Editing Hyperuricemia (section)

===Decreased excretion of uric acid===
{{Main|Uric acid#Low uric acid}}

The principal drugs that contribute to hyperuricemia by decreased excretion are the primary [[antiuricosuric]]s. Other drugs and agents include [[diuretic]]s, [[salicylate]]s, [[pyrazinamide]], [[ethambutol]], [[nicotinic acid]], [[ciclosporin]], 2-ethylamino-1,3,4-thiadiazole, and [[cytotoxic agent]]s.<ref name="pmid2070427">{{cite journal| author = Scott JT| title = Drug-induced gout| journal = Baillière's Clinical Rheumatology| volume = 5| issue = 1| pages = 39–60|date=April 1991| pmid = 2070427| doi = 10.1016/S0950-3579(05)80295-X}}</ref>

The gene [[SLC2A9]] encodes a protein that helps to transport uric acid in the kidney. Several [[single nucleotide polymorphism]]s of this gene are known to have a significant correlation with blood uric acid.<ref name="pmid18487473">{{cite journal|vauthors=Brandstätter A, Kiechl S, Kollerits B, Hunt SC, Heid IM, Coassin S, Willeit J, Adams TD, Illig T, Hopkins PN, Kronenberg F | title = Sex-specific association of the putative fructose transporter SLC2A9 variants with uric acid levels is modified by BMI| journal = Diabetes Care| volume = 31| issue = 8| pages = 1662–7|date=August 2008| pmid = 18487473| doi = 10.2337/dc08-0349| pmc = 2494626}}</ref> Hyperuricemia cosegregating with [[osteogenesis imperfecta]] has been shown to be associated with a mutation in [[GPATCH8]] using [[exome sequencing]]<ref>{{cite journal|last=Kaneko|first=Hiroshi|author2=Kitoh Hiroshi |author3=Matsuura Tohru |author4=Masuda Akio |author5=Ito Mikako |author6=Mottes Monica |author7=Rauch Frank |author8=Ishiguro Naoki |author9=Ohno Kinji  |date=Nov 2011|title=Hyperuricemia cosegregating with osteogenesis imperfecta is associated with a mutation in '''GPATCH8'''|journal=Hum. Genet.|volume=130|issue=5|pages=671–83| pmid = 21594610| doi = 10.1007/s00439-011-1006-9 |s2cid=1075364}}</ref>

A [[ketogenic diet]] impairs the ability of the kidney to excrete uric acid, due to competition for transport between uric acid and [[ketone]]s.<ref name="pmid488876">{{cite journal| author = Förster H| title = [Possibilities for weight reduction by means of diet]| language = de| journal = Fortschr. Med.| volume = 97| issue = 32| pages = 1339–44|date=August 1979| pmid = 488876}}</ref>

Elevated blood [[lead]] is significantly correlated with both impaired kidney function and hyperuricemia (although the causal relationship among these correlations is not known). In a study of over 2500 people resident in Taiwan, a [[blood lead level]] exceeding 7.5 microg/dL (a small elevation) had [[odds ratio]]s of 1.92 (95% CI: 1.18-3.10) for renal dysfunction and 2.72 (95% CI: 1.64-4.52) for hyperuricemia.<ref name="pmid18514766">{{cite journal|vauthors=Lai LH, Chou SY, Wu FY, Chen JJ, Kuo HW | title = Renal dysfunction and hyperuricemia with low blood lead levels and ethnicity in community-based study| journal = Sci. Total Environ.| volume = 401| issue = 1–3| pages = 39–43|date=August 2008| pmid = 18514766| doi = 10.1016/j.scitotenv.2008.04.004| bibcode =2008ScTEn.401...39L}}</ref><ref>Shadick NA, Kim R, Weiss S, Liang MH, Sparrow D, Hu H. (2000 ), ''Effect of low level lead exposure on hyperuricemia and gout among middle aged and elderly men: the normative aging study''; J Rheumatol. 2000 Jul; 27(7):1708–12 ([https://www.ncbi.nlm.nih.gov/pubmed/10914856 abstract]).</ref>