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Acute gouty arthritis occurs when crystals of monosodium urate form and deposit in joints and connective tissue. These crystals then provoke the characteristic acute inflammatory response of gout (Seegmiller, 1965), and may accumulate chronically forming gouty tophi.Although To determine the urate solubility of each solution, three ml of the solution to be tested was added to a 16 ml glass test tube containing a small magnetic stirring bar. The test tubes were placed on a magnetic stirrer and maintained at the desired temperature. After 16 hours the solutions were centrifuged at 12,000g in a 6 ml glass centrifuge tube and the supernatant was removed. The centrifugation was repeated until no precipitate was visible. Two centrifugations were usually sufficient. The final supernatant was then assayed for urate. Using this procedure, urate crystals could not be detected in the final supernatant by light microscopy. Care was taken to maintain the desired temperature closely during all steps of the procedure including centrifugation. URATE SOLUBILITY IN BUFFER SOLUTIONSThe effect of sodium on urate solubility was determined in 0-01 mol/l. potassium phosphate buffer, pH 7 40, containing appropriate amounts of sodium chloride. The desired pH was obtained by titrating solutions of monobasic and dibasic potassium phosphate.The effect of pH on urate solubility was determined in 0-01 mol/l. sodium phosphate buffer containing 015 mol/l. sodium chloride and adjusted to the desired pH by titrating solutions of monobasic and tribasic sodium phosphate. The effect of albumin on urate solubility was determined by adding the appropriate amount of albumin to 3 ml 0 01 mol/l. sodium phosphate buffer, pH 7*40, containing 0-15 mol/l. sodium chloride and 100 mg/100 ml sodium urate. The albumin was dissolved by gentle mixing.All buffers were boiled before use. Excess sodium urate (approximately 100 mg/100 ml) was added to solutions before titration to prevent pH changes due to the urate itself. URATE SOLUBILITY IN BIOLOGICAL FLUIDSAll blood and urine samples were obtained from normal volunteers. Blood was drawn in heparinized vacutainers, separated by centrifugation for 10 minutes at 3500 r.p.m. and the plasma frozen at -20°C until the time of assay (not

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Seven of 24 unrelated Israeli Jewish families affected with cystinuria were of Libyan origin. Five of these seven families were intensively investigated and heterozygotes were identified in four of them. This indicates that, contrary to other populations, in this community cystinuria is mainly of type II or III. Among randomly screened healthy school children of Libyan origin 3–4% were found to be heterozygotes for cystinuria. It is estimated that in this community the frequency of genetically determined cystine urolithiasis is about 1:2,500.