Control of renal uric acid excretion and gout.

Abstract

PURPOSE OF REVIEW:

Impaired renal uric acid excretion is the major mechanism of hyperuricemia in patients with primary gout. This review highlights recent advances in the knowledge of normal mechanisms of renal uric acid handling and derangement of these mechanisms in uric acid underexcretion.

RECENT FINDINGS:

The discovery of URAT1 has facilitated identification of other molecules potentially involved in uric acid transport in the renal tubules. Some of these molecules show gender differential expression in animal experiments. Sodium-dependent monocarboxylate cotransporters have been shown to transport lactate and butyrate, and may have roles in hyperuricemia associated with diabetic ketoacidosis and alcohol ingestion. Certain polymorphisms in SLC22A12 may be associated with the development of hyperuricemia or gout, although confirmation is needed. Mechanisms of hyperuricemia associated with uric acid underexcretion in patients with familial juvenile hyperuricemic nephropathy also remain to be clarified. Distal tubular salt wasting and compensatory upregulation of the resorption of sodium and uric acid in the proximal tubule may explain the hyperuricemia associated with this disorder.

SUMMARY:

Much progress has been made in understanding the mechanisms of renal uric acid handling. Elucidation of the mechanisms of hyperuricemia in patients with familial juvenile hyperuricemic nephropathy will shed light on the function of uromodulin, functional impairment of which eventually results in diminished uric acid excretion.

• Authors: Atsuo Taniguchi, Naoyuki Kamatani
• Journal: Current opinion in rheumatology (Curr Opin Rheumatol) Vol. 20 Issue 2 Pg. 192-7 (Mar 2008) ISSN: 1040-8711 [Print] United States
• PMID: 18349750 (Publication Type: Journal Article, Review)

Chemical References

• Organic Anion Transporters
• Organic Cation Transport Proteins
• SLC22A12 protein, human
• Uric Acid

Topics

• Genetic Predisposition to Disease
• Gout (genetics, physiopathology, urine)
• Humans
• Hyperuricemia (genetics, urine)
• Kidney Tubules, Proximal (physiology, physiopathology)
• Organic Anion Transporters (genetics)
• Organic Cation Transport Proteins (genetics)
• Polymorphism, Single Nucleotide
• Uric Acid (metabolism)