Editing Kidney stone disease

{{Short description|Formation of mineral 'stones' in the urinary tract}}
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{{Use American English|date=December 2024}}
{{Good article}}
{{Infobox medical condition
| name            = Kidney stone disease
| image           = Nefrolit.jpg
| alt             = A color photograph of a kidney stone, 8&nbsp;millimetres in length.
| caption         = A kidney stone, {{convert|8|mm|in|1|sp=us}} in [[diameter]]
| field           = [[Urology]], [[nephrology]]
| synonyms        = Urolithiasis, kidney stone, renal calculus, nephrolithiasis, kidney stone disease,<ref name=Sch2014/>
| symptoms        = Severe pain in the lower back or abdomen, blood in the urine, vomiting, nausea<ref name=NIH2013/>
| complications   =
| onset           =
| duration        =
| causes          = [[Genetics|Genetic]] and environmental factors<ref name=NIH2013 />
| risks           =
| diagnosis       =  Based on symptoms, [[urinalysis|urine testing]], [[medical imaging]]<ref name=NIH2013 />
| differential    = [[Abdominal aortic aneurysm]], [[diverticulitis]], [[appendicitis]], [[pyelonephritis]]<ref>{{cite book| vauthors = Knoll T, Pearle MS |title=Clinical Management of Urolithiasis|date=2012|publisher=Springer Science & Business Media|isbn=978-3-642-28732-9|page=21|url=https://books.google.com/books?id=A2uak6SVgBUC&pg=PA21|language=en|url-status=live|archive-url=https://web.archive.org/web/20170908221053/https://books.google.com/books?id=A2uak6SVgBUC&pg=PA21|archive-date=8 September 2017|df=dmy-all}}</ref>
| prevention      = Drinking fluids such that more than two liters of urine are produced per day<ref name=Qa2014 />
| treatment       = [[Analgesic|Pain medication]], [[extracorporeal shock wave lithotripsy]], [[ureteroscopy]], [[percutaneous nephrolithotomy]]<ref name=NIH2013 />
| medication      =
| prognosis       =
| frequency       = 22.1 million (2015)<ref name=GBD2015Pre/>
| deaths          = 16,100 (2015)<ref name=GBD2015De/>
}}

<!-- Definition and symptoms -->
'''Kidney stone disease''' is known as '''renal calculus disease''', '''nephrolithiasis''' or '''urolithiasis''' in medical terminology. "Renal" is Latin for kidney, while "nephro" is the Greek equivalent. "Lithiasis" (Gr.) and "calculus" (Lat.- pl. calculi) both mean stone(s). Kidney stone disease is a [[crystallopathy]] and occurs when there are too many minerals in the urine and not enough liquid or hydration. This imbalance causes tiny pieces of crystal to aggregate and form hard masses, or calculi (stones) in the upper [[urinary tract]].<ref name=NIH2013/> Because renal calculi typically form in the [[kidney]], if small enough, they are able to leave the urinary tract via the urine stream.<ref name=NIH2013/> A small calculus may pass without causing [[Signs and symptoms|symptoms]].<ref name=NIH2013/> However, if a stone grows to more than {{convert|5|mm|in|adj=off|1|abbr=off|sp=us}}, it can cause blockage of the [[ureter]], resulting in extremely sharp and severe pain ([[renal colic]])   in the lower back that often radiates downward to the groin.<ref name=NIH2013 /><ref name=Miller2007>{{cite journal | vauthors = Miller NL, Lingeman JE | title = Management of kidney stones | journal = BMJ | volume = 334 | issue = 7591 | pages = 468–72 | date = March 2007 | pmid = 17332586 | pmc = 1808123 | doi = 10.1136/bmj.39113.480185.80 | df = dmy-all }}</ref> A calculus may also result in [[Hematuria|blood in the urine]], vomiting (due to severe pain), or [[Dysuria|painful urination]].<ref name=NIH2013>{{cite web|title=Kidney Stones in Adults|url=http://www.niddk.nih.gov/health-information/health-topics/urologic-disease/kidney-stones-in-adults/Pages/facts.aspx|access-date=22 May 2015|date=February 2013|url-status=dead|archive-url=https://web.archive.org/web/20150511192215/http://www.niddk.nih.gov/health-information/health-topics/urologic-disease/kidney-stones-in-adults/Pages/facts.aspx|archive-date=11 May 2015|df=dmy-all}}</ref> About half of all people who have had a kidney stone are likely to develop another within ten years.<ref name=BMJ2016/>

<!-- Cause and diagnosis -->
[[File:Calcinosis kidney.jpg|thumb|Kidney with calcium deposits and a partially formed stag horn  calculus.]]
[[File:Kidney stones.jpg|thumb|Kidney stones. One entire stone (the bigger one) and another one fragmented in small pieces after extracorporeal shock wave [[Lithotripsy|lithotripsy]] (ESWL).]]
Most calculi form by a combination of [[genetics]] and environmental factors.<ref name=NIH2013 /> Risk factors include [[hypercalciuria|high urine calcium levels]], [[obesity]], certain foods, some medications, [[calcium supplement]]s, [[gout]],  [[hyperparathyroidism]] and not drinking enough fluids.<ref name=NIH2013 /><ref name=BMJ2016/> Calculi form in the kidney when [[mineral]]s in [[urine]] are at high concentration.<ref name=NIH2013 /> The [[Medical diagnosis|diagnosis]] is usually based on symptoms, [[urinalysis|urine testing]], and [[medical imaging]].<ref name=NIH2013 /> [[Blood test]]s may also be useful.<ref name=NIH2013 /> Calculi are typically classified by their location: nephrolithiasis (in the kidney), ureterolithiasis (in the [[ureter]]), [[bladder stone|cystolithiasis]] (in the [[urinary bladder|bladder]]), or by [[chemical composition|what they are made of]] ([[calcium oxalate]], [[uric acid]], [[struvite]], [[cystine]]).<ref name=NIH2013 />

<!-- Prevention and treatment -->
In those who have had renal calculi, drinking fluids, especially water,  
is a way to prevent them. Drinking fluids such that more than two liters of urine are produced per day is recommended.<ref name=Qa2014 /> If fluid intake alone is not effective to prevent renal calculi, the medications [[thiazide diuretic]], [[citrate]], or [[allopurinol]] may be suggested.<ref name=Qa2014 /> Soft drinks containing [[phosphoric acid]] (typically [[cola]]s) should be avoided.<ref name=Qa2014>{{cite journal | vauthors = Qaseem A, Dallas P, Forciea MA, Starkey M, Denberg TD | title = Dietary and pharmacologic management to prevent recurrent nephrolithiasis in adults: a clinical practice guideline from the American College of Physicians | journal = Annals of Internal Medicine | volume = 161 | issue = 9 | pages = 659–67 | date = November 2014 | pmid = 25364887 | doi = 10.7326/M13-2908 | doi-access = free }}</ref> When a calculus causes no symptoms, [[watchful waiting|no treatment]] is needed.<ref name=NIH2013 /> For those with symptoms, [[Analgesic|pain control]] is usually the first measure, using medications such as [[nonsteroidal anti-inflammatory drug]]s or [[opioid]]s.<ref name=Miller2007/><ref name=Af2015>{{cite journal | vauthors = Afshar K, Jafari S, Marks AJ, Eftekhari A, MacNeily AE | title = Nonsteroidal anti-inflammatory drugs (NSAIDs) and non-opioids for acute renal colic | journal = The Cochrane Database of Systematic Reviews | volume = 2015 | issue = 6 | pages = CD006027 | date = June 2015 | pmid = 26120804 | doi = 10.1002/14651858.CD006027.pub2 | pmc = 10981792 }}</ref> Larger calculi may be helped to pass with the medication [[tamsulosin]]<ref name=Wang2016>{{cite journal | vauthors = Wang RC, Smith-Bindman R, Whitaker E, Neilson J, Allen IE, Stoller ML, Fahimi J | title = Effect of Tamsulosin on Stone Passage for Ureteral Stones: A Systematic Review and Meta-analysis | journal = Annals of Emergency Medicine | volume = 69 | issue = 3 | pages = 353–361.e3 | date = March 2017 | pmid = 27616037 | doi = 10.1016/j.annemergmed.2016.06.044 | doi-access = free }}</ref> or may require procedures such as [[extracorporeal shock wave lithotripsy]], [[ureteroscopy]], or [[percutaneous nephrolithotomy]].<ref name=NIH2013 />

<!-- Epidemiology and history -->
Renal calculi have affected humans throughout history with a description of surgery to remove them dating from as early as 600 BC in ancient India by [[Sushruta]].<ref name="Sch2014">{{cite book| vauthors = Schulsinger DA |title=Kidney Stone Disease: Say NO to Stones! |date=2014 |publisher=Springer |isbn=978-3-319-12105-5 |page=27 |url= https://books.google.com/books?id=2ADRBQAAQBAJ&pg=PA27 |language=en |url-status=live |archive-url= https://web.archive.org/web/20170908221053/https://books.google.com/books?id=2ADRBQAAQBAJ&pg=PA27 |archive-date=8 September 2017|df=dmy-all}}</ref> Between 1% and 15% of people globally are affected by renal calculi at some point in their lives.<ref name=BMJ2016/><ref name=":3">{{cite journal | vauthors = Abufaraj M, Xu T, Cao C, Waldhoer T, Seitz C, D'andrea D, Siyam A, Tarawneh R, Fajkovic H, Schernhammer E, Yang L, Shariat SF | title = Prevalence and Trends in Kidney Stone Among Adults in the USA: Analyses of National Health and Nutrition Examination Survey 2007-2018 Data | journal = European Urology Focus | volume = 7 | issue = 6 | pages = 1468–1475 | date = November 2021 | pmid = 32900675 | doi = 10.1016/j.euf.2020.08.011 | s2cid = 221572651 | doi-access = free }}</ref> In 2015, 22.1 million cases occurred,<ref name=GBD2015Pre>{{cite journal | title = Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015 | journal = Lancet | volume = 388 | issue = 10053 | pages = 1545–1602 | date = October 2016 | pmid = 27733282 | pmc = 5055577 | doi = 10.1016/S0140-6736(16)31678-6 | collaboration = GBD 2015 Disease and Injury Incidence and Prevalence Collaborators | last1 = Vos | first1 = Theo | last2 = Allen | first2 = Christine | last3 = Arora | first3 = Megha | last4 = Barber | first4 = Ryan M. | last5 = Bhutta | first5 = Zulfiqar A. | last6 = Brown | first6 = Alexandria | last7 = Carter | first7 = Austin | last8 = Casey | first8 = Daniel C. | last9 = Charlson | first9 = Fiona J. | last10 = Chen | first10 = Alan Z. | last11 = Coggeshall | first11 = Megan | last12 = Cornaby | first12 = Leslie | last13 = Dandona | first13 = Lalit | last14 = Dicker | first14 = Daniel J. | last15 = Dilegge | first15 = Tina | last16 = Erskine | first16 = Holly E. | last17 = Ferrari | first17 = Alize J. | last18 = Fitzmaurice | first18 = Christina | last19 = Fleming | first19 = Tom | last20 = Forouzanfar | first20 = Mohammad H. | last21 = Fullman | first21 = Nancy | last22 = Gething | first22 = Peter W. | last23 = Goldberg | first23 = Ellen M. | last24 = Graetz | first24 = Nicholas | last25 = Haagsma | first25 = Juanita A. | last26 = Hay | first26 = Simon I. | last27 = Johnson | first27 = Catherine O. | last28 = Kassebaum | first28 = Nicholas J. | last29 = Kawashima | first29 = Toana | last30 = Kemmer | first30 = Laura }}</ref> resulting in about 16,100 deaths.<ref name=GBD2015De>{{cite journal | title = Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980-2015: a systematic analysis for the Global Burden of Disease Study 2015 | journal = Lancet | volume = 388 | issue = 10053 | pages = 1459–1544 | date = October 2016 | pmid = 27733281 | pmc = 5388903 | doi = 10.1016/s0140-6736(16)31012-1 | collaboration = GBD 2015 Disease and Injury Incidence and Prevalence Collaborators | last1 = Wang | first1 = Haidong | last2 = Naghavi | first2 = Mohsen | last3 = Allen | first3 = Christine | last4 = Barber | first4 = Ryan M. | last5 = Bhutta | first5 = Zulfiqar A. | last6 = Carter | first6 = Austin | last7 = Casey | first7 = Daniel C. | last8 = Charlson | first8 = Fiona J. | last9 = Chen | first9 = Alan Zian | last10 = Coates | first10 = Matthew M. | last11 = Coggeshall | first11 = Megan | last12 = Dandona | first12 = Lalit | last13 = Dicker | first13 = Daniel J. | last14 = Erskine | first14 = Holly E. | last15 = Ferrari | first15 = Alize J. | last16 = Fitzmaurice | first16 = Christina | last17 = Foreman | first17 = Kyle | last18 = Forouzanfar | first18 = Mohammad H. | last19 = Fraser | first19 = Maya S. | last20 = Fullman | first20 = Nancy | last21 = Gething | first21 = Peter W. | last22 = Goldberg | first22 = Ellen M. | last23 = Graetz | first23 = Nicholas | last24 = Haagsma | first24 = Juanita A. | last25 = Hay | first25 = Simon I. | last26 = Huynh | first26 = Chantal | last27 = Johnson | first27 = Catherine O. | last28 = Kassebaum | first28 = Nicholas J. | last29 = Kinfu | first29 = Yohannes | last30 = Kulikoff | first30 = Xie Rachel }}</ref> They have become more common in the [[Western world]] since the 1970s.<ref name=BMJ2016>{{cite journal | vauthors = Morgan MS, Pearle MS | title = Medical management of renal stones | journal = BMJ | volume = 352 | pages = i52 | date = March 2016 | pmid = 26977089 | doi = 10.1136/bmj.i52 | s2cid = 28313474 }}</ref><ref>{{cite journal |last1=Stamatelou |first1=Kiriaki K. |last2=Francis |first2=Mildred E. |last3=Jones |first3=Camille A. |last4=Nyberg |first4=Leroy M. |last5=Curhan |first5=Gary C. |date=May 2003 |title=Time trends in reported prevalence of kidney stones in the United States: 1976–199411.See Editorial by Goldfarb, p. 1951. |journal=Kidney International |language=en |volume=63 |issue=5 |pages=1817–1823 |doi=10.1046/j.1523-1755.2003.00917.x|pmid=12675858 |doi-access=free }}</ref> Generally, more men are affected than women.<ref name=NIH2013 /><ref name=":3" /> The prevalence and incidence of the disease rises worldwide and continues to be challenging for patients, physicians, and healthcare systems alike. In this context, epidemiological studies are striving to elucidate the worldwide changes in the patterns and the burden of the disease and identify modifiable risk factors that contribute to the development of renal calculi.<ref>{{cite journal |last1=Stamatelou |first1=Kyriaki |last2=Goldfarb |first2=David S. |date=January 2023 |title=Epidemiology of Kidney Stones |journal=Healthcare |language=en |volume=11 |issue=3 |pages=424 |doi=10.3390/healthcare11030424 |pmid=36766999 |pmc=9914194 |issn=2227-9032|doi-access=free }}{{Creative Commons text attribution notice|cc = by4|from this source = yes}}</ref>
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== Signs and symptoms ==
[[File:Pos-renal.png|thumb|upright=1.2|Diagram showing the typical location of [[renal colic]], below the rib cage to just above the [[pelvis]]]]
The hallmark of a stone that obstructs the ureter or renal pelvis is excruciating, intermittent pain that radiates from the flank to the groin or to the inner thigh.<ref name=Cutler2007 /> This is due to the transfer of referred pain signals from the lower thoracic splanchnic nerves to the lumbar splanchnic nerves as the stone passes down from the kidney or proximal ureter to the distal ureter. This pain, known as [[renal colic]], is often described as one of the strongest pain sensations known.<ref name=Wolf2011b /> Renal colic caused by kidney stones is commonly accompanied by [[urinary urgency]], restlessness, [[hematuria]], sweating, nausea, and vomiting. It typically comes in waves lasting 20 to 60 minutes caused by [[Peristalsis|peristaltic]] contractions of the ureter as it attempts to expel the stone.<ref name=Cutler2007 />

The [[embryology|embryological]] link between the urinary tract, the [[Reproductive system|genital system]], and the [[Human gastrointestinal tract|gastrointestinal tract]] is the basis of the radiation of pain to the [[gonad]]s, as well as the nausea and vomiting that are also common in urolithiasis.<ref name=Pearle2007 /> [[Postrenal azotemia]] and hydronephrosis can be observed following the obstruction of urine flow through one or both ureters.<ref name=Cavendish2008 />

Pain in the lower-left quadrant can sometimes be confused with [[diverticulitis]] because the [[sigmoid colon]] overlaps the ureter, and the exact location of the pain may be difficult to isolate due to the proximity of these two structures.

== Risk factors ==
[[Dehydration]] from low fluid intake is a factor in stone formation.<ref name=Cutler2007 /><ref name="Curhan-1996">{{cite journal | vauthors = Curhan GC, Willett WC, Rimm EB, Spiegelman D, Stampfer MJ | title = Prospective study of beverage use and the risk of kidney stones | journal = American Journal of Epidemiology | volume = 143 | issue = 3 | pages = 240–7 | date = February 1996 | pmid = 8561157 | doi = 10.1093/oxfordjournals.aje.a008734 | doi-access = free }}</ref> Individuals living in warm climates are at higher risk due to increased fluid loss.<ref name=":0">{{cite book|title=Medical-surgical nursing : assessment and management of clinical problems| vauthors = Lewis SM |isbn=978-0-323-32852-4|oclc=944472408|year = 2017| publisher = Elsevier }}</ref> Obesity, immobility, and sedentary lifestyles are other leading risk factors.<ref name=":0" />

High dietary intake of animal [[protein]],<ref name=Cutler2007 /> [[sodium]], sugars including honey, refined [[sugar]]s, [[fructose]] and [[high fructose corn syrup]],<ref name=HFCS /> and excessive consumption of fruit juices may increase the risk of kidney stone formation due to increased [[uric acid]] excretion and elevated [[Oxalate|urinary oxalate]] levels (whereas tea, coffee, wine and beer may decrease the risk).<ref name=":0" /><ref name="Curhan-1996" />

Kidney stones can result from an underlying metabolic condition, such as [[distal renal tubular acidosis]],<ref name=Moe2006 /> [[Dent's disease]],<ref name=Thakker2000 /> [[hyperparathyroidism]],<ref name=NIDDK2006 /> primary [[hyperoxaluria]],<ref name=Hoppe2003 /> or [[medullary sponge kidney]]. 3–20% of people who form kidney stones have medullary sponge kidney.<ref name=Reilly2005Ch13 /><ref name=NIDDK20086235 />

Kidney stones are more common in people with [[Crohn's disease]];<ref name=NDDIC2006 /> Crohn's disease is associated with [[hyperoxaluria]] and malabsorption of magnesium.<ref name="pmid4416806">{{cite journal | vauthors = Farmer RG, Mir-Madjlessi SH, Kiser WS | title = Urinary excretion of oxalate, calcium, magnesium, and uric acid in inflammatory bowel disease | journal = Cleveland Clinic Quarterly | volume = 41 | issue = 3 | pages = 109–17 | year = 1974 | pmid = 4416806 | doi = 10.3949/ccjm.41.3.109 | doi-broken-date = 9 December 2024 | url = http://www.ccjm.org/content/41/3/109.short | access-date = 1 November 2013 | archive-date = 20 March 2020 | archive-url = https://web.archive.org/web/20200320210418/https://www.ccjm.org/content/41/3/109.short | url-status = live }}</ref>

A person with recurrent kidney stones may be screened for such disorders. This is typically done with a 24-hour urine collection. The urine is analyzed for features that promote stone formation.<ref name=Cavendish2008 />

=== Calcium oxalate ===
[[File:Kidney stone composed of calcium oxalate showing sharp edges.jpg|thumb|A kidney stone (yellow) composed of calcium oxalate, next to a tourmaline gemstone for scale]]Calcium is one component of the most common type of human kidney stones, [[calcium oxalate]]. Some studies suggest that people who take calcium or [[vitamin D]] as a [[dietary supplement]] have a higher risk of developing kidney stones.<ref name=IOM2010p413 /><ref name=Johri2010 />  In the [[United States]], kidney stone formation was used as an indicator of excess calcium intake by the [[Reference Daily Intake]] committee for calcium in adults.<ref name=IOM2010p8 />

In the early 1990s, a study conducted for the [[Women's Health Initiative]] in the US found that postmenopausal women who consumed&nbsp;1000&nbsp;mg of supplemental calcium and 400&nbsp;[[international unit]]s of [[vitamin D]] per day for seven years had a 17% higher risk of developing kidney stones than subjects taking a [[placebo]].<ref name=IOM2010p413 /> The [[Nurses' Health Study]] also showed an association between supplemental calcium intake and kidney stone formation.<ref name=Johri2010 />

Unlike supplemental calcium, high intakes of dietary calcium do not appear to cause kidney stones and may actually protect against their development.<ref name=Johri2010 /><ref name=IOM2010p413 /> This is perhaps related to the role of calcium in binding ingested oxalate in the gastrointestinal tract. As the amount of calcium intake decreases, the amount of oxalate available for absorption into the bloodstream increases; this oxalate is then excreted in greater amounts into the urine by the kidneys. In the urine, oxalate is a very strong promoter of calcium oxalate precipitation—about 15 times stronger than calcium.

A 2004 study found that diets low in calcium are associated with a higher overall risk for kidney stone formation.<ref name=Parmar2004 /> For most individuals, other risk factors for kidney stones, such as high intakes of dietary oxalates and low fluid intake, play a greater role than calcium intake.<ref name=Liebman2011 />

=== Other electrolytes ===
Calcium is not the only [[electrolyte]] that influences the formation of kidney stones. For example, by increasing urinary calcium excretion, high dietary sodium may increase the risk of stone formation.<ref name=Johri2010 />

Drinking [[Water fluoridation|fluoridated tap water]] may increase the risk of kidney stone formation by a similar mechanism, though further epidemiologic studies are warranted to determine whether fluoride in drinking water is associated with an increased incidence of kidney stones.<ref name=NAS2006 /> High dietary intake of [[potassium]] appears to reduce the risk of stone formation because potassium promotes the urinary excretion of [[citrate]], an inhibitor of calcium crystal formation.<ref>{{cite journal | vauthors = Ferraro PM, Mandel EI, Curhan GC, Gambaro G, Taylor EN | title = Dietary Protein and Potassium, Diet-Dependent Net Acid Load, and Risk of Incident Kidney Stones | journal = Clinical Journal of the American Society of Nephrology | volume = 11 | issue = 10 | pages = 1834–1844 | date = October 2016 | pmid = 27445166 | pmc = 5053786 | doi = 10.2215/CJN.01520216 }}</ref>

Kidney stones are more likely to develop, and to grow larger, if a person has low [[Magnesium in biology|dietary magnesium]]. Magnesium inhibits stone formation.<ref name="Riley-2013">{{cite journal | vauthors = Riley JM, Kim H, Averch TD, Kim HJ | title = Effect of magnesium on calcium and oxalate ion binding | journal = Journal of Endourology | volume = 27 | issue = 12 | pages = 1487–92 | date = December 2013 | pmid = 24127630 | pmc = 3883082 | doi = 10.1089/end.2013.0173 }}</ref>

=== Animal protein ===
[[Western pattern diet|Diets in Western nations]] typically contain a large proportion of [[protein#nutrition|animal protein]]. Eating animal protein creates an acid load that increases urinary excretion of calcium and uric acid and reduced citrate. Urinary excretion of excess sulfurous [[amino acid]]s (e.g., [[cysteine]] and [[methionine]]), uric acid, and other acidic [[metabolite]]s from animal protein acidifies the urine, which promotes the formation of kidney stones.<ref name="Negri-2013">{{cite journal | vauthors = Negri AL, Spivacow FR, Del Valle EE | title = [Diet in the treatment of renal lithiasis. Pathophysiological basis] | journal = Medicina | volume = 73 | issue = 3 | pages = 267–71 | year = 2013 | pmid = 23732207 }}</ref> Low urinary-citrate excretion is also commonly found in those with a high dietary intake of animal protein, whereas vegetarians tend to have higher levels of citrate excretion.<ref name=Johri2010 /> Low urinary citrate, too, promotes stone formation.<ref name="Negri-2013" />

=== Vitamins ===
The evidence linking [[vitamin C]] supplements with an increased rate of kidney stones is inconclusive.<ref name=Goodwin1998 /><ref>{{cite journal | vauthors = Traxer O, Pearle MS, Gattegno B, Thibault P | title = [Vitamin C and stone risk. Review of the literature] | journal = Progres en Urologie | volume = 13 | issue = 6 | pages = 1290–4 | date = December 2003 | pmid = 15000301 }}</ref> The excess dietary intake of vitamin C might increase the risk of calcium-oxalate stone formation.<ref>{{cite journal | vauthors = Ferraro PM, Curhan GC, Gambaro G, Taylor EN | title = Total, Dietary, and Supplemental Vitamin C Intake and Risk of Incident Kidney Stones | journal = American Journal of Kidney Diseases | volume = 67 | issue = 3 | pages = 400–7 | date = March 2016 | pmid = 26463139 | pmc = 4769668 | doi = 10.1053/j.ajkd.2015.09.005 }}</ref> The link between vitamin D intake and kidney stones is also tenuous.

Excessive vitamin D supplementation may increase the risk of stone formation by increasing the intestinal absorption of calcium; correction of a deficiency does not.<ref name=Johri2010 />

== Pathophysiology ==
[[File:Staghorn Kidney Stone Progression.png|thumb|Small crystals formed in the kidney. The most common crystals are made of calcium oxalate and they are generally 4–5&nbsp;mm. Staghorn kidney stones are considerably larger. 1. Calcium and oxalate come together to make the crystal nucleus. Supersaturation promotes their combination (as does inhibition.) 2. Continued deposition at the renal papillae leads to the growth of the kidney stones. 3. Kidney stones grow and collect debris. In the case where the kidney stones block all routes to the renal papillae, this can cause extreme discomfort and pain. 4. The complete staghorn stone forms and retention occurs. Smaller solids that break off can become trapped in the urinary glands causing discomfort. 5. Displaced stones travel through the ureter. If they cannot be broken down, they must be physically removed by a surgeon.]]

=== Supersaturation of urine ===
Kidney stones are primarily composed of calcium salts, with the most common being calcium oxalate (70-80%), followed by calcium phosphate and uric acid. When urine contains high concentrations of these ions, they can form crystals and eventually stones.<ref name="pmid26439475">{{cite journal |vauthors=Phillips R, Hanchanale VS, Myatt A, Somani B, Nabi G, Biyani CS |title=Citrate salts for preventing and treating calcium containing kidney stones in adults |journal=Cochrane Database Syst Rev |volume=2015 |issue=10 |pages=CD010057 |date=October 2015 |pmid=26439475 |pmc=9578669 |doi=10.1002/14651858.CD010057.pub2 |url=}}</ref>

The formation of kidney stones occurs in three main phases:<ref name="pmid26439475"/>
# [[nucleation]] (initial crystal formation)
# growth (expansion of single crystals)
# aggregation (clumping together of multiple crystals)<ref name="pmid26439475"/>

When the urine becomes [[Supersaturation|supersaturated]] (when the urine [[solvent]] contains more [[wikt:Special:Search/solute|solutes]] than it can hold in [[Solution (chemistry)|solution]]) with one or more calculogenic (crystal-forming) substances, initial [[seed crystal]]s may form through the process of [[nucleation]].<ref name=Reilly2005Ch13 /> Heterogeneous nucleation (where there is a solid surface present on which a crystal can grow) proceeds more rapidly than homogeneous nucleation (where a crystal must grow in a liquid medium with no such surface), because it requires less energy. Adhering to cells on the surface of a [[renal papilla]], a seed crystal can grow and aggregate into an organized mass. Depending on the chemical composition of the crystal, the stone-forming process may proceed more rapidly when the urine pH is unusually high or low.<ref name=Reilly2005Ch14 />

Supersaturation of the urine with respect to a calculogenic compound is pH-dependent. For example, at a pH of 7.0, the solubility of uric acid in urine is 158&nbsp;mg/100&nbsp;mL. Reducing the pH to 5.0 decreases the [[solubility]] of [[uric acid]] to less than 8&nbsp;mg/100&nbsp;mL. The formation of uric-acid stones requires a combination of [[hyperuricosuria]] (high urine uric-acid levels) and low urine pH; hyperuricosuria alone is not associated with uric-acid stone formation if the urine pH is alkaline.<ref name=Knudsen2007 /> Supersaturation of the urine is a necessary, but not a sufficient, condition for the development of any urinary calculus.<ref name=Reilly2005Ch13 /> Supersaturation is likely the underlying cause of uric acid and [[cystine]] stones, but calcium-based stones (especially [[calcium oxalate]] stones) may have a more complex cause.<ref name=Wolf2011p />

=== Randall's plaque ===
While supersaturation of urine may lead to [[crystalluria]], it does not necessarily promote the formation of a kidney stone because the particle may not reach the sufficient size needed for renal attachment.<ref>{{cite journal | vauthors = Robertson WG, Peacock M, Nordin BE | title = Calcium crystalluria in recurrent renal-stone formers | journal = Lancet | volume = 2 | issue = 7610 | pages = 21–24 | date = July 1969 | pmid = 4182793 | doi = 10.1016/S0140-6736(69)92598-7 }}</ref><ref>{{cite journal | vauthors = Elliot JS, Rabinowitz IN | title = Calcium oxalate crystalluria: crystal size in urine | journal = The Journal of Urology | volume = 123 | issue = 3 | pages = 324–327 | date = March 1980 | pmid = 7359628 | doi = 10.1016/S0022-5347(17)55918-2 }}</ref> On the other hand, Randall's plaques, which were first identified by Alexander Randall in 1937,<ref>{{cite journal | vauthors = Randall A | title = The Origin and Growth of Renal Calculi | journal = Annals of Surgery | volume = 105 | issue = 6 | pages = 1009–1027 | date = June 1937 | pmid = 17856988 | pmc = 1390483 | doi = 10.1097/00000658-193706000-00014 }}</ref> are [[calcium phosphate]] deposits that form in the papillary interstitium and are thought to be the nidus required for stone development.<ref>{{cite journal | vauthors = Ratkalkar VN, Kleinman JG | title = Mechanisms of Stone Formation | journal = Clinical Reviews in Bone and Mineral Metabolism | volume = 9 | issue = 3–4 | pages = 187–197 | date = December 2011 | pmid = 22229020 | pmc = 3252394 | doi = 10.1007/s12018-011-9104-8 }}</ref> In addition to Randall's plugs, which form in the [[Duct of Bellini]], these structures can generate reactive oxygen species that further enhance stone formation.<ref>{{cite journal | vauthors = Khan SR | title = Reactive oxygen species, inflammation and calcium oxalate nephrolithiasis | journal = Translational Andrology and Urology | volume = 3 | issue = 3 | pages = 256–276 | date = September 2014 | pmid = 25383321 | pmc = 4220551 | doi = 10.3978/j.issn.2223-4683.2014.06.04 }}</ref>

=== Pathogenic bacteria ===
Some [[bacteria]] have roles in promoting stone formation. Specifically, [[urease-positive]] bacteria, such as ''[[Proteus mirabilis]]'' can produce the [[enzyme]] [[urease]], which converts [[urea]] to [[ammonia]] and [[carbon dioxide]].<ref>{{cite journal | vauthors = Jones BD, Mobley HL | title = Proteus mirabilis urease: genetic organization, regulation, and expression of structural genes | journal = Journal of Bacteriology | volume = 170 | issue = 8 | pages = 3342–3349 | date = August 1988 | pmid = 2841283 | pmc = 211300 | doi = 10.1128/jb.170.8.3342-3349.1988 }}</ref> This increases the urinary [[pH]] and promotes [[struvite]] stone formation. Additionally, non-urease producing bacteria can provide bacterial components that promote [[calcium oxalate]] crystallization, though this mechanism is poorly understood.<ref>{{cite journal | vauthors = Chmiel JA, Stuivenberg GA, Alathel A, Gorla J, Grohe B, Razvi H, Burton JP, Bjazevic J | title = High-Throughput in vitro Gel-Based Plate Assay to Screen for Calcium Oxalate Stone Inhibitors | journal = Urologia Internationalis | pages = 616–622 | date = December 2021 | volume = 106 | issue = 6 | pmid = 34883484 | doi = 10.1159/000519842 | s2cid = 245012979 }}</ref><ref>{{cite journal | vauthors = Kanlaya R, Naruepantawart O, Thongboonkerd V | title = Flagellum Is Responsible for Promoting Effects of Viable ''Escherichia coli'' on Calcium Oxalate Crystallization, Crystal Growth, and Crystal Aggregation | journal = Frontiers in Microbiology | volume = 10 | pages = 2507 | date = 2019-11-05 | pmid = 31749785 | pmc = 6848068 | doi = 10.3389/fmicb.2019.02507 | doi-access = free }}</ref>

=== Inhibitors of stone formation ===
Normal [[urine]] contains [[Chelation|chelating]] agents, such as [[Citric acid|citrate]], that inhibit the [[nucleation]], [[Crystal growth|growth]], and aggregation of calcium-containing crystals. Other [[endogenous]] inhibitors include [[calgranulin]] (an [[S-100 protein|S-100 calcium-binding protein]]), [[Tamm–Horsfall protein]], [[glycosaminoglycan]]s, uropontin (a form of [[osteopontin]]), [[nephrocalcin]] (an acidic [[glycoprotein]]), pro[[thrombin]] F1 peptide, and [[Alpha-1-microglobulin/bikunin precursor|bikunin]] ([[uronic acid]]-rich protein). The biochemical mechanisms of action of these substances have not yet been thoroughly elucidated. However, when these substances fall below their normal proportions, stones can form from an aggregation of crystals.<ref name=Coe2005 />

Sufficient dietary intake of [[magnesium]] and [[citrate]] inhibits the formation of calcium oxalate and calcium phosphate stones; in addition, magnesium and citrate operate synergistically to inhibit kidney stones. The efficacy of magnesium in subduing stone formation and growth is [[dose-dependent]].<ref name=Johri2010 /><ref name="Riley-2013" /><ref name="del Valle-2013">{{cite journal | vauthors = del Valle EE, Spivacow FR, Negri AL | title = [Citrate and renal stones] | journal = Medicina | volume = 73 | issue = 4 | pages = 363–8 | year = 2013 | pmid = 23924538 }}</ref>

=== Hypocitraturia ===
Hypocitraturia or low urinary-citrate excretion (variably defined as less than 320&nbsp;mg/day) can be a contributing cause of kidney stones in up to 2/3 of cases. The protective role of citrate is linked to several mechanisms; citrate reduces urinary supersaturation of calcium salts by forming soluble complexes with calcium ions and by inhibiting crystal growth and aggregation. Therapy with [[potassium citrate]]  is commonly prescribed in clinical practice to increase urinary citrate and to reduce stone formation rates. [[Alkali citrate]] is also used to increase urine citrate levels. It can be prescribed or found over-the-counter in pill, liquid or powder form.<ref>{{cite web |title=Educate Your Patients about Kidney Stones |url=https://www.kidney.org/sites/default/files/moonstone-professional-education-teaching-card-final.pdf |archive-url=https://web.archive.org/web/20201026133550/https://www.kidney.org/sites/default/files/moonstone-professional-education-teaching-card-final.pdf |archive-date=2020-10-26 |url-status=live |website=kidney.org}}</ref><ref>{{cite journal | vauthors = Caudarella R, Vescini F | title = Urinary citrate and renal stone disease: the preventive role of alkali citrate treatment | journal = Archivio Italiano di Urologia, Andrologia | volume = 81 | issue = 3 | pages = 182–7 | date = September 2009 | pmid = 19911682 |url=https://www.researchgate.net/publication/38087757 }}</ref>

== Diagnosis ==
Diagnosis of kidney stones is made on the basis of information obtained from the history, physical examination, [[urinalysis]], and [[radiography|radiographic]] studies.<ref name=Anoia2009 /> [[Medical diagnosis|Clinical diagnosis]] is usually made on the basis of the location and severity of the pain, which is typically colicky in nature (comes and goes in [[spasm]]odic  waves). Pain in the back occurs when calculi produce an obstruction in the kidney.<ref name=Weaver2002 /> Physical examination may reveal fever and [[Murphy's punch sign|tenderness at the costovertebral angle]] on the affected side.<ref name=Anoia2009 />

=== Imaging studies ===
Calcium-containing stones are relatively [[Radiodensity|radiodense]] (opaque to [[X-ray]]s), and they can often be detected by a traditional [[radiography]] of the [[abdomen]] that includes the [[kidneys, ureters, and bladder x-ray|kidneys, ureters, and bladder]] (KUB film{{Clarify|date=February 2024}}).<ref name=Pietrow2006 /> KUB{{Clarify|date=February 2024}} radiography, although useful in monitoring size of stone or passage of stone in stone formers, might not be useful in the acute setting due to low sensitivity.<ref>{{cite journal |last1=Brisbane |first1=Wayne |last2=Bailey |first2=Michael R. |last3=Sorensen |first3=Mathew D. |date=November 2016 |title=An overview of kidney stone imaging techniques |journal=Nature Reviews. Urology |volume=13 |issue=11 |pages=654–662 |doi=10.1038/nrurol.2016.154 |issn=1759-4812 |pmc=5443345 |pmid=27578040}}</ref> Some 60% of all renal stones are radiopaque.<ref name=SmithCentennial2000 /><ref name=Bushinsky2007 /> In general, calcium phosphate stones have the greatest density, followed by calcium oxalate and magnesium ammonium phosphate stones. [[Cystine]] calculi are only faintly [[radiodense]], while [[uric acid]] stones are usually entirely [[radiolucent]].<ref name=Smith1999 />

In people with a history of stones, those who are less than 50 years of age and are presenting with the symptoms of stones without any concerning signs do not require [[Helical cone beam computed tomography|helical CT scan]] imaging.<ref>{{cite web|author1=American College of Emergency Physicians|title=Ten Things Physicians and Patients Should Question|url=http://www.choosingwisely.org/doctor-patient-lists/american-college-of-emergency-physicians/|website=Choosing Wisely|access-date=14 January 2015|date=27 October 2014|url-status=live|archive-url=https://web.archive.org/web/20140307012443/http://www.choosingwisely.org/doctor-patient-lists/american-college-of-emergency-physicians/|archive-date=7 March 2014|df=dmy-all}}</ref> A [[CT scan|computed tomography]] (CT) scan is also not typically recommended in children.<ref>{{cite web|title=American Urological Association {{!}} Choosing Wisely|url=http://www.choosingwisely.org/societies/american-urological-association/|website=www.choosingwisely.org|access-date=28 May 2017|url-status=dead|archive-url=https://web.archive.org/web/20170223133729/http://www.choosingwisely.org/societies/american-urological-association/|archive-date=23 February 2017|df=dmy-all}}</ref>

Otherwise a noncontrast helical CT scan with {{convert|5|mm|in|1|sp=us}} sections is the diagnostic method to use to detect kidney stones and confirm the diagnosis of kidney stone disease.<ref name=Pearle2007 /><ref name=Anoia2009 /><ref name=SmithCentennial2000 /><ref name=Fang2009 /><ref name=Miller2007 /> Near all stones are detectable on CT scans with the exception of those composed of certain drug residues in the urine,<ref name=Pietrow2006 /> such as from [[indinavir]].

Where a CT scan is unavailable, an [[intravenous pyelogram]] may be performed to help confirm the diagnosis of [[urolithiasis]]. This involves [[Intravenous therapy|intravenous injection]] of a [[Radiocontrast|contrast agent]] followed by a KUB film. [[Urolith]]s present in the kidneys, ureters, or bladder may be better defined by the use of this contrast agent. Stones can also be detected by a [[retrograde pyelogram]], where a similar contrast agent is injected directly into the distal ostium of the ureter (where the ureter terminates as it enters the bladder).<ref name=SmithCentennial2000 />

[[Renal ultrasonography]] can sometimes be useful, because it gives details about the presence of [[hydronephrosis]], suggesting that the stone is blocking the outflow of urine.<ref name=Pietrow2006 /> Radiolucent stones, which do not appear on KUB, may show up on ultrasound imaging studies. Other advantages of renal ultrasonography include its low cost and absence of [[Radiology|radiation exposure]]. Ultrasound imaging is useful for detecting stones in situations where X-rays or CT scans are discouraged, such as in children or pregnant women.<ref name="semins">{{cite journal | vauthors = Semins MJ, Matlaga BR | title = Management of urolithiasis in pregnancy | journal = International Journal of Women's Health | volume = 5 | pages = 599–604 | date = September 2013 | pmid = 24109196 | pmc = 3792830 | doi = 10.2147/ijwh.s51416 | doi-access = free }}</ref> Despite these advantages, renal ultrasonography in 2009 was not considered a substitute for noncontrast helical CT scan in the initial diagnostic evaluation of urolithiasis.<ref name=Fang2009 /> The main reason for this is that, compared with CT, renal ultrasonography more often fails to detect small stones (especially ureteral stones) and other serious disorders that could be causing the symptoms.<ref name=Cutler2007 />

On the contrary, a 2014 study suggested that ultrasonography should be used as the initial diagnostic imaging test, with further imaging studies be performed at the discretion of the physician on the basis of clinical judgment, and using [[ultrasonography]] rather than [[CT scan|CT]] as an initial diagnostic test results in less radiation exposure and equally good outcome.<ref>{{cite journal | vauthors = Smith-Bindman R, Aubin C, Bailitz J, Bengiamin RN, Camargo CA, Corbo J, Dean AJ, Goldstein RB, Griffey RT, Jay GD, Kang TL, Kriesel DR, Ma OJ, Mallin M, Manson W, Melnikow J, Miglioretti DL, Miller SK, Mills LD, Miner JR, Moghadassi M, Noble VE, Press GM, Stoller ML, Valencia VE, Wang J, Wang RC, Cummings SR | title = Ultrasonography versus computed tomography for suspected nephrolithiasis | journal = The New England Journal of Medicine | volume = 371 | issue = 12 | pages = 1100–10 | date = September 2014 | pmid = 25229916 | doi = 10.1056/NEJMoa1404446 | s2cid = 4511678 | url = https://escholarship.org/content/qt1cm5f8cd/qt1cm5f8cd.pdf?t=nwl44w | access-date = 25 September 2019 | archive-date = 14 March 2020 | archive-url = https://web.archive.org/web/20200314051953/https://escholarship.org/content/qt1cm5f8cd/qt1cm5f8cd.pdf?t=nwl44w | url-status = live }}</ref>

<gallery>
File:Kidney stones abdominal X-ray.jpg|Bilateral kidney stones can be seen on this [[Kidneys, ureters, and bladder x-ray|KUB radiograph]]. There are [[phlebolith]]s in the pelvis, which can be misinterpreted as [[bladder stone]]s.
File:3mmstone.png|[[Transverse plane|Axial]] [[X-ray computed tomography|CT scan]] of abdomen without contrast, showing a 3-mm stone (marked by an arrow) in the left proximal [[ureter]]
File:Ultrasonography of renal stone located at the pyeloureteric junction.jpg|[[Renal ultrasonograph]] of a stone located at the pyeloureteric junction with accompanying hydronephrosis.
File:CT measurement of kidney stone in soft tissue and bone window.jpg|Measurement of a 5.6&nbsp;mm large kidney stone in soft tissue versus skeletal [[CT scan#Process|CT window]].
</gallery>

=== Laboratory examination ===
[[File:Struvite crystals dog with scale 1.JPG|thumb|[[Struvite]] crystals found on [[Urine microscopy|microscopic examination]] of the urine]]

Laboratory investigations typically carried out include:<ref name=Anoia2009 /><ref name=Fang2009 /><ref name=Pietrow2006 /><ref name=NIDDK2007 />
* [[Urine microscopy|microscopic examination]] of the urine, which may show [[red blood cell]]s, bacteria, [[leukocyte]]s, [[urinary cast]]s, and crystals;
* urine culture to identify any infecting organisms present in the urinary tract and [[Kirby-Bauer antibiotic testing|sensitivity]] to determine the susceptibility of these organisms to specific antibiotics;
* [[complete blood count]], looking for [[neutrophilia]] (increased [[neutrophil granulocyte]] count) suggestive of bacterial infection, as seen in the setting of struvite stones;
* [[renal function]] tests to look for abnormally high blood calcium levels ([[Hypercalcaemia|hypercalcemia]]);
* 24&nbsp;hour urine collection to measure total daily urinary volume, magnesium, sodium, uric acid, calcium, citrate, oxalate, and [[phosphate]];
* collection of stones (by urinating through a StoneScreen kidney stone collection cup or a simple [[tea strainer]]) is useful. Chemical analysis of collected stones can establish their composition, which in turn can help to guide future preventive and therapeutic management.
{{clear}}

=== Composition ===

{| class="wikitable"
|- style="line-height:133%"
! Kidney<br>stone<br>type
! Relative<br>incidence<br>(adults)<ref name=Frassetto2011>{{cite journal | author= Frassetto L, Kohlstadt I | title= Treatment and prevention of kidney stones: an update. | journal= Am Fam Physician | year= 2011 | volume= 84 | issue= 11 | pages= 1234–42 | pmid= 22150656 | doi=  | pmc=  | url= https://pubmed.ncbi.nlm.nih.gov/22150656 | archive-date= 22 September 2023 | access-date= 28 August 2023 | archive-url= https://web.archive.org/web/20230922163226/https://pubmed.ncbi.nlm.nih.gov/22150656/ | url-status= live }}<br>Including cystine stone incidence of 1%</ref>
! Circumstances
! Color and<br>microscopy<br>appearance
! Radio-density
! Details
|-
| [[Calcium oxalate|Calcium<br>oxalate]]
| 60%
| when urine is acidic (decreased pH)<ref>{{cite book| vauthors = Becker KL |title=Principles and practice of endocrinology and metabolism|date=2001|publisher=Lippincott, Williams & Wilkins|location=Philadelphia, Pa. [u.a.]|isbn=978-0-7817-1750-2|page=684|edition=3|url=https://books.google.com/books?id=FVfzRvaucq8C&pg=PA684|url-status=live|archive-url=https://web.archive.org/web/20170908221053/https://books.google.com/books?id=FVfzRvaucq8C&pg=PA684|archive-date=8 September 2017|df=dmy-all}}</ref>
| Black/dark brown [[File:Calcium oxalate crystal.jpg|center|70 px]]
| Radio-opaque
| Some of the oxalate in urine is produced by the body. Calcium and oxalate in the diet play a part but are not the only factors that affect the formation of calcium oxalate stones. Dietary oxalate is found in many vegetables, fruits, and nuts. Calcium from bone may also play a role in kidney stone formation.
|-
| [[Calcium phosphate|Calcium<br>phosphate]]
| 10–20%
| when urine is alkaline (high pH)
| Dirty white [[File:Calcium phosphate crystal.jpg|center|70 px]]
| Radio-opaque
| Tends to grow in alkaline urine especially when [[Proteus (bacterium)|''Proteus'' bacteria]] are present. The most common type among pregnant women.<ref name=Frassetto2011/>
|-
| [[Uric acid]]
| 10–20%
| when urine is persistently acidic
| Yellow/reddish brown [[File:Uric acid crystal.jpg|center|70 px]]
| Radio-lucent
| Diets rich in animal proteins and purines: substances found naturally in all food but especially in organ meats, fish, and shellfish.
|-
| [[Struvite]]
| {{0}}3%
| infections in the kidney and when urine is alkaline (high pH)
| Dirty white [[File:Struvite crystals.jpg|center|70 px]]
| Radio-opaque
| Prevention of struvite stones depends on staying infection-free. Diet has not been shown to affect struvite stone formation.
|-
| [[Cystine]]
| {{0}}1–2%<ref>{{cite web|title=Cystine stones|url=http://www.uptodate.com/contents/cystine-stones|work=[[UpToDate]]|access-date=20 February 2014|url-status=live|archive-url=https://web.archive.org/web/20140226110022/http://www.uptodate.com/contents/cystine-stones|archive-date=26 February 2014|df=dmy-all}}</ref>
| rare genetic disorder
| Pink/yellow [[File:Cystine crystals.jpg|center|70 px]]
| Radio-opaque
| Cystine, an amino acid (a dimer of cysteine, of the building blocks of protein), leaks through the kidneys and into the urine to form crystals.
|-
| [[Xanthine]]<ref>Bailey & Love's/25th/1296</ref>
|
| extremely rare
| Brick red
| Radio-lucent
|
|}

[[File:Surface of a kidney stone.jpg|thumb|Scanning electron micrograph of the surface of a kidney stone showing tetragonal crystals of [[weddellite]] (calcium oxalate dihydrate) emerging from the amorphous central part of the stone (the horizontal length of the picture represents 0.5 mm of the figured original)]]
[[File:Kidney stones, Uric acid.JPG|thumb|Multiple kidney stones composed of [[uric acid]] and a small amount of [[calcium oxalate]]]]
[[File:Lenticular kidney stone.jpg|thumb|A lenticular kidney stone, excreted in the urine]]

==== Calcium-containing stones ====
By far, the most common type of kidney stones worldwide contains calcium. For example, calcium-containing stones represent about 80% of all cases in the United States; these typically contain [[calcium oxalate]] either alone or in combination with [[calcium phosphate]] in the form of [[apatite]] or [[brushite]].<ref name=Reilly2005Ch13 /><ref name=Coe2005 /> Factors that promote the [[Precipitation (chemistry)|precipitation]] of oxalate crystals in the urine, such as [[primary hyperoxaluria]], are associated with the development of calcium oxalate stones.<ref name=Hoppe2003 /> The formation of calcium phosphate stones is associated with conditions such as [[hyperparathyroidism]]<ref name=NIDDK2006 /> and [[renal tubular acidosis]].<ref name=NIDDK20084696 />

[[Oxaluria]] is increased in patients with certain gastrointestinal disorders including inflammatory bowel disease such as [[Crohn's disease]] or in patients who have undergone resection of the small bowel or small-bowel bypass procedures. Oxaluria is also increased in patients who consume increased amounts of oxalate (found in vegetables and nuts). Primary hyperoxaluria is a rare autosomal recessive condition that usually presents in childhood.<ref name="De Mais">{{cite book | vauthors = De Mais D |title= ASCP Quick Compendium of Clinical Pathology |edition= 2nd |publisher= ASCP Press |location= Chicago |year= 2009 }}</ref>

Calcium oxalate crystals can come in two varieties. Calcium oxalate monohydrate can appear as 'dumbbells' or as long ovals that resemble the individual posts in a picket fence. Calcium oxalate dihydrate have a tetragonal "envelope" appearance.<ref name="De Mais" />

==== Struvite stones ====
About 10–15% of urinary calculi are composed of [[struvite]] (hexa-hydrated [[ammonium magnesium phosphate]], NH<sub>4</sub>MgPO<sub>4</sub>·6H<sub>2</sub>O).<ref name=Heptinstall2007 /> Struvite stones (also known as "infection stones," [[urease]], or triple-phosphate stones) form most often in the presence of infection by urea-splitting [[bacteria]]. Using the enzyme urease, these organisms [[Metabolism|metabolize]] [[urea]] into [[ammonia]] and [[carbon dioxide]]. This [[alkalinity|alkalinizes]] the urine, resulting in favorable conditions for the formation of struvite stones. ''[[Proteus mirabilis]]'', ''[[Proteus vulgaris]]'', and ''[[Morganella morganii]]'' are the most common organisms isolated; less common organisms include ''[[Ureaplasma urealyticum]]'' and some species of ''[[Providencia (bacterium)|Providencia]]'', ''[[Klebsiella]]'', ''[[Serratia]]'', and ''[[Enterobacter]]''. These infection stones are commonly observed in people who have factors that predispose them to [[urinary tract infection]]s, such as those with [[spinal cord injury]] and other forms of [[neurogenic bladder]], [[ileal conduit urinary diversion]], [[vesicoureteral reflux]], and [[Obstructive uropathy|obstructive uropathies]]. They are also commonly seen in people with underlying metabolic disorders, such as [[idiopathic]] [[hypercalciuria]], [[hyperparathyroidism]], and [[gout]]. Infection stones can grow rapidly, forming large calyceal staghorn ([[antler]]-shaped) calculi requiring invasive surgery such as percutaneous nephrolithotomy for definitive treatment.<ref name=Heptinstall2007 />

Struvite stones (triple-phosphate/magnesium ammonium phosphate) have a 'coffin lid' morphology by microscopy.<ref name="De Mais" />

==== Uric acid stones ====
About 5–10% of all stones are formed from [[uric acid]].<ref name=Moe2006 /> People with certain metabolic abnormalities, including [[obesity]],<ref name=Johri2010 /> may produce uric acid stones. They also may form in association with conditions that cause [[hyperuricosuria]] (an excessive amount of uric acid in the urine) with or without [[hyperuricemia]] (an excessive amount of uric acid in the [[blood serum|serum]]). They may also form in association with disorders of acid/base metabolism where the urine is excessively acidic (low [[pH]]), resulting in precipitation of uric acid crystals. A diagnosis of uric acid [[urolithiasis]] is supported by the presence of a [[Radiodensity|radiolucent]] stone in the face of persistent urine acidity, in conjunction with the finding of uric acid crystals in fresh urine samples.<ref name=Halabe1994 />

As noted above (section on calcium oxalate stones), people with [[inflammatory bowel disease]] ([[Crohn's disease]], [[ulcerative colitis]]) tend to have [[hyperoxaluria]] and form oxalate stones. They also have a tendency to form urate stones. Urate stones are especially common after [[Colectomy|colon resection]].

Uric acid stones appear as [[Pleomorphism (cytology)|pleomorphic]] crystals, usually diamond-shaped.  They may also look like squares or rods which are polarizable.<ref name="De Mais" />

==== Other types ====
[[File:Cystine Crystals in Canine Urine Sediment.jpg|alt=Translucent, hexagon-shaped crystals seen through a microscope|thumb|Microscopic [[cystine]] crystals have a distinctive hexagonal shape and are present in the urine of people with kidney stones composed of cystine]]
People with certain rare [[Inborn error of metabolism|inborn errors of metabolism]] have a propensity to accumulate crystal-forming substances in their urine. For example, those with [[cystinuria]], [[cystinosis]], and [[Fanconi syndrome]] may form stones composed of [[cystine]]. Cystine stone formation can be treated with urine alkalinization and dietary protein restriction.  People affected by [[xanthinuria]] often produce stones composed of [[xanthine]]. People affected by [[adenine phosphoribosyltransferase deficiency]] may produce [[2,8-dihydroxyadenine]] stones,<ref name=Kamatani1996 /> [[Alkaptonuria|alkaptonurics]] produce [[homogentisic acid]] stones, and [[Iminoglycinuria|iminoglycinurics]] produce stones of [[glycine]], [[proline]], and [[hydroxyproline]].<ref name=Rosenberg1968 /><ref name=Coskun1993 /> Urolithiasis has also been noted to occur in the setting of therapeutic drug use, with crystals of drug forming within the renal tract in some people currently being treated with agents such as [[indinavir]],<ref name=Crixivan2010 /> [[sulfadiazine]],<ref name=Schlossberg2011 /> and [[triamterene]].<ref name=Carr1990 />

=== Location ===
[[File:Blausen 0595 KidneyStones.png|thumb|Illustration of kidney stones]]

Urolithiasis refers to stones originating anywhere in the urinary system, including the kidneys and bladder.<ref name=Pearle2007 /> Nephrolithiasis refers to the presence of such stones in the kidneys. Calyceal calculi are aggregations in either the [[minor calyx|minor]] or [[major calyx]], parts of the kidney that pass urine into the ureter (the tube connecting the kidneys to the urinary bladder). The condition is called ureterolithiasis when a calculus is located in the ureter. Stones may also form or pass into the bladder, a condition referred to as [[bladder stone]]s.<ref name=McNutt1893 />

===Size===
[[File:Staghorn Kidney Stone 08779.jpg|thumb|Radiograph showing a large staghorn calculus involving the [[major calyx|major calyces]] and [[renal pelvis]] in a person with severe [[scoliosis]]]]
Stones less than {{convert|5|mm|in|1|abbr=on}} in diameter pass spontaneously in up to 98% of cases, while those measuring {{convert|5|to|10|mm|in|1|abbr=on}} in diameter pass spontaneously in less than 53% of cases.<ref name=Gettman2005 />

{{anchor|staghorn}}Stones that are large enough to fill out the renal calyces are called ''staghorn stones'' and are composed of [[struvite]] in a vast majority of cases, which forms only in the presence of [[Urease#As diagnostic test|urease-forming bacteria]]. Other forms that can possibly grow to become staghorn stones are those composed of cystine, calcium oxalate monohydrate, and uric acid.<ref name="Segura1997">{{cite journal | vauthors = Segura JW | title = Staghorn calculi | journal = The Urologic Clinics of North America | volume = 24 | issue = 1 | pages = 71–80 | date = February 1997 | pmid = 9048853 | doi = 10.1016/S0094-0143(05)70355-4 }}</ref>

== Prevention ==
Preventative measures depend on the type of stones. In those with calcium stones, drinking plenty of fluids, [[thiazide]] [[diuretic]]s and citrate are effective as is allopurinol in those with high uric acid levels in urine.<ref name=Fink2013>{{cite journal | vauthors = Fink HA, Wilt TJ, Eidman KE, Garimella PS, MacDonald R, Rutks IR, Brasure M, Kane RL, Ouellette J, Monga M | title = Medical management to prevent recurrent nephrolithiasis in adults: a systematic review for an American College of Physicians Clinical Guideline | journal = Annals of Internal Medicine | volume = 158 | issue = 7 | pages = 535–43 | date = April 2013 | pmid = 23546565 | doi = 10.7326/0003-4819-158-7-201304020-00005 | doi-access = free }}</ref><ref name=Qas2014 />

=== Dietary measures ===
{{See also|#Hypocitraturia|label1= Hypocitraturia}}
Specific therapy should be tailored to the type of stones involved. Diet can have an effect on the development of kidney stones. Preventive strategies include some combination of dietary modifications and medications with the goal of reducing the excretory load of calculogenic compounds on the kidneys.<ref name=Parmar2004 /><ref name=Goldfarb1999 /><ref name=Finkielstein2006 /> Dietary recommendations to minimize the formation of kidney stones include:
* increasing total fluid intake to achieve more than two liters per day of urine output;<ref name=AHRQ2012>{{cite journal |publisher=Agency for Healthcare Research and Quality |location=Rockvill, MD | vauthors = Fink HA, Wilt TJ, Eidman KE, Garimella PS, MacDonald R, Rutks IR, Brasure M, Kane RL, Monga M | title = Recurrent Nephrolithiasis in Adults: Comparative Effectiveness of Preventive Medical Strategies |journal=Comparative Effectiveness Reviews |number=61 | date = July 2012 | pmid = 22896859 }}</ref>
* limiting [[cola]], including sugar-sweetened soft drinks;<ref name=Fink2013 /><ref name=AHRQ2012/><ref name="FerraroTaylor2013">{{cite journal | vauthors = Ferraro PM, Taylor EN, Gambaro G, Curhan GC | title = Soda and other beverages and the risk of kidney stones | journal = Clinical Journal of the American Society of Nephrology | volume = 8 | issue = 8 | pages = 1389–95 | date = August 2013 | pmid = 23676355 | pmc = 3731916 | doi = 10.2215/CJN.11661112 }}</ref> to less than one liter per week.<ref>{{cite web |url=http://www.kidney.org.au/ForPatients/Management/KidneyStones/tabid/838/Default.aspx |title=What are kidney stones? |website=kidney.org |access-date=19 August 2013 |url-status=dead |archive-url=https://web.archive.org/web/20130514122900/http://kidney.org.au/ForPatients/Management/KidneyStones/tabid/838/Default.aspx |archive-date=14 May 2013 |df=dmy-all }}</ref>
* limiting animal protein intake to no more than two meals daily (an association between animal [[Protein (nutrient)|protein]] and recurrence of kidney stones has been shown in men);<ref name=Taylor2006>{{cite journal | vauthors = Taylor EN, Curhan GC | title = Diet and fluid prescription in stone disease | journal = Kidney International | volume = 70 | issue = 5 | pages = 835–9 | date = September 2006 | pmid = 16837923 | doi = 10.1038/sj.ki.5001656 | doi-access = free }}</ref>
* increasing citrate, including from lemon and [[lime juice]];<ref name="Gul_2014">{{cite journal | vauthors = Gul Z, Monga M | title = Medical and dietary therapy for kidney stone prevention | journal = Korean Journal of Urology | volume = 55 | issue = 12 | pages = 775–9 | date = December 2014 | pmid = 25512810 | pmc = 4265710 | doi = 10.4111/kju.2014.55.12.775 }}</ref> citric acid in its natural form, such as from citrus fruits, "prevents small stones from becoming 'problem stones' by coating them and preventing other material from attaching and building onto the stones";<ref>{{cite web |title=Citric Acid and Kidney Stones |url=https://www.uwhealth.org/files/uwhealth/docs/pdf/kidney_citric_acid.pdf |archive-url=https://web.archive.org/web/20100705033118/http://www.uwhealth.org/files/uwhealth/docs/pdf/kidney_citric_acid.pdf |archive-date=2010-07-05 |url-status=live |website=uwhealth.org}}</ref> citrate inhibits the formation of kidney stones on all phases[[Nucleation|{{emdash}}nucleation]], growth and aggregation{{emdash}}by raising the limit at which oxalate remain stable, slowing oxalate crystal growth, and notably, reducing crystal aggregation within the [[kidney tubules]];<ref name="pmid26439475"/>
* increase alkaline load by consuming more fruits and vegetables (because uric acid crystals form in acidic environment);<ref name="Gul_2014"/>
* reducing sodium intake is associated with a reduction in urine calcium excretion.<ref name="pmid38931286">{{cite journal |vauthors=Balawender K, Łuszczki E, Mazur A, Wyszyńska J |title=The Multidisciplinary Approach in the Management of Patients with Kidney Stone Disease-A State-of-the-Art Review |journal=Nutrients |volume=16 |issue=12 |date=June 2024 |page=1932 |pmid=38931286 |pmc=11206918 |doi=10.3390/nu16121932|doi-access=free }}</ref>

Maintenance of dilute urine by means of vigorous fluid therapy is beneficial in all forms of kidney stones, so increasing urine volume is a key principle for the prevention of kidney stones. Fluid intake should be sufficient to maintain a urine output of at least {{convert|2|L|USoz|lk=on}} per day.<ref name=Qas2014>{{cite journal | vauthors = Qaseem A, Dallas P, Forciea MA, Starkey M, Denberg TD | title = Dietary and pharmacologic management to prevent recurrent nephrolithiasis in adults: a clinical practice guideline from the American College of Physicians | journal = Annals of Internal Medicine | volume = 161 | issue = 9 | pages = 659–67 | date = November 2014 | pmid = 25364887 | doi = 10.7326/m13-2908 | doi-access = free }}</ref> A high fluid intake may reduce the likelihood of kidney stone recurrence or may increase the time between stone development without unwanted effects.

Calcium binds with available oxalate in the [[gastrointestinal tract]], thereby preventing its absorption into the [[Circulatory system|bloodstream]]. Reducing oxalate absorption decreases kidney stone risk in susceptible people.<ref name=Heaney2006 /> Because of this, some doctors recommend increasing dairy intake so that its calcium content will serve as an oxalate binder'''.''' Taking calcium citrate tablets during or after meals containing high oxalate foods<ref name=Tiselius2003 /> may be useful if dietary calcium cannot be increased by other means as in those with lactose intolerance. The preferred calcium supplement for people at risk of stone formation is calcium citrate, as opposed to calcium carbonate, because it helps to increase urinary citrate excretion.<ref name=Finkielstein2006 />

Aside from vigorous oral hydration and eating more dietary calcium, other prevention strategies include avoidance of higher doses of supplemental {{nowrap|vitamin C}} (since [[ascorbate]] is metabolized to oxalate) and restriction of oxalate-rich foods such as [[List of common leaf vegetables|leaf vegetables]], [[rhubarb]], [[Soybean|soy products]] and [[chocolate]].<ref name=Taylor2004 /> However, no randomized, controlled trial of oxalate restriction has been performed to test the hypothesis that oxalate restriction reduces stone formation.<ref name=Tiselius2003 /> Some evidence indicates [[magnesium]] intake decreases the risk of symptomatic kidney stones.<ref name=Taylor2004 />

=== Urine alkalinization ===
The mainstay for medical management of uric acid stones is [[Alkalinity|alkalinization]] (increasing the [[pH]]) of the urine. Uric acid stones are among the few types amenable to dissolution therapy, referred to as [[Lysis|chemolysis]]. Chemolysis is usually achieved through the use of oral medications, although in some cases, intravenous agents or even instillation of certain irrigating agents directly onto the stone can be performed, using antegrade [[nephrostomy]] or [[retrograde ureteral]] catheters.<ref name=Knudsen2007 /> [[Acetazolamide]] is a medication that alkalinizes the urine. In addition to acetazolamide or as an alternative, certain dietary supplements are available that produce a similar alkalinization of the urine. These include [[alkali citrate]], [[sodium bicarbonate]], [[potassium citrate]], [[magnesium citrate]], and [[bicitrate]] (a combination of citric acid monohydrate and sodium citrate dihydrate).<ref>{{cite journal | vauthors = Cicerello E, Merlo F, Maccatrozzo L | title = Urinary alkalization for the treatment of uric acid nephrolithiasis | journal = Archivio Italiano di Urologia, Andrologia | volume = 82 | issue = 3 | pages = 145–8 | date = September 2010 | pmid = 21121431 }}</ref> Aside from alkalinization of the urine, these supplements have the added advantage of increasing the urinary citrate level, which helps to reduce the aggregation of calcium oxalate stones.<ref name=Knudsen2007 />

Increasing the urine pH to around 6.5 provides optimal conditions for [[Dissolution (chemistry)|dissolution]] of uric acid stones. Increasing the urine pH to a value higher than 7.0 may increase the risk of calcium phosphate stone formation, though this concept is controversial since citrate does inhibit calcium phosphate crystallization. Testing the urine periodically with [[nitrazine]] paper can help to ensure the urine pH remains in this optimal range. Using this approach, stone dissolution rate can be expected to be around {{convert|10|mm|in|1|abbr=on}} of stone radius per month.<ref name=Knudsen2007 />

==== Slaked lime ====
[[Calcium hydroxide]] decreases urinary calcium when combined with food rich in oxalic acid such as green leafy vegetables.<ref>{{cite web |url=https://www.researchgate.net/publication/287536542 |title=Effect of addition of calcium hydroxide to foods rich in oxalic acid on calcium and oxalic acid metabolism {{!}} Request PDF<!-- Bot generated title --> |access-date=6 March 2021 |archive-date=7 November 2021 |archive-url=https://web.archive.org/web/20211107061411/https://www.researchgate.net/publication/287536542_Effect_of_addition_of_calcium_hydroxide_to_foods_rich_in_oxalic_acid_on_calcium_and_oxalic_acid_metabolism |url-status=live }}</ref>

=== Diuretics ===
One of the recognized medical therapies for prevention of stones is the [[thiazide]] and [[thiazide-like diuretic]]s, such as [[Chlortalidone|chlorthalidone]] or [[indapamide]]. These drugs inhibit the formation of calcium-containing stones by reducing urinary calcium excretion.<ref name=Cutler2007 /> Sodium restriction is necessary for clinical effect of thiazides, as sodium excess promotes calcium excretion. Thiazides work best for renal leak hypercalciuria (high urine calcium levels), a condition in which high urinary calcium levels are caused by a primary kidney defect. Thiazides are useful for treating absorptive hypercalciuria, a condition in which high urinary calcium is a result of excess absorption from the gastrointestinal tract.<ref name=Coe2005 />

=== Allopurinol ===
For people with [[hyperuricosuria]] and calcium stones, [[allopurinol]] is one of the few treatments that have been shown to reduce kidney stone recurrences. Allopurinol interferes with the production of uric acid in the [[liver]]. The drug is also used in people with [[gout]] or hyperuricemia (high [[Serum (blood)|serum]] uric acid levels).<ref name=Cameron1987 /> Dosage is adjusted to maintain a reduced urinary excretion of uric acid. Serum uric acid level at or below 6&nbsp;mg/100&nbsp;mL is often a therapeutic goal. Hyperuricemia is not necessary for the formation of uric acid stones; hyperuricosuria can occur in the presence of normal or even [[hypouricemia|low serum uric acid]]. Some practitioners advocate adding allopurinol only in people in whom hyperuricosuria and hyperuricemia persist, despite the use of a urine-[[alkalinizing agent]] such as [[sodium bicarbonate]] or [[potassium citrate]].<ref name=Knudsen2007 />

== Treatment ==
Stone size influences the rate of spontaneous stone passage. For example, up to 98% of small stones (less than {{convert|5|mm|in|1|abbr=on}} in diameter) may pass spontaneously through urination within four weeks of the onset of symptoms,<ref name=Miller2007 /> but for larger stones ({{convert|5|to|10|mm|in|1|abbr=on}} in diameter), the rate of spontaneous passage decreases to less than 53%.<ref name=Gettman2005 /> Initial stone location also influences the likelihood of spontaneous stone passage. Rates increase from 48% for stones located in the proximal ureter to 79% for stones located at the vesicoureteric junction, regardless of stone size.<ref name=Gettman2005 /> Assuming no high-grade obstruction or associated infection is found in the urinary tract, and symptoms are relatively mild, various nonsurgical measures can be used to encourage the passage of a stone.<ref name=Knudsen2007 /> Repeat stone formers benefit from more intense management, including proper fluid intake and use of certain medications, as well as careful monitoring.<ref name=Macaluso1999 />

=== Pain management ===
Management of pain often requires intravenous administration of [[Nonsteroidal anti-inflammatory drug|NSAIDs]] or opioids.<ref name=Cutler2007 /> NSAIDs appear somewhat better than opioids or [[paracetamol]] in those with normal kidney function.<ref>{{cite journal |vauthors= Pathan SA, Mitra B, Cameron PA |title= A Systematic Review and Meta-analysis Comparing the Efficacy of Nonsteroidal Anti-inflammatory Drugs, Opioids, and Paracetamol in the Treatment of Acute Renal Colic |journal= European Urology |volume= 73 |issue= 4 |pages= 583–595 |date= April 2018 |pmid= 29174580 |doi= 10.1016/j.eururo.2017.11.001 }}</ref> Medications by mouth are often effective for less severe discomfort.<ref name=semins/> The use of [[antispasmodic]]s does not have further benefit.<ref name=Af2015 />

=== Medical expulsive therapy ===
The use of medications to speed the spontaneous passage of stones in the ureter is referred to as medical expulsive therapy.<ref name=MET09>{{cite journal | vauthors = Seitz C, Liatsikos E, Porpiglia F, Tiselius HG, Zwergel U | title = Medical therapy to facilitate the passage of stones: what is the evidence? | journal = European Urology | volume = 56 | issue = 3 | pages = 455–71 | date = September 2009 | pmid = 19560860 | doi = 10.1016/j.eururo.2009.06.012 }}</ref><ref name=Camp2018>{{cite journal | vauthors = Campschroer T, Zhu X, Vernooij RW, Lock MT | title = Alpha-blockers as medical expulsive therapy for ureteral stones | journal = The Cochrane Database of Systematic Reviews | volume = 2018 | pages = CD008509 | date = April 2018 | issue = 4 | pmid = 29620795 | doi = 10.1002/14651858.CD008509.pub3 | pmc = 6494465 }}</ref> Several agents, including [[Alpha blocker|alpha adrenergic blockers]] (such as [[tamsulosin]]) and [[calcium channel blocker]]s (such as [[nifedipine]]), may be effective.<ref name=MET09 /> Alpha-blockers likely result in more people passing their stones, and they may pass their stones in a shorter time.<ref name=Camp2018/> People taking alpha-blockers may also use less pain medication and may not need to visit the hospital.<ref name="Camp2018" /> Alpha-blockers appear to be more effective for larger stones (over 5&nbsp;mm in size) than smaller stones.<ref name=Camp2018/> However, use of alpha-blockers may be associated with a slight increase in serious, unwanted effects from this medication.<ref name="Camp2018" /> A combination of tamsulosin and a [[corticosteroid]] may be better than tamsulosin alone.<ref name=MET09 /> These treatments also appear to be useful in addition to lithotripsy.<ref name=Miller2007 />

=== Lithotripsy ===
[[File:Lithotriptor machine.jpg|thumb|A [[Extracorporeal shock wave lithotripsy|lithotriptor machine]] with a [[X-ray image intensifier#Mobile Fluoroscopic System AKA "portable C-arm"|mobile fluoroscopic system]] ("C-arm") is seen in an [[Operating theater|operating room]]; other equipment is seen in the background including an [[Anaesthetic machine|anesthesia machine]].]]
[[Extracorporeal shock wave lithotripsy]] (ESWL) is a [[noninvasive]] technique for the removal of kidney stones. Most ESWL is carried out when the stone is present near the [[renal pelvis]]. ESWL involves the use of a [[Extracorporeal shockwave therapy|lithotriptor]] machine to deliver externally applied, focused, high-intensity pulses of [[ultrasound|ultrasonic energy]] to cause fragmentation of a stone over a period of around 30–60&nbsp;minutes. Following its introduction in the United States in February 1984, ESWL was rapidly and widely accepted as a treatment alternative for renal and ureteral stones.<ref name=AUA2009 /> It is currently used in the treatment of uncomplicated stones located in the kidney and upper ureter, provided the aggregate stone burden (stone size and number) is less than {{convert|20|mm|in|1|abbr=on}} and the anatomy of the involved kidney is normal.<ref name=Lingeman2007 /><ref name=Preminger2007 />

For a stone greater than {{convert|10|mm|in}}, ESWL may not help break the stone in one treatment; instead, two or three treatments may be needed. Some 80-85% of simple renal calculi can be effectively treated with ESWL.<ref name=Miller2007 /> A number of factors can influence its efficacy, including chemical composition of the stone, presence of anomalous renal anatomy and the specific location of the stone within the kidney, presence of hydronephrosis, [[body mass index]], and distance of the stone from the surface of the skin.<ref name=AUA2009 />

Common adverse effects of ESWL include acute [[Trauma (medicine)|trauma]], such as [[bruise|bruising]] at the site of shock administration, and damage to blood vessels of the kidney.<ref name=Evan1996 /><ref name=Evan2007 /> In fact, the vast majority of people who are treated with a typical dose of shock waves using currently accepted treatment settings are likely to experience some degree of [[acute kidney injury]].<ref name=AUA2009 /> ESWL-induced acute kidney injury is dose-dependent (increases with the total number of shock waves administered and with the power setting of the lithotriptor) and can be severe,<ref name=AUA2009 /> including [[internal bleeding]] and subcapsular [[hematoma]]s. On rare occasions, such cases may require [[blood transfusion]] and even lead to acute [[kidney failure]]. Hematoma rates may be related to the type of lithotriptor used; hematoma rates of less than 1% and up to 13% have been reported for different lithotriptor machines.<ref name=Evan2007 /> Recent studies show reduced acute tissue injury when the treatment protocol includes a brief pause following the initiation of treatment, and both improved stone breakage and a reduction in injury when ESWL is carried out at slow shock wave rate.<ref name=AUA2009 />

In addition to the aforementioned potential for acute kidney injury, animal studies suggest these acute injuries may progress to scar formation, resulting in loss of functional renal volume.<ref name=Evan1996 /><ref name=Evan2007 /> Recent [[Prospective cohort study|prospective studies]] also indicate elderly people are at increased risk of developing new-onset hypertension following ESWL. In addition, a [[Retrospective cohort study|retrospective case-control study]] published by researchers from the [[Mayo Clinic]] in 2006 has found an increased risk of developing [[diabetes mellitus]] and [[hypertension]] in people who had undergone ESWL, compared with age and gender-matched people who had undergone nonsurgical treatment. Whether or not acute trauma progresses to long-term effects probably depends on multiple factors that include the shock wave dose (i.e., the number of shock waves delivered, rate of delivery, power setting, acoustic characteristics of the particular lithotriptor, and frequency of retreatment), as well as certain intrinsic predisposing pathophysiologic risk factors.<ref name=AUA2009 />

To address these concerns, the [[American Urological Association]] established the Shock Wave Lithotripsy Task Force to provide an expert opinion on the safety and [[Risk-benefit analysis|risk-benefit ratio]] of ESWL. The task force published a [[white paper]] outlining their conclusions in 2009. They concluded the risk-benefit ratio remains favorable for many people.<ref name=AUA2009 /> The advantages of ESWL include its noninvasive nature, the fact that it is technically easy to treat most upper urinary tract calculi, and that, at least acutely, it is a well-tolerated, low-[[morbidity]] treatment for the vast majority of people. However, they recommended slowing the shock wave firing rate from 120&nbsp;pulses per minute to 60&nbsp;pulses per minute to reduce the risk of renal injury and increase the degree of stone fragmentation.<ref name=AUA2009 />

[[Alpha blocker|Alpha-blockers]] are sometimes prescribed after shock wave lithotripsy to help the pieces of the stone leave the person's body.<ref name=":1">{{cite journal | vauthors = Oestreich MC, Vernooij RW, Sathianathen NJ, Hwang EC, Kuntz GM, Koziarz A, Scales CD, Dahm P | title = Alpha-blockers after shock wave lithotripsy for renal or ureteral stones in adults | journal = The Cochrane Database of Systematic Reviews | volume = 2020 | pages = CD013393 | date = November 2020 | issue = 11 | pmid = 33179245 | doi = 10.1002/14651858.CD013393.pub2 | pmc = 8092672 | collaboration = Cochrane Urology Group }}</ref> By relaxing muscles and helping to keep blood vessels open, alpha blockers may relax the ureter muscles to allow the kidney stone fragments to pass. When compared to usual care or placebo treatment, alpha blockers may lead to faster clearing of stones, a reduced need for extra treatment and fewer unwanted effects.<ref name=":1" /> They may also clear kidney stones in more adults than the standard shock wave lithotripsy procedure. The unwanted effects associated with alpha blockers are hospital emergency visits and return to hospital for stone-related issues, but these effects were more common in adults who did not receive [[Alpha blocker|alpha-blockers]] as a part of their treatment.<ref name=":1" />

=== Surgery ===
{{multiple image
| align             = right
| direction         = vertical
| width             = 220
| image1            = Ureterstent double J 3D legend.jpg
| alt1              =
| caption1          = [[X-ray computed tomography#Three-dimensional reconstruction|Three-dimensional reconstructed CT scan]] image of a [[Ureteric stent|ureteral stent]] in the left kidney (indicated by yellow arrow), with a kidney stone in the inferior [[renal pelvis]] (highest red arrow) and one in the [[ureter]] beside the stent (lower red arrow)
| image2            = Kidney Stone Image 4172-PH.jpg
| alt2              =
| caption2          = A kidney stone at the tip of an [[ultrasound|ultrasonic]] stone disintegration apparatus
}}

Most stones under {{convert|5|mm|in|1|abbr=on}} pass spontaneously.<ref name=Parmar2004 /><ref name=Miller2007 /> Prompt surgery may, nonetheless, be required in persons with only one working kidney, bilateral obstructing stones, a urinary tract infection and thus, it is presumed, an infected kidney, or intractable pain.<ref name=Young2011 /> Beginning in the mid-1980s, less invasive treatments such as extracorporeal shock wave lithotripsy, [[ureteroscopy]], and [[percutaneous nephrolithotomy]] began to replace open surgery as the modalities of choice for the surgical management of urolithiasis.<ref name=Miller2007 />  More recently, flexible ureteroscopy has been adapted to facilitate retrograde nephrostomy creation for percutaneous nephrolithotomy.  This approach is still under investigation, though early results are favorable.<ref>{{cite journal | vauthors = Wynberg JB, Borin JF, Vicena JZ, Hannosh V, Salmon SA | title = Flexible ureteroscopy-directed retrograde nephrostomy for percutaneous nephrolithotomy: description of a technique | journal = Journal of Endourology | volume = 26 | issue = 10 | pages = 1268–74 | date = October 2012 | pmid = 22563900 | doi = 10.1089/end.2012.0160 }}</ref> Percutaneous nephrolithotomy or, rarely, [[lithotomy|anatrophic nephrolithotomy]], is the treatment of choice for large or complicated stones (such as calyceal staghorn calculi) or stones that cannot be extracted using less invasive procedures.<ref name=Anoia2009 /><ref name=Miller2007 />

==== Ureteroscopic surgery ====
[[Ureteroscopy]] has become increasingly popular as flexible and rigid [[optical fiber|fiberoptic]] ureteroscopes have become smaller. One ureteroscopic technique involves the placement of a [[Ureteric stent|ureteral stent]] (a small tube extending from the bladder, up the ureter and into the kidney) to provide immediate relief of an obstructed kidney. Stent placement can be useful for saving a kidney at risk for [[Acute kidney injury#Postrenal|postrenal acute kidney failure]] due to the increased hydrostatic pressure, [[edema|swelling]] and infection ([[pyelonephritis]] and [[pyonephrosis]]) caused by an obstructing stone. Ureteral stents vary in length from {{convert|24|to|30|cm|in|abbr=on}} and most have a shape commonly referred to as a "double-J" or "double pigtail", because of the curl at both ends. They are designed to allow urine to flow past an obstruction in the ureter. They may be retained in the ureter for days to weeks as infections resolve and as stones are dissolved or fragmented by ESWL or by some other treatment. The stents dilate the ureters, which can facilitate instrumentation, and they also provide a clear landmark to aid in the visualization of the ureters and any associated stones on radiographic examinations. The presence of indwelling ureteral stents may cause minimal to moderate discomfort, frequency or urgency incontinence, and infection, which in general resolves on removal. Most ureteral stents can be removed cystoscopically during an office visit under [[Topical anesthetic|topical anesthesia]] after resolution of urolithiasis.<ref name=Lam2007 /> Research is currently uncertain if placing a temporary stent during ureteroscopy leads to different outcomes than not placing a stent in terms of number of hospital visits for post operative problems, short or long term pain, need for narcotic pain medication, risk of UTI, need for a repeat procedure or narrowing of the ureter from scarring.<ref>{{cite journal | vauthors = Ordonez M, Hwang EC, Borofsky M, Bakker CJ, Gandhi S, Dahm P | title = Ureteral stent versus no ureteral stent for ureteroscopy in the management of renal and ureteral calculi | journal = The Cochrane Database of Systematic Reviews | volume = 2019 | pages = CD012703 | date = February 2019 | issue = 2 | pmid = 30726554 | pmc = 6365118 | doi = 10.1002/14651858.CD012703.pub2 | collaboration = Cochrane Urology Group }}</ref>

More definitive ureteroscopic techniques for stone extraction (rather than simply bypassing the obstruction) include basket extraction and ultrasound ureterolithotripsy. [[Laser lithotripsy]] is another technique, which involves the use of a [[holmium]]:[[yttrium aluminium garnet]] (Ho:YAG) laser to fragment stones in the bladder, ureters, and kidneys.<ref name="Marks2011" />

Ureteroscopic techniques are generally more effective than ESWL for treating stones located in the lower ureter, with success rates of 93–100% using Ho:YAG laser lithotripsy.<ref name=Gettman2005 /> Although ESWL has been traditionally preferred by many practitioners for treating stones located in the upper ureter, more recent experience suggests ureteroscopic techniques offer distinct advantages in the treatment of upper ureteral stones. Specifically, the overall success rate is higher, fewer repeat interventions and postoperative visits are needed, and treatment costs are lower after ureteroscopic treatment when compared with ESWL. These advantages are especially apparent with stones greater than {{convert|10|mm|in|1|abbr=on}} in diameter. However, because ureteroscopy of the upper ureter is much more challenging than ESWL, many urologists still prefer to use ESWL as a first-line treatment for stones of less than 10&nbsp;mm, and ureteroscopy for those greater than 10&nbsp;mm in diameter.<ref name=Gettman2005 /> Ureteroscopy is the preferred treatment in pregnant and morbidly obese people, as well as those with [[Bleeding diathesis|bleeding disorders]].<ref name=Miller2007 />
{{Clear}}

== Epidemiology ==
{| class="wikitable" style="float: right; margin-left:15px; text-align:center"
! Country
! Earliest prevalence (years)<ref name=RevUrol2010 />
! Latest prevalence (years)<ref name=RevUrol2010 />
|-
| United States
| 2.6% (1964–1972)
| 5.2% (1988–1994)
|-
| Italy
| 1.2% (1983)
| 1.7% (1993–1994)
|-
| Scotland
| 3.8% (1977)
| 3.5% (1987)
|-
| Spain
| 0.1% (1977)
| 10.0% (1991)
|-
| Turkey
| n/a
| 14.8% (1989)
|-
|}
{| class="wikitable" style="float: right; margin-left:15px; text-align:center"
! Country
! New cases per 100,000 (year)<ref name=RevUrol2010 />
! Trend
|-
| United States
| 116 (2000)
| decreasing
|-
| Germany
| 720 (2000)
| increasing
|-
| Japan
| 114.3 (2005)
| increasing
|-
| Spain
| 270 (1984)
| decreasing
|-
| Sweden
| 200 (1969)
| increasing
|-
|}
[[File:Urolithiasis world map-Deaths per million persons-WHO2012.svg|thumb|upright=1.3|Urolithiasis deaths per million persons in 2012 {{Div col|small=yes|colwidth=10em}}{{legend|#ffff20|0–0}}{{legend|#ffa020|1–1}}{{legend|#f08015|2–2}}{{legend|#d85010|3–3}}{{legend|#d02010|4–20}}{{div col end}}]]
Kidney stones affect all geographical, cultural, and racial groups. The [[Cumulative incidence|lifetime risk]] is about 10-15% in the developed world, but can be as high as 20-25% in the [[Middle East]]. The increased risk of dehydration in hot climates, coupled with a diet 50% lower in calcium and 250% higher in oxalates compared to Western diets, accounts for the higher net risk in the Middle East.<ref name=Potts2004 /> In the Middle East, uric acid stones are more common than calcium-containing stones.<ref name=Reilly2005Ch13 /> The number of deaths due to kidney stones is estimated at 19,000 per year being fairly consistent between 1990 and 2010.<ref name=Loz2012>{{cite journal |vauthors= Lozano R, Naghavi M, Foreman K, Lim S, Shibuya K, Aboyans V, Abraham J, Adair T, Aggarwal R, Ahn SY, Alvarado M, Anderson HR, Anderson LM, Andrews KG, Atkinson C, Baddour LM, Barker-Collo S, Bartels DH, Bell ML, Benjamin EJ, Bennett D, Bhalla K, Bikbov B, Bin Abdulhak A, Birbeck G, Blyth F, Bolliger I, Boufous S, Bucello C, Burch M, Burney P, Carapetis J, Chen H, Chou D, Chugh SS, Coffeng LE, Colan SD, Colquhoun S, Colson KE, Condon J, Connor MD, Cooper LT, Corriere M, Cortinovis M, de Vaccaro KC, Couser W, Cowie BC, Criqui MH, Cross M, Dabhadkar KC, Dahodwala N, De Leo D, Degenhardt L, Delossantos A, Denenberg J, Des Jarlais DC, Dharmaratne SD, Dorsey ER, Driscoll T, Duber H, Ebel B, Erwin PJ, Espindola P, Ezzati M, Feigin V, Flaxman AD, Forouzanfar MH, Fowkes FG, Franklin R, Fransen M, Freeman MK, Gabriel SE, Gakidou E, Gaspari F, Gillum RF, Gonzalez-Medina D, Halasa YA, Haring D, Harrison JE, Havmoeller R, Hay RJ, Hoen B, Hotez PJ, Hoy D, Jacobsen KH, James SL, Jasrasaria R, Jayaraman S, Johns N, Karthikeyan G, Kassebaum N, Keren A, Khoo JP, Knowlton LM, Kobusingye O, Koranteng A, Krishnamurthi R, Lipnick M, Lipshultz SE, Ohno SL, Mabweijano J, MacIntyre MF, Mallinger L, March L, Marks GB, Marks R, Matsumori A, Matzopoulos R, Mayosi BM, McAnulty JH, McDermott MM, McGrath J, Mensah GA, Merriman TR, Michaud C, Miller M, Miller TR, Mock C, Mocumbi AO, Mokdad AA, Moran A, Mulholland K, Nair MN, Naldi L, Narayan KM, Nasseri K, Norman P, O'Donnell M, Omer SB, Ortblad K, Osborne R, Ozgediz D, Pahari B, Pandian JD, Rivero AP, Padilla RP, Perez-Ruiz F, Perico N, Phillips D, Pierce K, Pope CA, Porrini E, Pourmalek F, Raju M, Ranganathan D, Rehm JT, Rein DB, Remuzzi G, Rivara FP, Roberts T, De León FR, Rosenfeld LC, Rushton L, Sacco RL, Salomon JA, Sampson U, Sanman E, Schwebel DC, Segui-Gomez M, Shepard DS, Singh D, Singleton J, Sliwa K, Smith E, Steer A, Taylor JA, Thomas B, Tleyjeh IM, Towbin JA, Truelsen T, Undurraga EA, Venketasubramanian N, Vijayakumar L, Vos T, Wagner GR, Wang M, Wang W, Watt K, Weinstock MA, Weintraub R, Wilkinson JD, Woolf AD, Wulf S, Yeh PH, Yip P, Zabetian A, Zheng ZJ, Lopez AD, Murray CJ, AlMazroa MA, Memish ZA |title= Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010 |journal= Lancet |volume= 380 |issue= 9859 |pages= 2095–128 |date= December 2012 |pmid= 23245604 |doi= 10.1016/S0140-6736(12)61728-0 |pmc= 10790329 |hdl= 10536/DRO/DU:30050819 |s2cid= 1541253 |url= https://zenodo.org/record/2557786 |archive-url=https://web.archive.org/web/20200519152712/https://zenodo.org/record/2557786 |archive-date=May 19, 2020|hdl-access= free }}</ref>

In North America and Europe, the annual [[incidence (epidemiology)|number of new cases per year]] of kidney stones is roughly 0.5%. In the United States, the frequency in the population of urolithiasis has increased from 3.2% to 5.2% from the mid-1970s to the mid-1990s.<ref name=Moe2006 /> In the United States, about 9% of the population has had a kidney stone.<ref name=NIH2013 />

The total cost for treating urolithiasis was US$2&nbsp;billion in 2003.<ref name=Pietrow2006 /> About 65–80% of those with kidney stones are men; most stones in women are due to either metabolic defects (such as [[cystinuria]]) or infections in the case of [[struvite stone]]s.<ref name=Heptinstall2007 /><ref>{{cite book| vauthors = Windus D |title=The Washington manual nephrology subspecialty consult |year=2008 |publisher=Wolters Kluwer Health/Lippincott Williams & Wilkins Health|location=Philadelphia |isbn=978-0-7817-9149-6 |page=235 |url=https://books.google.com/books?id=sPgGqotdzqAC&pg=PA235 |edition=2nd |url-status= live|archive-url=https://web.archive.org/web/20160909114412/https://books.google.com/books?id=sPgGqotdzqAC&pg=PA235 |archive-date=9 September 2016 |df=dmy-all}}</ref><ref name=":0" /> Urinary tract calculi disorders are more common in men than in women.  Men most commonly experience their first episode between 30 and 40 years of age, whereas for women, the age at first presentation is somewhat later.<ref name=Heptinstall2007 /> The age of onset shows a [[bimodal distribution]] in women, with episodes peaking at 35 and 55 years.<ref name=Pietrow2006 /> Recurrence rates are estimated at 50% over a 10-year and 75% over 20-year period,<ref name=Moe2006 /> with some people experiencing ten or more episodes over the course of a lifetime.<ref name=Heptinstall2007 />

A 2010 review concluded that rates of disease are increasing.<ref name=RevUrol2010>{{cite journal | vauthors = Romero V, Akpinar H, Assimos DG | title = Kidney stones: a global picture of prevalence, incidence, and associated risk factors | journal = Reviews in Urology | volume = 12 | issue = 2–3 | pages = e86-96 | year = 2010 | pmid = 20811557 | pmc = 2931286 }}</ref>

== History ==
{{See also|List of kidney stone formers}}
The existence of kidney stones was first recorded thousands of years ago, with various explanations given; Joseph Glanville's ''[[Saducismus Triumphatus]],'' for example, gives a detailed description of Abraham Mechelburg's voiding of small stones through his penis' virga, attributing the issue to witchcraft.<ref>{{cite book |last=Glanvill |first=Joseph |url=http://worldcat.org/oclc/943229347 |title=Saducismus triumphatus, or, Full and plain evidence concerning witches and apparitions : in two parts, the first treating of their possibility, the second of their real existence |isbn=1-171-33286-6 |oclc=943229347}}</ref>

In 1901, a stone discovered in the [[pelvis]] of an ancient Egyptian [[mummy]] was dated to 4,800&nbsp;BC.

Medical texts from ancient [[Mesopotamia]], [[History of India|India]], [[History of China|China]], [[Achaemenid Empire|Persia]], [[Ancient Greece|Greece]], and [[Ancient Rome|Rome]] all mentioned calculous disease. Part of the [[Hippocratic Oath]] suggests there were practicing surgeons in ancient Greece to whom physicians were to defer for [[Lithotomy|lithotomies]], or the surgical removal of stones. The Roman medical treatise ''[[De Medicina]]'' by [[Aulus Cornelius Celsus]] contained a description of lithotomy,<ref name="Collier1831" /> and this work served as the basis for this procedure until the 18th century.<ref name="Shah2002" />

Examples of people who had kidney stone disease include [[Napoleon]] I, [[Epicurus]], [[Napoleon III]], [[Peter the Great]], [[Louis XIV of France|Louis XIV]], [[George IV of the United Kingdom|George IV]], [[Oliver Cromwell]], [[Lyndon B. Johnson]], [[Benjamin Franklin]], [[Michel de Montaigne]], [[Francis Bacon]], [[Isaac Newton]], [[Samuel Pepys]], [[William Harvey]], [[Herman Boerhaave]], and [[Antonio Scarpa]].<ref name=Ellis1969 />

New techniques in lithotomy began to emerge starting in 1520, but the operation remained risky. After [[Henry Jacob Bigelow]] popularized the technique of [[litholapaxy]] in 1878,<ref name=Bigelow1878 /> the [[mortality rate]] dropped from about 24% to 2.4%. However, other treatment techniques continued to produce a high level of mortality, especially among inexperienced urologists.<ref name=Shah2002 /><ref name=Ellis1969 /> In 1980, [[Dornier Flugzeugwerke|Dornier MedTech]] introduced extracorporeal shock wave lithotripsy for breaking up stones via acoustical pulses, and this technique has since come into widespread use.<ref name=AUA2009 />

=== Etymology ===
The term ''renal calculus'' is from the [[Latin]] ''rēnēs'', meaning "kidneys", and ''[[Calculus (medicine)|calculus]]'', meaning "pebble". Lithiasis (stone formation) in the kidneys is called nephrolithiasis ({{IPAc-en|ˌ|n|ɛ|f|r|oʊ|l|ɪ|ˈ|θ|aɪ|ə|s|ᵻ|s}}), from ''[[wikt:nephro-|nephro]]-'', meaning kidney, + ''[[wikt:-lith|-lith]]'', meaning stone, and ''[[wikt:-iasis#Suffix|-iasis]]'', meaning disorder. A distinction between nephrolithiasis and urolithiasis can be made because not all urinary stones (uroliths) form in the kidney; they can also form in the bladder. But the distinction is often clinically irrelevant (with similar disease process and treatment either way) and the words are thus often used loosely as synonyms.

== Children ==
Although kidney stones do not often occur in children, the incidence is increasing.<ref name="Dwyer2012">{{cite journal | vauthors = Dwyer ME, Krambeck AE, Bergstralh EJ, Milliner DS, Lieske JC, Rule AD | title = Temporal trends in incidence of kidney stones among children: a 25-year population based study | journal = The Journal of Urology | volume = 188 | issue = 1 | pages = 247–52 | date = July 2012 | pmid = 22595060 | pmc = 3482509 | doi = 10.1016/j.juro.2012.03.021 }}</ref> These stones are in the kidney in two thirds of reported cases, and in the [[ureter]] in the remaining cases. Older children are at greater risk independent of whether or not they are male or female.<ref>{{cite web |url=http://www.pediatriconcall.com/fordoctor/DiseasesandCondition/Diet_diseases/diet_for_renal.asp |archive-url=https://web.archive.org/web/20071117030318/http://www.pediatriconcall.com/fordoctor/DiseasesandCondition/Diet_diseases/diet_for_renal.asp |url-status=dead |archive-date=17 November 2007 |title=Diet and Definition of Kidney Stones, Renal Calculi |access-date=11 October 2013}}</ref>

As with adults, most pediatric kidney stones are predominantly composed of [[calcium oxalate]]; [[struvite]] and [[calcium phosphate]] stones are less common. Calcium oxalate stones in children are associated with high amounts of calcium, oxalate, and magnesium in acidic urine.<ref name="Kirejczyk-2013">{{cite journal | vauthors = Kirejczyk JK, Porowski T, Filonowicz R, Kazberuk A, Stefanowicz M, Wasilewska A, Debek W | title = An association between kidney stone composition and urinary metabolic disturbances in children | journal = Journal of Pediatric Urology | volume = 10 | issue = 1 | pages = 130–5 | date = February 2014 | pmid = 23953243 | doi = 10.1016/j.jpurol.2013.07.010 | doi-access = free }}</ref>

Treatment of kidney stones in children is similar to treatments for adults, including shock wave lithotripsy, medication, and treatment using scope through the bladder, kidney or skin.<ref name=":2">{{cite journal | vauthors = Barreto L, Jung JH, Abdelrahim A, Ahmed M, Dawkins GP, Kazmierski M | title = Medical and surgical interventions for the treatment of urinary stones in children | journal = The Cochrane Database of Systematic Reviews | volume = 6 | pages = CD010784 | date = June 2018 | issue = 6 | pmid = 29859007 | pmc = 6513049 | doi = 10.1002/14651858.CD010784.pub2 | collaboration = Cochrane Urology Group }}</ref> Of these treatments, research is uncertain if shock waves are more effective than medication or a scope through the bladder, but it is likely less successful than a scope through skin into the kidney.<ref name=":2" /> When going in with a scope through the kidney, a regular and a mini-sized scope likely have similar success rates of stone removal. Alpha-blockers, a type of medication, may increase the successful removal of kidney stones when compared with a placebo and without ibuprofen.<ref name=":2" />

== Research ==
[[Metabolic syndrome]] and its associated diseases of obesity and diabetes as general risk factors for kidney stone disease are under research  to determine if urinary excretion of calcium, oxalate and urate are higher than in people with normal weight or underweight, and if diet and physical activity have roles.<ref name="Aune">{{cite journal | vauthors = Aune D, Mahamat-Saleh Y, Norat T, Riboli E | title = Body fatness, diabetes, physical activity and risk of kidney stones: a systematic review and meta-analysis of cohort studies | journal = European Journal of Epidemiology | volume = 33 | issue = 11 | pages = 1033–1047 | date = November 2018 | pmid = 30066054 | pmc = 6208979 | doi = 10.1007/s10654-018-0426-4 }}</ref><ref name="Trinch">{{cite journal | vauthors = Trinchieri A, Croppi E, Montanari E | title = Obesity and urolithiasis: evidence of regional influences | journal = Urolithiasis | volume = 45 | issue = 3 | pages = 271–278 | date = June 2017 | pmid = 27488444 | doi = 10.1007/s00240-016-0908-3 | s2cid = 4585476 }}</ref> Dietary, fluid intake, and lifestyle factors remain major topics for research on prevention of kidney stones, as of 2017.<ref name="Zisman">{{cite journal | vauthors = Zisman AL | title = Effectiveness of Treatment Modalities on Kidney Stone Recurrence | journal = Clinical Journal of the American Society of Nephrology | volume = 12 | issue = 10 | pages = 1699–1708 | date = October 2017 | pmid = 28830863 | pmc = 5628726 | doi = 10.2215/cjn.11201016 }}</ref>

=== Gut microbiota ===
The [[gut microbiota]] has been explored as a contributing factor for stone disease, indicating that some bacteria may be different in people forming kidney stones.<ref>{{cite journal |last1=Stanford |first1=Jordan |last2=Charlton |first2=Karen |last3=Stefoska-Needham |first3=Anita |last4=Ibrahim |first4=Rukayat |last5=Lambert |first5=Kelly |title=The gut microbiota profile of adults with kidney disease and kidney stones: a systematic review of the literature |journal=BMC Nephrology|date=5 June 2020 |language=en |volume=21 |issue=1 |pages=215 |doi=10.1186/s12882-020-01805-w |issn=1471-2369 |pmc=7275316 |pmid=32503496 |doi-access=free }}</ref> One bacterium, ''[[Oxalobacter formigenes]]'', is potentially beneficial for mitigating calcium oxalate stones because of its ability to metabolize oxalate as its sole carbon source,<ref>{{cite journal |last1=Duncan |first1=Sylvia H. |last2=Richardson |first2=Anthony J. |last3=Kaul |first3=Poonam |last4=Holmes |first4=Ross P. |last5=Allison |first5=Milton J. |last6=Stewart |first6=Colin S. |date=2002-08-01 |title=Oxalobacter formigenes and Its Potential Role in Human Health |journal=Applied and Environmental Microbiology |language=en |volume=68 |issue=8 |pages=3841–3847 |doi=10.1128/AEM.68.8.3841-3847.2002 |issn=0099-2240 |pmc=124017 |pmid=12147479|bibcode=2002ApEnM..68.3841D }}</ref> but 2018 research suggests that it is instead part of a network of oxalate degrading bacteria.<ref>{{cite journal |last1=Ticinesi |first1=Andrea |last2=Milani |first2=Christian |last3=Guerra |first3=Angela |last4=Allegri |first4=Franca |last5=Lauretani |first5=Fulvio |last6=Nouvenne |first6=Antonio |last7=Mancabelli |first7=Leonardo |last8=Lugli |first8=Gabriele Andrea |last9=Turroni |first9=Francesca |last10=Duranti |first10=Sabrina |last11=Mangifesta |first11=Marta |title=Understanding the gut–kidney axis in nephrolithiasis: an analysis of the gut microbiota composition and functionality of stone formers |url=https://gut.bmj.com/lookup/doi/10.1136/gutjnl-2017-315734|date=28 April 2018 |journal=Gut |language=en |volume=67 |issue=12 |pages=2097–2106 |doi=10.1136/gutjnl-2017-315734 |pmid=29705728 |s2cid=14055215 |issn=0017-5749}}</ref> Additionally, one study found that oral [[antibiotic]] use, which alters the gut microbiota,<ref>{{cite journal |last1=Ramirez |first1=Jaime |last2=Guarner |first2=Francisco |last3=Bustos Fernandez |first3=Luis |last4=Maruy |first4=Aldo |last5=Sdepanian |first5=Vera Lucia |last6=Cohen |first6=Henry |date=2020-11-24 |title=Antibiotics as Major Disruptors of Gut Microbiota |journal=Frontiers in Cellular and Infection Microbiology |volume=10 |pages=572912 |doi=10.3389/fcimb.2020.572912 |issn=2235-2988 |pmc=7732679 |pmid=33330122|doi-access=free }}</ref> can increase the odds of a person developing a kidney stone.<ref>{{cite journal |last1=Tasian |first1=Gregory E. |last2=Jemielita |first2=Thomas |last3=Goldfarb |first3=David S. |last4=Copelovitch |first4=Lawrence |last5=Gerber |first5=Jeffrey S. |last6=Wu |first6=Qufei |last7=Denburg |first7=Michelle R. |date=2018-06-01 |title=Oral Antibiotic Exposure and Kidney Stone Disease |journal=Journal of the American Society of Nephrology |language=en |volume=29 |issue=6 |pages=1731–1740 |doi=10.1681/ASN.2017111213 |issn=1046-6673 |pmc=6054354 |pmid=29748329}}</ref>

==In other animals==
Among [[ruminant]]s, uroliths more commonly cause problems in males than in females; the sigmoid flexure of the ruminant male urinary tract is more likely to obstruct passage. Early-castrated males are at greater risk, because of lesser urethral diameter.<ref name="PughBaird2012">{{cite book | vauthors = Pugh DG, Baird N | title = Sheep & Goat Medicine - E-Book | url = https://books.google.com/books?id=s-Z311q6CIcC | date = 27 May 2012 | publisher = Elsevier Health Sciences | isbn = 978-1-4377-2354-0 | access-date = 17 June 2018 | archive-date = 14 April 2021 | archive-url = https://web.archive.org/web/20210414055355/https://books.google.com/books?id=s-Z311q6CIcC | url-status = live }}</ref>

Low Ca:P intake ratio is conducive to phosphatic (e.g. struvite) urolith formation.<ref name=PughBaird2012/>  Incidence among wether lambs can be minimized by maintaining a dietary Ca:P intake ratio of 2:1.<ref name=PughBaird2012/><ref>{{cite journal | vauthors = Bushman DH, Emerick RJ, Embry LB | title = Experimentally induced ovine phosphatic urolithiasis: relationships involving dietary calcium, phosphorus and magnesium | journal = The Journal of Nutrition | volume = 87 | issue = 4 | pages = 499–504 | date = December 1965 | pmid = 5841867 | doi = 10.1093/jn/87.4.499 }}</ref>

Alkaline (higher) [[pH]] favors formation of [[#Composition|carbonate and phosphate calculi]]. For domestic ruminants, dietary cation: anion balance is sometimes adjusted to assure a slightly acidic urine pH, for prevention of calculus formation.<ref name=PughBaird2012/>

Differing generalizations regarding effects of pH on formation of silicate uroliths may be found.<ref name=PughBaird2012/><ref>{{cite journal | vauthors = Stewart SR, Emerick RJ, Pritchard RH | title = Effects of dietary ammonium chloride and variations in calcium to phosphorus ratio on silica urolithiasis in sheep | journal = Journal of Animal Science | volume = 69 | issue = 5 | pages = 2225–9 | date = May 1991 | pmid = 1648554 | doi = 10.2527/1991.6952225x | url = http://pdfs.semanticscholar.org/b1f1/b2a896e57ed8350fe826cffcb23496d2be2c.pdf | archive-url = https://web.archive.org/web/20190302075532/http://pdfs.semanticscholar.org/b1f1/b2a896e57ed8350fe826cffcb23496d2be2c.pdf | url-status = dead | archive-date = 2019-03-02 | s2cid = 10130833 }}</ref>  In this connection, it may be noted that under some circumstances, calcium carbonate accompanies silica in siliceous uroliths.<ref>{{cite journal | vauthors = Forman SA, Whiting F, Connell R | title = Silica Urolithiasis In Beef Cattle : 3. Chemical and Physical Composition of the Uroliths | journal = Canadian Journal of Comparative Medicine and Veterinary Science | volume = 23 | issue = 5 | pages = 157–62 | date = May 1959 | pmid = 17649146 | pmc = 1581990 }}</ref>

Pelleted feeds may be conducive to formation of phosphate uroliths, because of increased urinary phosphorus excretion.  This is attributable to lower saliva production where pelleted rations containing finely ground constituents are fed.  With less blood phosphate partitioned into saliva, more tends to be excreted in urine.<ref>{{cite journal | vauthors = Scott D, Buchan W | title = The effects of feeding pelleted diets made from either coarsely or finely ground hay on phosphorus balance and on the partition of phosphorus excretion between urine and faeces in the sheep | journal = Quarterly Journal of Experimental Physiology | volume = 73 | issue = 3 | pages = 315–22 | date = May 1988 | pmid = 3399614 | doi = 10.1113/expphysiol.1988.sp003148 | doi-access = free }}</ref>  (Most saliva phosphate is fecally excreted.<ref>{{cite journal | vauthors = Bravo D, Sauvant D, Bogaert C, Meschy F | title = III. Quantitative aspects of phosphorus excretion in ruminants | journal = Reproduction, Nutrition, Development | volume = 43 | issue = 3 | pages = 285–300 | year = 2003 | pmid = 14620634 | doi = 10.1051/rnd:2003021 | url = https://hal.archives-ouvertes.fr/hal-00900449/file/hal-00900449.pdf | doi-access = free | access-date = 29 August 2019 | archive-date = 16 April 2021 | archive-url = https://web.archive.org/web/20210416000942/https://hal.archives-ouvertes.fr/hal-00900449/file/hal-00900449.pdf | url-status = live }}</ref>)

Oxalate uroliths can occur in ruminants, although such problems from oxalate ingestion may be relatively uncommon.  Ruminant urolithiasis associated with oxalate ingestion has been reported.<ref>Waltner-Toews, D. and D. H. Meadows.  1980.  Case report:  Urolithiasis in a herd of beef cattle associated with oxalate ingestion.  Can. Vet. J. 21: 61-62</ref>   However, no renal tubular damage or visible deposition of calcium oxalate crystals in kidneys was found in yearling wether sheep fed diets containing soluble oxalate at 6.5 percent of dietary dry matter for about 100 days.<ref>{{cite journal | vauthors = James LF, Butcher JE | title = Halogeton poisoning of sheep: effect of high level oxalate intake | journal = Journal of Animal Science | volume = 35 | issue = 6 | pages = 1233–1238 | date = December 1972 | pmid = 4647453 | doi = 10.2527/jas1972.3561233x }}</ref>

Conditions limiting water intake can result in stone formation.<ref name=Kahn2005>{{cite book | veditors = Kahn CM | date = 2005 | title = Merck veterinary manual | edition = 9th | publisher = Merck & Co., Inc. | location = Whitehouse Station }}</ref>

Various surgical interventions, e.g.  amputation of the urethral process at its base near the glans penis in male ruminants, perineal [[urethrostomy]], or tube [[Suprapubic cystostomy|cystostomy]] may be considered for relief of obstructive urolithiasis.<ref name=Kahn2005/>

== See also ==
* [[Nephrocalcinosis]]
* [[Kidney disease]]
* [[Renal stone formation in space|Kidney stone formation in space]]

== References ==
{{Reflist|30em|refs=

<ref name=Anoia2009>{{cite book|veditors=Graham SD, Keane TE|title=Glenn's Urologic Surgery|edition=7th|vauthors=Anoia EJ, Paik ML, Resnick MI|chapter=Ch. 7: Anatrophic Nephrolithomy|pages=45–50|publisher=Lippincott Williams & Wilkins|location=Philadelphia|year=2009|isbn=978-0-7817-9141-0|chapter-url=https://books.google.com/books?id=GahMzaKgMKAC&q=nephrolithiasis+diagnosis+radiographic&pg=PA45|access-date=6 November 2020|archive-date=14 April 2021|archive-url=https://web.archive.org/web/20210414030139/https://books.google.com/books?id=GahMzaKgMKAC&q=nephrolithiasis+diagnosis+radiographic&pg=PA45|url-status=live}}</ref>

<ref name=AUA2009>{{cite web|author=Shock Wave Lithotripsy Task Force|title=Current Perspective on Adverse Effects in Shock Wave Lithotripsy|work=Clinical Guidelines|publisher=[[American Urological Association]]|location=Linthicum, Maryland|year=2009|url=https://www.auanet.org/common/pdf/education/clinical-guidance/Shock-Wave-Therapy-WP.pdf|access-date=13 October 2015|url-status=dead|archive-url=https://web.archive.org/web/20130718072759/http://www.auanet.org/common/pdf/education/clinical-guidance/Shock-Wave-Therapy-WP.pdf|archive-date=18 July 2013|df=dmy-all}}</ref>

<ref name=Bigelow1878>{{cite book|vauthors=Bigelow HJ|author-link=Henry Jacob Bigelow|title=Litholapaxy or rapid lithotrity with evacuation|page=29|publisher=A. Williams and Company|location=Boston|year=1878|url=https://books.google.com/books?id=UUkSAAAAYAAJ|access-date=25 August 2020|archive-date=14 April 2021|archive-url=https://web.archive.org/web/20210414060039/https://books.google.com/books?id=UUkSAAAAYAAJ|url-status=live}}</ref>

<ref name=Bushinsky2007>{{cite book | veditors = Brenner BM |title=Brenner and Rector's The Kidney|edition=8th|volume=1| vauthors = Bushinsky D, Coe FL, Moe OW | chapter = Ch. 37: Nephrolithiasis|pages=1299–349|publisher=WB Saunders|location=Philadelphia|year=2007|isbn=978-1-4160-3105-5|chapter-url=http://www.expertconsultbook.com/expertconsult/op/book.do?method=display&type=bookPage&decorator=none&eid=4-u1.0-B978-1-4160-3105-5..50039-6&isbn=978-1-4160-3105-5#lpState=open&lpTab=contentsTab&content=4-u1.0-B978-1-4160-3105-5..50039-6%3Bfrom%3Dtoc%3Btype%3DbookPage%3Bisbn%3D978-1-4160-3105-5&search=none|url-status=dead|archive-url=https://web.archive.org/web/20111008090923/http://www.expertconsultbook.com/expertconsult/op/book.do?method=display&type=bookPage&decorator=none&eid=4-u1.0-B978-1-4160-3105-5..50039-6&isbn=978-1-4160-3105-5#lpState=open&lpTab=contentsTab&content=4-u1.0-B978-1-4160-3105-5..50039-6%3Bfrom%3Dtoc%3Btype%3DbookPage%3Bisbn%3D978-1-4160-3105-5&search=none|archive-date=8 October 2011|df=dmy-all}}</ref>

<ref name=Cameron1987>{{cite journal | vauthors = Cameron JS, Simmonds HA | title = Use and abuse of allopurinol | journal = British Medical Journal | volume = 294 | issue = 6586 | pages = 1504–5 | date = June 1987 | pmid = 3607420 | pmc = 1246665 | doi = 10.1136/bmj.294.6586.1504 }}</ref>

<ref name=Carr1990>{{cite journal | vauthors = Carr MC, Prien EL, Babayan RK | title = Triamterene nephrolithiasis: renewed attention is warranted | journal = The Journal of Urology | volume = 144 | issue = 6 | pages = 1339–40 | date = December 1990 | pmid = 2231920 | doi = 10.1016/S0022-5347(17)39734-3 }}</ref>

<ref name=Cavendish2008>{{cite book|vauthors=Cavendish M|title=Diseases and Disorders|edition=1st|volume=2|chapter=Kidney disorders|pages=490–3|publisher=Marshall Cavendish Corporation|location=Tarrytown, New York|year=2008|isbn=978-0-7614-7772-3|chapter-url=https://books.google.com/books?id=L5fGm_7ThKEC&q=0761477721&pg=PA507|access-date=6 November 2020|archive-date=14 April 2021|archive-url=https://web.archive.org/web/20210414055706/https://books.google.com/books?id=L5fGm_7ThKEC&q=0761477721&pg=PA507|url-status=live}}</ref>

<ref name=Coe2005>{{cite journal | vauthors = Coe FL, Evan A, Worcester E | title = Kidney stone disease | journal = The Journal of Clinical Investigation | volume = 115 | issue = 10 | pages = 2598–608 | date = October 2005 | pmid = 16200192 | pmc = 1236703 | doi = 10.1172/JCI26662 }}</ref>

<ref name=Collier1831>{{cite book  | vauthors = Celsus AC |author-link=Aulus Cornelius Celsus| veditors = Collier GF |title=A translation of the eight books of Aul. Corn. Celsus on medicine|edition=2nd|chapter=Book VII, Chapter XXVI: Of the operation necessary in a suppression of urine, and lithotomy |pages=306–14 |publisher=Simpkin and Marshall |location=London |year=1831 |chapter-url=https://books.google.com/books?id=p2kFAAAAQAAJ&pg=PA311|url-status=live|archive-url= https://web.archive.org/web/20140708104311/http://books.google.com/books?id=p2kFAAAAQAAJ&pg=PA311 |archive-date=8 July 2014 |df=dmy-all}}</ref>

<ref name=Coskun1993>{{cite journal | vauthors = Coşkun T, Ozalp I, Tokatli A | title = Iminoglycinuria: a benign type of inherited aminoaciduria | journal = The Turkish Journal of Pediatrics | volume = 35 | issue = 2 | pages = 121–5 | year = 1993 | pmid = 7504361 }}</ref>

<ref name=Cutler2007>{{cite book|veditors=Cutler RE|vauthors=Preminger GM|title=The Merck Manual of Medical Information Home Edition|edition=3rd|chapter=Chapter 148: Stones in the Urinary Tract|publisher=[[Merck & Co.|Merck Sharp and Dohme Corporation]]|location=Whitehouse Station, New Jersey|year=2007|chapter-url=http://www.merckmanuals.com/home/sec12/ch148/ch148a.html|title-link=Merck Manual of Diagnosis and Therapy|access-date=7 August 2011|archive-date=8 December 2014|archive-url=https://web.archive.org/web/20141208070004/http://www.merckmanuals.com/home/sec12/ch148/ch148a.html|url-status=live}}</ref>

<ref name=Crixivan2010>{{cite web |title=Patient Information about Crixivan for HIV (Human Immunodeficiency Virus) Infection|work=Crixivan® (indinavir sulfate) Capsules|publisher=Merck Sharp & Dohme Corporation|location=Whitehouse Station, New Jersey|year=2010|url=http://www.merck.com/product/usa/pi_circulars/c/crixivan/crixivan_ppi.pdf|access-date=27 July 2011|url-status=live|archive-url=https://web.archive.org/web/20110815003924/http://www.merck.com/product/usa/pi_circulars/c/crixivan/crixivan_ppi.pdf|archive-date=15 August 2011|df=dmy-all}}</ref>

<!-- Not in use
<ref name=Eknoyan2004>{{cite journal| vauthors = Eknoyan G |title=History of urolithiasis|journal=Clinical Reviews in Bone and Mineral Metabolism|volume=2|issue=3|pages=177–85|year=2004|issn=1534-8644|doi=10.1385/BMM:2:3:177|s2cid=71156397}}</ref>
Not in use-->

<ref name=Ellis1969>{{cite book| vauthors = Ellis H |title=A History of Bladder Stone|publisher=Blackwell Scientific Publications|location=Oxford, England|year=1969|isbn=978-0-632-06140-2}}</ref>

<ref name=Evan1996>{{cite book | vauthors = Evan AP, McAteer JA |chapter= Ch. 28: Q-effects of Shock Wave Lithotripsy |title= Kidney Stones: Medical and Surgical Management | url = https://archive.org/details/kidneystonesmedi0000unse | url-access = registration | veditors = Coe FL, Favus MJ, Pak CY, Parks JH, Preminger GM |location= Philadelphia |publisher= Lippincott-Raven |year= 1996 |pages= [https://archive.org/details/kidneystonesmedi0000unse/page/549 549]–60|isbn= 978-0-7817-0263-8 }}</ref>

<ref name=Evan2007>{{cite book | vauthors = Evan AP, Willis LR |year= 2007 |chapter= Ch. 41: Extracorporeal Shock Wave Lithotripsy: Complications |title= Smith's Textbook on Endourology | veditors = Smith AD, Badlani GH, Bagley DH, Clayman RV, Docimo SG |location= Hamilton, Ontario, Canada |publisher= B C Decker, Inc. |pages= 353–65 }}</ref>

<ref name=Fang2009>{{cite book|veditors=Goroll AH, Mulley AG|title=Primary care medicine: office evaluation and management of the adult patient|edition=6th|vauthors=Fang LS|chapter=Chapter 135: Approach to the Paient with Nephrolithiasis|pages=962–7|publisher=Lippincott Williams & Wilkins|location=Philadelphia|year=2009|isbn=978-0-7817-7513-7|chapter-url=https://books.google.com/books?id=bIZvJPcSEXMC&q=nephrolithiasis+%22physical+examination%22&pg=PA964|access-date=6 November 2020|archive-date=21 March 2021|archive-url=https://web.archive.org/web/20210321183305/https://books.google.com/books?id=bIZvJPcSEXMC&q=nephrolithiasis+%22physical+examination%22&pg=PA964|url-status=live}}</ref>

<ref name=Finkielstein2006>{{cite journal | vauthors = Finkielstein VA, Goldfarb DS | title = Strategies for preventing calcium oxalate stones | journal = CMAJ | volume = 174 | issue = 10 | pages = 1407–9 | date = May 2006 | pmid = 16682705 | pmc = 1455427 | doi = 10.1503/cmaj.051517 | url = http://www.cmaj.ca/cgi/reprint/174/10/1407 | archive-url = https://web.archive.org/web/20081015202450/http://www.cmaj.ca/cgi/reprint/174/10/1407 | df = dmy-all | url-status = live | archive-date = 15 October 2008 }}</ref>

<ref name=Gettman2005>{{cite journal | vauthors = Gettman MT, Segura JW | title = Management of ureteric stones: issues and controversies | journal = BJU International | volume = 95 | issue = Suppl 2 | pages = 85–93 | date = March 2005 | pmid = 15720341 | doi = 10.1111/j.1464-410X.2005.05206.x | s2cid = 36265416 }}</ref>

<ref name=Goldfarb1999>{{cite journal | vauthors = Goldfarb DS, Coe FL | title = Prevention of recurrent nephrolithiasis | journal = American Family Physician | volume = 60 | issue = 8 | pages = 2269–76 | date = November 1999 | pmid = 10593318 | url = http://www.aafp.org/afp/991115ap/2269.html | archive-url = https://web.archive.org/web/20050822183805/http://www.aafp.org/afp/991115ap/2269.html | df = dmy-all | url-status = live | archive-date = 22 August 2005 }}</ref>

<ref name=Goodwin1998>{{cite journal | vauthors = Goodwin JS, Tangum MR | title = Battling quackery: attitudes about micronutrient supplements in American academic medicine | journal = Archives of Internal Medicine | volume = 158 | issue = 20 | pages = 2187–91 | date = November 1998 | pmid = 9818798 | doi = 10.1001/archinte.158.20.2187 }}</ref>

<ref name=Halabe1994>{{cite journal | vauthors = Halabe A, Sperling O | title = Uric acid nephrolithiasis | journal = Mineral and Electrolyte Metabolism | volume = 20 | issue = 6 | pages = 424–31 | year = 1994 | pmid = 7783706 }}</ref>

<ref name=Heaney2006>{{cite journal | vauthors = Heaney RP | title = Nutrition and chronic disease | journal = Mayo Clinic Proceedings | volume = 81 | issue = 3 | pages = 297–9 | date = March 2006 | pmid = 16529131 | doi = 10.4065/81.3.297 | df = dmy-all | doi-access = free }}</ref>

<ref name=Heptinstall2007>{{cite book|veditors=Jennette JC, Olson JL, Schwartz MM, Silva FG|title=Heptinstall's Pathology of the Kidney|edition=6th|volume=2|vauthors=Weiss M, Liapis H, Tomaszewski JE, Arend LJ|chapter=Chapter 22: Pyelonephritis and Other Infections, Reflux Nephropathy, Hydronephrosis, and Nephrolithiasis|pages=991–1082|publisher=Lippincott Williams & Wilkins|location=Philadelphia|year=2007|isbn=978-0-7817-4750-9|chapter-url=https://books.google.com/books?id=oWymx2hp1OoC&q=%22AA+amyloidosis%22+pyelonephritis&pg=PA886|access-date=6 November 2020|archive-date=20 March 2021|archive-url=https://web.archive.org/web/20210320231125/https://books.google.com/books?id=oWymx2hp1OoC&q=%22AA+amyloidosis%22+pyelonephritis&pg=PA886|url-status=live}}</ref>

<ref name=HFCS>{{cite journal | vauthors = Knight J, Assimos DG, Easter L, Holmes RP | title = Metabolism of fructose to oxalate and glycolate | journal = Hormone and Metabolic Research | volume = 42 | issue = 12 | pages = 868–73 | date = November 2010 | pmid = 20842614 | pmc = 3139422 | doi = 10.1055/s-0030-1265145 }}</ref>

<ref name=Hoppe2003>{{cite journal | vauthors = Hoppe B, Langman CB | title = A United States survey on diagnosis, treatment, and outcome of primary hyperoxaluria | journal = Pediatric Nephrology | volume = 18 | issue = 10 | pages = 986–91 | date = October 2003 | pmid = 12920626 | doi = 10.1007/s00467-003-1234-x | s2cid = 23503869 }}</ref>

<ref name=IOM2010p8>"Summary". In {{harvnb|Committee to Review Dietary Reference Intakes for Vitamin D and Calcium|2011|pp= 1–14}}.</ref>

<ref name=IOM2010p413>"Tolerable upper intake levels: Calcium and vitamin D". In {{harvnb|Committee to Review Dietary Reference Intakes for Vitamin D and Calcium|2011|pp= 403–56}}.</ref>

<ref name=Johri2010>{{cite journal | vauthors = Johri N, Cooper B, Robertson W, Choong S, Rickards D, Unwin R | title = An update and practical guide to renal stone management | journal = Nephron Clinical Practice | volume = 116 | issue = 3 | pages = c159-71 | year = 2010 | pmid = 20606476 | doi = 10.1159/000317196 | url = https://www.karger.com/Article/PDF/000317196 | doi-access = free | access-date = 18 May 2019 | archive-date = 31 January 2021 | archive-url = https://web.archive.org/web/20210131093917/https://www.karger.com/Article/PDF/000317196 | url-status = live }}</ref>

<ref name=Kamatani1996>{{cite journal | vauthors = Kamatani N | title = [Adenine phosphoribosyltransferase(APRT) deficiency] | language = ja | journal = Nihon Rinsho. Japanese Journal of Clinical Medicine | volume = 54 | issue = 12 | pages = 3321–7 | date = December 1996 | pmid = 8976113 }}</ref>

<ref name=Knudsen2007>{{citation | vauthors = Knudsen BE, Beiko DT, Denstedt JD |title=  ''Ch. 16: "Uric Acid Urolithiasis"'' |postscript= .}} In {{harvnb|Stoller|Meng|2007|pp= 299–308}}.</ref>

<ref name=Lam2007>{{citation | vauthors = Lam JS, Gupta M |title= ''Ch. 25: "Ureteral Stents"'' |postscript= .}} In {{harvnb|Stoller|Meng|2007|pp= 465–83}}.</ref>

<ref name=Liebman2011>{{cite journal | vauthors = Liebman M, Al-Wahsh IA | title = Probiotics and other key determinants of dietary oxalate absorption | journal = Advances in Nutrition | volume = 2 | issue = 3 | pages = 254–60 | date = May 2011 | pmid = 22332057 | pmc = 3090165 | doi = 10.3945/an.111.000414 | url = http://advances.nutrition.org/content/2/3/254.full.pdf | archive-url = https://web.archive.org/web/20160116135506/http://advances.nutrition.org/content/2/3/254.full.pdf | df = dmy-all | url-status = live | archive-date = 16 January 2016 }}</ref>

<ref name=Lingeman2007>{{cite book | vauthors = Lingeman JE, Matlaga BR, Evan AP |year= 2007 |chapter= Surgical Management of Urinary Lithiasis |title= Campbell-Walsh Urology | veditors = Wein AJ, Kavoussi LR, Novick AC, Partin AW, Peters CA |location= Philadelphia |publisher= W. B. Saunders |pages= 1431–1507}}</ref>

<ref name=Macaluso1999>{{cite journal | vauthors = Macaluso JN | title = Management of stone disease--bearing the burden | journal = The Journal of Urology | volume = 156 | issue = 5 | pages = 1579–80 | date = November 1996 | pmid = 8863542 | doi = 10.1016/S0022-5347(01)65452-1 }}</ref>

<ref name=Marks2011>{{citation | vauthors = Marks AJ, Qiu J, Milner TE, Chan KF, Teichman JM |title= ''Ch. 26: "Laser Lithotripsy Physics"'' |date= 6 January 2011 |publisher= Springer |isbn= 978-1-84800-362-0 |url=https://books.google.com/books?id=LlJy5XJOkSkC&pg=PA302 |access-date=6 November 2020|url-status=live|archive-date=20 February 2021|archive-url=https://web.archive.org/web/20210220110253/https://books.google.com/books?id=LlJy5XJOkSkC&pg=PA302}} in {{harvnb|Rao|Preminger|Kavanagh|2011|pp=301–310}}.</ref>

<ref name=McNutt1893>{{cite book| vauthors = McNutt WF |title=Diseases of the Kidneys and Bladder: A Text-Book for Students of Medicine|chapter=Section IV: Diseases of the Bladder, Chapter VII: Vesical Calculi (Cysto-lithiasis)|pages=185–6|publisher=J.B. Lippincott Company|location=Philadelphia|year=1893|chapter-url=https://books.google.com/books?id=RP0oAAAAYAAJ&q=cystolithiasis+symptoms&pg=PA185|access-date=6 November 2020|archive-date=14 April 2021|archive-url=https://web.archive.org/web/20210414030140/https://books.google.com/books?id=RP0oAAAAYAAJ&q=cystolithiasis+symptoms&pg=PA185|url-status=live}}</ref>

<ref name=Moe2006>{{cite journal | vauthors = Moe OW | title = Kidney stones: pathophysiology and medical management | journal = Lancet | volume = 367 | issue = 9507 | pages = 333–44 | date = January 2006 | pmid = 16443041 | doi = 10.1016/S0140-6736(06)68071-9 | s2cid = 26581831 | url = http://emed.chris-barton.com/PDF/kidney%20stones%20pathophys%20and%20rx.pdf | archive-url = https://web.archive.org/web/20110815154001/http://emed.chris-barton.com/PDF/kidney%20stones%20pathophys%20and%20rx.pdf | df = dmy-all | url-status = live | archive-date = 15 August 2011 }}</ref>

<ref name=NAS2006>{{cite book|author=Committee on Fluoride in Drinking Water of the National Academy of Sciences|title=Fluoride in Drinking Water: A Scientific Review of EPA's Standards|chapter=Chapter 9: Effects on the Renal System|pages=236–48|publisher=The National Academies Press|location=Washington, DC|year=2006|isbn=978-0-309-65799-0|chapter-url=http://www.nap.edu/openbook.php?record_id=11571&page=268|url-status=live|archive-url=https://web.archive.org/web/20110730220401/http://www.nap.edu/openbook.php?record_id=11571&page=268|archive-date=30 July 2011|df=dmy-all}}</ref>

<ref name=NDDIC2006>{{cite web|author=National Digestive Diseases Information Clearinghouse|author-link=National Digestive Diseases Information Clearinghouse|title=Crohn's Disease (NIH Publication No. 06–3410)|work=Digestive Diseases: A-Z List of Topics and Titles|publisher=National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, United States Public Health Service, United States Department of Health and Human Services|location=Bethesda, Maryland|year=2006|url=http://digestive.niddk.nih.gov/ddiseases/pubs/crohns/|access-date=27 July 2011|url-status=dead|archive-url=https://web.archive.org/web/20140609002323/http://digestive.niddk.nih.gov/ddISeases/pubs/crohns/|archive-date=9 June 2014|df=dmy-all}}</ref>

<ref name=NIDDK2006>{{cite web|author=National Endocrine and Metabolic Diseases Information Service|author-link=Endocrine and Metabolic Diseases Information Service|title=Hyperparathyroidism (NIH Publication No. 6–3425)|work=Information about Endocrine and Metabolic Diseases: A-Z list of Topics and Titles|publisher=National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Public Health Service, US Department of Health and Human Services|location=Bethesda, Maryland|year=2006|url=http://www.endocrine.niddk.nih.gov/pubs/hyper/hyper.htm|access-date=27 July 2011|url-status=dead|archive-url=https://web.archive.org/web/20110524101254/http://www.endocrine.niddk.nih.gov/pubs/hyper/hyper.htm|archive-date=24 May 2011|df=dmy-all}}</ref>

<ref name=NIDDK2007>{{cite web|author=National Kidney and Urologic Diseases Information Clearinghouse|title=Kidney Stones in Adults (NIH Publication No. 08–2495)|work=Kidney & Urologic Diseases: A-Z list of Topics and Titles|publisher=National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Public Health Service, US Department of Health and Human Services|location=Bethesda, Maryland|year=2007|url=http://kidney.niddk.nih.gov/kudiseases/pubs/stonesadults/|access-date=27 July 2011|url-status=dead|archive-url=https://web.archive.org/web/20110726181803/http://kidney.niddk.nih.gov/kudiseases/pubs/stonesadults/|archive-date=26 July 2011|df=dmy-all}}</ref>

<ref name=NIDDK20084696>{{cite web|author=National Endocrine and Metabolic Diseases Information Service|title=Renal Tubular Acidosis (NIH Publication No. 09–4696)|work=Kidney & Urologic Diseases: A-Z list of Topics and Titles|publisher=National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Public Health Service, US Department of Health and Human Services|location=Bethesda, Maryland|year=2008|url=http://kidney.niddk.nih.gov/kudiseases/pubs/tubularacidosis/|access-date=27 July 2011|url-status=dead|archive-url=https://web.archive.org/web/20110728025351/http://kidney.niddk.nih.gov/kudiseases/pubs/tubularacidosis/|archive-date=28 July 2011|df=dmy-all}}</ref>

<ref name=NIDDK20086235>{{cite web|author=National Kidney and Urologic Diseases Information Clearinghouse|title=Medullary Sponge Kidney (NIH Publication No. 08–6235)|work=Kidney & Urologic Diseases: A-Z list of Topics and Titles|publisher=National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Public Health Service, US Department of Health and Human Services|location=Bethesda, Maryland|year=2008|url=http://kidney.niddk.nih.gov/kudiseases/pubs/medullaryspongekidney/|access-date=27 July 2011|url-status=dead|archive-url=https://web.archive.org/web/20110807163748/http://kidney.niddk.nih.gov/kudiseases/pubs/medullaryspongekidney/|archive-date=7 August 2011|df=dmy-all}}</ref>

<ref name=Parmar2004>{{cite journal | vauthors = Parmar MS | title = Kidney stones | journal = BMJ | volume = 328 | issue = 7453 | pages = 1420–4 | date = June 2004 | pmid = 15191979 | pmc = 421787 | doi = 10.1136/bmj.328.7453.1420 }}</ref>

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<ref name=Paterson2010>{{cite journal | vauthors = Paterson R, Fernandez A, Razvi H, Sutton R | title = Evaluation and medical management of the kidney stone patient | journal = Canadian Urological Association Journal | volume = 4 | issue = 6 | pages = 375–9 | date = December 2010 | pmid = 21191493 | pmc = 2997825 | doi = 10.5489/cuaj.10166 }}</ref>-->

<ref name=Pearle2007>{{cite book| veditors = Litwin MS, Saigal CS |title=Urologic Diseases in America (NIH Publication No. 07–5512)| vauthors = Pearle MS, Calhoun EA, Curhan GC |chapter=Ch. 8: Urolithiasis|pages=283–319|publisher=[[National Institute of Diabetes and Digestive and Kidney Diseases]], [[National Institutes of Health]], [[United States Public Health Service]], [[United States Department of Health and Human Services]]|location=Bethesda, Maryland|year=2007|chapter-url=http://kidney.niddk.nih.gov/statistics/uda/Urologic_Diseases_in_America.pdf|url-status=live|archive-url=https://web.archive.org/web/20111018023922/http://kidney.niddk.nih.gov/statistics/UDA/Urologic_Diseases_in_America.pdf|archive-date=18 October 2011|df=dmy-all}}</ref>

<ref name=Pietrow2006>{{cite journal | vauthors = Pietrow PK, Karellas ME | title = Medical management of common urinary calculi | journal = American Family Physician | volume = 74 | issue = 1 | pages = 86–94 | date = July 2006 | pmid = 16848382 | url = http://www.aafp.org/afp/2006/0701/p86.pdf | archive-url = https://web.archive.org/web/20111123060406/http://www.aafp.org/afp/2006/0701/p86.pdf | df = dmy-all | url-status = live | archive-date = 23 November 2011 }}</ref>

<ref name=Potts2004>{{cite book| veditors = Potts JM |title=Essential Urology: A Guide to Clinical Practice| url = https://archive.org/details/essentialurology0000unse | url-access = registration |edition=1st| vauthors = Lieske JC, Segura JW |chapter= Ch. 7: Evaluation and Medical Management of Kidney Stones|pages=[https://archive.org/details/essentialurology0000unse/page/117 117]–52|publisher=Humana Press|location=Totowa, New Jersey|year=2004|isbn=978-1-58829-109-7}}</ref>

<ref name=Preminger2007>{{cite journal | vauthors = Preminger GM, Tiselius HG, Assimos DG, Alken P, Buck C, Gallucci M, Knoll T, Lingeman JE, Nakada SY, Pearle MS, Sarica K, Türk C, Wolf JS | title = 2007 guideline for the management of ureteral calculi | journal = The Journal of Urology | volume = 178 | issue = 6 | pages = 2418–34 | date = December 2007 | pmid = 17993340 | doi = 10.1016/j.juro.2007.09.107 }}</ref>

<ref name=Reilly2005Ch13>{{citation | vauthors = Reilly RF |title= ''Ch. 13: "Nephrolithiasis"'' |postscript= .}} In {{harvnb|Reilly|Perazella|2005|pp= 192–207}}.</ref>

<ref name=Reilly2005Ch14>{{citation | vauthors = Perazella MA |title= ''Ch. 14: "Urinalysis"'' |postscript= .}} In {{harvnb|Reilly|Perazella|2005|pp=209–26}}.</ref>

<ref name=Rosenberg1968>{{cite journal | vauthors = Rosenberg LE, Durant JL, Elsas LJ | title = Familial iminoglycinuria. An inborn error of renal tubular transport | journal = The New England Journal of Medicine | volume = 278 | issue = 26 | pages = 1407–13 | date = June 1968 | pmid = 5652624 | doi = 10.1056/NEJM196806272782601 }}</ref>

<ref name=Schlossberg2011>{{cite book|vauthors=Schlossberg D, Samuel R|title=Antibiotic Manual: A Guide to Commonly Used Antimicrobials|edition=1st|chapter=Sulfadiazine|pages=411–12|publisher=People's Medical Publishing House|location=Shelton, Connecticut|year=2011|isbn=978-1-60795-084-4|chapter-url=https://books.google.com/books?id=sCXn0xOVKNoC|access-date=25 August 2020|archive-date=20 March 2021|archive-url=https://web.archive.org/web/20210320092903/https://books.google.com/books?id=sCXn0xOVKNoC|url-status=live}}</ref>

<ref name=Shah2002>{{cite journal | vauthors = Shah J, Whitfield HN | title = Urolithiasis through the ages | journal = BJU International | volume = 89 | issue = 8 | pages = 801–10 | date = May 2002 | pmid = 11972501 | doi = 10.1046/j.1464-410X.2002.02769.x | s2cid = 44311421 }}</ref>

<ref name=Smith1999>{{cite journal | vauthors = Smith RC, Levine J, Rosenfeld AT | title = Helical CT of urinary tract stones. Epidemiology, origin, pathophysiology, diagnosis, and management | journal = Radiologic Clinics of North America | volume = 37 | issue = 5 | pages = 911–52, v | date = September 1999 | pmid = 10494278 | doi = 10.1016/S0033-8389(05)70138-X }}</ref>

<ref name=SmithCentennial2000>{{cite journal | vauthors = Smith RC, Varanelli M | title = Diagnosis and management of acute ureterolithiasis: CT is truth | journal = AJR. American Journal of Roentgenology | volume = 175 | issue = 1 | pages = 3–6 | date = July 2000 | pmid = 10882237 | doi = 10.2214/ajr.175.1.1750003 | s2cid = 73387308 }}</ref>

<ref name=Taylor2004>{{cite journal | vauthors = Taylor EN, Stampfer MJ, Curhan GC | title = Dietary factors and the risk of incident kidney stones in men: new insights after 14 years of follow-up | journal = Journal of the American Society of Nephrology | volume = 15 | issue = 12 | pages = 3225–32 | date = December 2004 | pmid = 15579526 | doi = 10.1097/01.ASN.0000146012.44570.20 | url = http://jasn.asnjournals.org/content/15/12/3225.full.pdf | doi-access = free | access-date = 3 June 2011 | archive-date = 21 September 2017 | archive-url = https://web.archive.org/web/20170921054542/http://jasn.asnjournals.org/content/15/12/3225.full.pdf | url-status = live }}</ref>

<ref name=Thakker2000>{{cite journal | vauthors = Thakker RV | title = Pathogenesis of Dent's disease and related syndromes of X-linked nephrolithiasis | journal = Kidney International | volume = 57 | issue = 3 | pages = 787–93 | date = March 2000 | pmid = 10720930 | doi = 10.1046/j.1523-1755.2000.00916.x | url = http://www.nature.com/ki/journal/v57/n3/pdf/4491399a.pdf | archive-url = https://web.archive.org/web/20121105121823/http://www.nature.com/ki/journal/v57/n3/pdf/4491399a.pdf | df = dmy-all | url-status = live | archive-date = 5 November 2012 | doi-access = free }}</ref>

<ref name=Tiselius2003>{{cite journal | vauthors = Tiselius HG | title = Epidemiology and medical management of stone disease | journal = BJU International | volume = 91 | issue = 8 | pages = 758–67 | date = May 2003 | pmid = 12709088 | doi = 10.1046/j.1464-410X.2003.04208.x | s2cid = 28256459 }}</ref>

<ref name=Weaver2002>{{cite book |vauthors= Weaver SH, Jenkins P |year= 2002 |chapter= Ch. 14: Renal and Urological Care |title= Illustrated Manual of Nursing Practice |edition= 3rd |publisher= Lippincott Williams & Wilkins |isbn= 978-1-58255-082-4 |chapter-url-access= registration |chapter-url= https://archive.org/details/illustratedmanua0000unse }}</ref>

<ref name=Wolf2011b>{{EMedicine|article|437096|Nephrolithiasis|Overview}} § Background.</ref>

<ref name=Wolf2011p>{{EMedicine|article|437096|Nephrolithiasis|Overview}} § Pathophysiology.</ref>

<ref name=Young2011>{{citation | vauthors = Young JG, Keeley FX |title= ''Ch. 38: "Indications for Surgical Removal, Including Asymptomatic Stones"''}} in {{harvnb|Rao|Preminger|Kavanagh|2011|pp=441–454}}.</ref>
}}

=== Notes ===
{{Refbegin|30em}}
* {{cite book|veditors=Ross AC, Taylor CL, Yaktine AL, Del HB|author=Committee to Review Dietary Reference Intakes for Vitamin D and Calcium, Institute of Medicine of the National Academies|title=Dietary Reference Intakes for Calcium and Vitamin D|publisher=The National Academies Press|location=Washington, DC|year=2011|isbn=978-0-309-16394-1|url=http://www.nap.edu/catalog.php?record_id=13050|ref={{Harvid|Committee to Review Dietary Reference Intakes for Vitamin D and Calcium|2011}}|doi=10.17226/13050|pmid=21796828|s2cid=58721779 |access-date=21 June 2011|archive-date=9 September 2014|archive-url=https://web.archive.org/web/20140909000908/http://www.nap.edu/catalog.php?record_id=13050|url-status=live}}
* {{cite book|veditors=Rao PN, Preminger GM, Kavanagh JP|title=Urinary Tract Stone Disease|edition=1st |publisher=Springer-Verlag|location=London|year=2011|isbn=978-1-84800-361-3|doi=10.1007/978-1-84800-362-0_26}}
* {{cite book|veditors=Reilly RF, Perazella MA|title=Nephrology in 30 Days|edition=1st|publisher=The McGraw-Hill Companies, Inc.|location=New York|year=2005|isbn=978-0-07-143701-1|url=https://books.google.com/books?id=tBGhK_1L6rAC&pg=PA195|access-date=25 August 2020|archive-date=14 April 2021|archive-url=https://web.archive.org/web/20210414030630/https://books.google.com/books?id=tBGhK_1L6rAC&pg=PA195|url-status=live}}
* {{cite book|veditors=Stoller ML, Meng MV|title=Urinary stone disease: the practical guide to medical and surgical management|edition=1st|publisher=Humana Press|location=Totowa, New Jersey|year=2007 |isbn=978-1-59259-972-1}}
{{Refend}}

== External links ==
{{Commons category}}
* [https://web.archive.org/web/20160922193247/http://patients.uroweb.org/i-am-a-urology-patient/kidney-and-ureteral-stones/ Information from the European Urological Association]
* [https://kidneystones.uchicago.edu/kidney-stone-book/ Kidney Stone Guide Book] {{Webarchive|url=https://web.archive.org/web/20200803210414/https://kidneystones.uchicago.edu/kidney-stone-book/ |date=3 August 2020 }} – [[University of Chicago]] Kidney Stone Program
{{Medical resources
 | ICD10           = {{ICD10|N|20|0|n|20}} – {{ICD10|N|20|9|n|20}}
 | ICD9            = {{ICD9|592.0}} – {{ICD9|594.9}}
 | DiseasesDB      = 11346
 | MedlinePlus     = 000458
 |OMIM=167030
 | eMedicineSubj   = med
 | eMedicineTopic  = 1600
 | MeshID          = D052878
}}
{{Urinary tract disease}}
{{Authority control}}
{{Use dmy dates|date=April 2018}}

[[Category:Kidney diseases]]
[[Category:Urological conditions]]
[[Category:Acute pain]]
[[Category:Wikipedia medicine articles ready to translate]]
[[Category:Wikipedia emergency medicine articles ready to translate]]