Editing Azotemia (section)

===Prerenal azotemia===
Prerenal azotemia is caused by a decrease in blood flow ([[hypoperfusion]]) to the kidneys. However, there is no inherent kidney disease. It can occur following [[hemorrhage]], [[shock (circulatory)|shock]], [[volume depletion]], [[congestive heart failure]], adrenal insufficiency, and narrowing of the renal artery among other things.<ref name=robbins7 />

The BUN:Cr in prerenal azotemia is greater than 20. The reason for this lies in the mechanism of filtration of urea and creatinine. Renal Plasma Flow (RPF) is decreased due to hypoperfusion which results in a proportional decrease in [[Glomerular filtration rate|Glomerular Filtration Rate]] (GFR). In turn, the decreased flow and pressure to the kidney will be sensed by baroreceptors in the Juxtaglomerular (JG) Cells of the afferent arteriole. If the decrease in blood pressure is systemic (rather than occlusion of the renal artery), baroreceptors in the carotid sinus and aortic arch will be stimulated. This leads to sympathetic nerve activation, resulting in <!--renal afferent arteriolar vasoconstriction (in hypovolemic states vasodilation predominates due to autoregulatory mechanisms) > alpha1 vasoconstriction--> [[renin]] secretion through [[Beta-1 adrenergic receptor|β<sub>1</sub> receptor]]s. Constriction of the afferent arterioles causes a decrease in the intraglomerular pressure, reducing GFR proportionally. Renin is the main effector of the juxtaglomerular baroreceptors. Renin is secreted from granules in the JG cells, and once in the blood stream, it acts as a protease to convert [[angiotensin]]ogen to angiotensin I, which is converted by [[Angiotensin-converting enzyme|angiotensin converting enzyme]], to angiotensin II, which, in turn, stimulates aldosterone release. Increased [[aldosterone]] levels results in salt and water absorption in the distal collecting tubule.<ref>{{Cite journal |last=Blantz |first=Roland C. |date=1998-02-01 |title=Pathophysiology of pre-renal azotemia |journal=Kidney International |language=en |volume=53 |issue=2 |pages=512–523 |doi=10.1046/j.1523-1755.2003_t01-1-00784.x |pmid=9461116 |issn=0085-2538|doi-access=free }}</ref>

A decrease in volume or pressure is a non-osmotic stimulus for antidiuretic hormone production in the hypothalamus, which exerts its effect in the medullary collecting duct for water reabsorption. Through unknown mechanisms, activation of the sympathetic nervous system leads to enhanced proximal tubular reabsorption of salt and water, as well as urea (BUN), calcium, uric acid, and bicarbonate. The net result of these 4 mechanisms of salt and water retention is decreased output and decreased urinary excretion of sodium (< 20mEq/L). The increased reabsorption of Na leads to increased water and urea reabsorption from the [[proximal tubule]]s of the kidney back into the blood. In contrast, creatinine is actually secreted in the proximal tubule. This generally leads to a BUN:Cr ratio greater than 20, a [[Fractional sodium excretion|fractional excretion of Na]] of less than 1%, and an elevated urine osmolarity.<ref>{{Citation |last1=Tyagi |first1=Alka |title=Azotemia |date=2022 |url=http://www.ncbi.nlm.nih.gov/books/NBK538145/ |work=StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=30844172 |access-date=2022-06-15 |last2=Aeddula |first2=Narothama R.}}</ref>