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Look for hyperuricosuria in patients with renal calculus formation. Identification of overexcretors re: risks of stone formation, identification of genetic defects, influence of overexcretion on therapy of gout. Uric acid nephrolithiasis occurs in primary gout or in secondary hyperuricemia (eg, malignant diseases). Uric acid nephrolithiasis may complicate ulcerative colitis, Crohn's disease, and surgical jejunoileal bypass. Most subjects with uric acid stones do not have gout.1 Evaluate uric acid metabolism in gout.
Even mild renal failure decreases uric acid excretion. Uric acid excretion is decreased with hypertension.
A young patient with acute gouty arthritis, uric acid stones, and any patient who excretes >1000 mg uric acid/24 hours, should be evaluated for HPRT deficiency.2 The uric acid:creatinine ratio has been used as a test for Lesch-Nyhan syndrome (HPRTase deficiency). Normal control patients 0.21−0.59; partial enzyme deficient group 0.62−2.00; complete enzyme deficiency 1.98−5.35.3
The ratio of uric acid:creatinine in morning samples of urine has been used as a test for detection of the Lesch-Nyhan syndrome, which is associated with virtually complete absence of activity of the enzyme hypoxanthine-guanine phosphoribosyltransferase. This ratio has also been applied to 24-hour urine samples from adult patients with gout for detection of partial deficiency of the same enzyme. The uric acid:creatinine ratio in the urine of normal control patients is reported to range from 0.21−0.59. Patients with gout exhibit ratios of 0.15−0.73, whereas those patients with hyperuricemia associated with another disorder such as leukemia or glycogen-storage disease have ratios of 0.25−1.77. The ratio is 0.27−0.58 for patients with nongouty arthritis. Patients with complete hypoxanthine-guanine phosphoribosyltransferase deficiency are reported to have urinary uric acid:creatinine ratios of 1.98−5.35, as compared to 0.62−2.00 for patients with gout accompanied by partial enzyme deficiency.
The ratio of uric acid:creatinine concentration on a random urine specimen has also been shown to be >1.0 in patients with acute renal failure secondary to acute uric acid nephropathy, but <1.0 in patients with acute renal failure resulting from other causes.
1. Pak CY. Renal calculi. In: Wyngaarden JB, Smith LH Jr, eds. Cecil Textbook of Medicine. 18th ed, vol 1. Philadelphia, Pa: WB Saunders Co;1988:638-644.
2. Wilson JM, Young AB, Kelley WN. Hypoxanthine-guanine phosphoribosyltransferase deficiency. The molecular basis of the clinical syndromes. N Engl J Med. 1983 Oct 13; 309(15):900-910 (review). PubMed 6136913
3. Pesce AJ, Kaplan LA. Methods in Clinical Chemistry. St Louis, Mo: Mosby-Year Book Inc;1987: 32.
