Renal function abnormalities in patients with asymptomatic hyperuricemia

✍ Scribed by James R. Klinenberg; Harvey C. Gonick; Leslie Dornfeld

• Publisher: John Wiley and Sons
• Year: 1975
• Tongue: English
• Weight: 419 KB
• Volume: 18
• Category: Article
• ISSN: 0004-3591
• DOI: 10.1002/art.1780180714

✦ Synopsis

Uremia is the major cause of death in patients with gout, accounting for approximately 25y0 of the overall mortality (1). Initially tlie damage to the kidney was thought to be secondary to deposition of urate crystals in the collecting tubules with resulting intrarenal hydroneplirosis, proximal tubular atrophy, secondary necrosis, and fibrosis and complicating pyelonephritis (1-5). More recent studies (6,7) have suggested that the increased filtered urate load per se may be nephrotoxic and lead to glomerular hyalinization, tubular atrophy, and interstitial inflammation in tlie absence of demonstrable obstructive changes. If this thesis is correct, then asymptomatic liyperuricemia should also be associated with renal abnormalities.

I n a n effort to define further the role of the filtered urate load in the etiology of tlie renal lesion, renal function was studied in two groups of hyperuricemic patients. T h e first group consisted of 50 consecutive unselected patients with overt clinical gout. T h e second group consisted of 20 patients with From the Cedars-