A 64-year-old male with renal hypouricemia associated with a uric acid bladder stone and benign prostatic hyperplasia is reported. Transurethral prostatectomy and cystolithotripsy was performed. The crystalline component of the stone was uric acid dihydrate by infrared spectrophotometry. Further examination revealed that impaired renal tubular absorption of uric acid was responsible for the hypouricemia in this case.
We studied the solubility of anhydrous uric acid stones, and compared it with that of anhydrous uric acid and urinary uric acid (uric acid dihydrate). As reported previously, the solubility of urinary crystals was 2.1 to 2.9 times higher than that of anhydrous uric acid. However the solubility of uric acid stones was only slightly higher than that of anhydrous uric acid. If uric acid crystals formed in the urine are dihydrate in form and they change to anhydrous form subsequently, uric acid stone formation can be prevented by alkalinization based on the solubility of urinary uric acid crystals. On the other hand, much stronger alkalinization is necessary to dissolve the stones.

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A 42 year-old man who had had recurrent renal colic episodes since he was 25 year-old was found to have hypouricemia at the age of 37. Several times he passed tiny stones composed mainly of calcium oxalate. X-rays showed staghorn stones in both kidneys. Physical examination disclosed no abnormality. Routine hematological and blood chemistry values were all within the normal range, except for a low uric acid level (1.9 mg/dl). The creatinine clearance was 88.4 ml/min and uric acid clearance ranged from 50.7 to 53.3ml/min. The average urinary uric acid excretion was 482.5 mg/24hr on a low purine diet. There was neither glycosuria nor abnormal amino acid pattern in urine. The urinary calcium excretion ranged from 158.4 to 306.0 mg/24hr under a regular hospital diet. Administration of pyrazinamide almost completely suppressed uric acid excretion, while that of benzbromarone did not cause a significant change in uric acid excretion. These suggested that the hypouricemia in this patient was caused by the defect in tubular reabsorption of uric acid at the postsecretory site.
Since hyperuricosuria was suspected to be one of the causes contributory to the formation of calcium oxalate stone, this patient was given allopurinol therapy. Although 8years administration of allopurinol (200mg/day ) did not reduce the renal calculi on X ray film, it relieved him of stone discharge with colic. Therefore, we conclude that allopurinol may be beneficial in the present case and it may be applicable to some patients who suffer from recurrent colic of renal calcium oxalate calculi associated with idiopathic renal hypouricemia.

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We measured the concentration ofserum lipoprotein(a)[Lp(a)], lipids, high density lipoprotein cholesterol (HDL-C) and apolipoprotein B (apo B) in patients with primary gout and control subjects.
The serum concentrations of Lp (a), triglyceride and apo B were significantly higher (p<0.01) in the patients with primary gout than those in the control subjects, while the concentration of HDL-C was significantly lower (p<0.01) in the former than in the latter. No association was noted among Lp (a) concentration, and age, alcohol intake, body mass index, serum lipids, apo B and HDL-C concentrations in the patients with primary gout or in the control subjects.
These findings suggest that an increase in Lp (a) concentration contributes to the development of atherosclerosis in primary gout in addition to a low level of HDL-C and a high level of apo B.

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