Editing Gout (section)

===Genetics===
Gout is partly genetic, contributing to about 60% of [[Genetic variability|variability]] in uric acid level.<ref name=Lancet2010/> The ''[[SLC2A9]]'', ''[[SLC22A12]]'', and ''[[ABCG2]]'' genes have been found to be commonly associated with gout and variations in them can approximately double the risk.<ref>{{cite journal|last=Merriman|first=TR|author2=Dalbeth, N|author2-link= Nicola Dalbeth |title=The genetic basis of hyperuricaemia and gout|journal= Joint Bone Spine|year=2011|volume=78|issue=1|pages=35–40|pmid=20472486|doi=10.1016/j.jbspin.2010.02.027}}</ref><ref name="Reginato2012">{{cite journal |vauthors=Reginato AM, Mount DB, Yang I, Choi HK |title=The genetics of hyperuricaemia and gout |journal=Nature Reviews Rheumatology|year=2012 |pmid=22945592 |doi=10.1038/nrrheum.2012.144 |volume=8 |issue=10 |pages=610–621 |pmc=3645862 }}</ref> [[Loss-of-function mutation]]s in ''SLC2A9'' and ''SLC22A12'' causes low blood uric acid levels by reducing urate absorption and unopposed urate secretion.<ref name=Reginato2012/> The rare genetic disorders [[Tamm-Horsfall protein|familial juvenile hyperuricemic nephropathy]], [[medullary cystic kidney disease]], [[PRPSAP1|phosphoribosylpyrophosphate synthetase]] superactivity and [[hypoxanthine-guanine phosphoribosyltransferase]] deficiency as seen in [[Lesch–Nyhan syndrome]], are complicated by gout.<ref name=Lancet2010/>