Urate nephropathy, chronic

In acute uric acid nephropathy, acute renal failure occurs as a result of blockage of urine flow secondary to massive precipitation of uric acid crystals in the collecting ducts and ureters. This syndrome is a well-recognized complication in patients with myeloproliferative or lymphopro-liferative disorders and results from massive malignant cell turnover, particularly after initiation of chemotherapy. Chronic urate nephropathy is caused by the long-term deposition of urate crystals in the renal parenchyma. 

Questions are often raised regarding the indications for drug therapy for asymptomatic hyperuricemia. The purported heneflts from treatment include prevention of acute gouty arthritis, tophi formation, nephrolithiasis, and chronic urate nephropathy. The first three complications are easily controlled shonld they develop therefore antihyperuricemic therapy is not warranted to prevent these conditions. 

Emmerson BT. The renal excretion of urate in chronic lead nephropathy. Austr Ann Med 1965 14 295-303. 

Renal disease is a eommon complication of hyperuricaemia. Several types of renal disease have been identified. The most comnutn is urate nephropathy which is caused by the deposition of urate crystals in renal tissue or the urinary tract to form urate stones. This mtiy be associated with chronic hyperuricaemia. Acute renal failure can be cau.sed by the rapid precipitation of uric acid crystals w hich commonly occurs during treatment of patients with leukaemias and lymphomas. In the acute tumour lysis syndrome (p. 129), nucleic acids are released as a result of tumour cell breakdown and arc rapidly metabolized to uric acid. 

Renal Disease is a well recognized complication of gout, and the typical histologic features of chronic gouty nephropathy have been carefully studied, however, early evolution of the nephropathy and its precise relationship to hyperuricemia and uricosuria have been difficult to study in the human subject. Unfortunately, animal models of sustained hyperuricemia are difficult to produce and maintain. Recently, Stavric and colleagues described the production of hyperuricemia and urate nephropathy in rats fed orally with oxonic acid and uric acid, oxonic acid is a potent, hepatic uricase inhibitor and this chemical, combined with uric acid or RNA dietry supplements, consistently leads to hyperuricemia in this species. 

Of particular interest was the fact that the cohort surviving into the 1%0 s had developed a high prevalence of gouty arthritis in comparison with patients with chronic nephritis due to causes other than lead. There was also a disproportionate hyperuricemia in these patients with chronic lead nephropathy, which was caused by a significantly lower urate clearance for any particular degree of renal insufficiency [32]. Studies of discrete tubular functions suggest that this was due to excessive reabsorption of filtered urate [33]. 

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