[Primary hyperuricemia due to decreased renal uric acid excretion].
Hyperuricemia reflects extracellular fluid supersaturation for uric acid. Although dietary, genetic, or disease-related excesses in urate production underlie hyperuricemia in some cases, impaired renal excretion of uric acid is the dominant cause of hyperuricemia. This type of hyperuricemia may be primary (idiopathic) and unassociated with an identifiable disorder. Two important candidates that may affect renal urate excretion were identified recently. One is an organic anion transporter (OAT) family member called urate transporter (URAT) 1. URAT1 has highly specific urate transport activity, exchanging this anion with others including most of the endogenous organic anions and drug anions that are known to affect renal uric acid transport. Another is uromodulin (UMOD), which is the key protein for the pathogenesis of familial juvenile hyperuricemic nephropathy that is characterized by early onset of hyperuricemia and renal failure. The role of these proteins in the cause of hyperuricemia is under investigation.
Yamauchi
Takahiro
T
Department of Internal Medicine 1, University of Fukui.
Ueda
Takanori
T
D001692:Biological Transport / Q000235:genetics; D006801:Humans; D033461:Hyperuricemia / Q000145:classification / Q000209:etiology* / Q000235:genetics; D007668:Kidney / Q000378:metabolism*; D009088:Mucoproteins / Q000502:physiology; D027361:Organic Anion Transporters / Q000502:physiology; D027701:Organic Cation Transport Proteins / Q000502:physiology; D051437:Renal Insufficiency / Q000209:etiology; D014527:Uric Acid / Q000378:metabolism*; D058949:Uromodulin
D009088:Mucoproteins; D027361:Organic Anion Transporters; D027701:Organic Cation Transport Proteins; C491241:SLC22A12 protein, human; C548612:UMOD protein, human; D058949:Uromodulin; D014527:Uric Acid