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Renal excretion of uric acid was studied in 48 patients with recurrent calcium nephrolithiasis. Hyperuricosuria was found in 16 patients (33%) and among them 10 patients had increased values of urate clearance and fractional excretion. The tubular transport of urate was evaluated by means of pharmacological tests with pyrazinamide (PZA) and benzbromarone (BB) in these 11 patients with hyperuricosuria of renal origin. PZA suppression test was normal in 10 patients while in one case uric acid excretion was not suppressed sufficiently by PZA. Maximal uricorusirc response to BB was increased in two patients, normal in one patient and impaired in eight patients. PZA and BB tests revealed isolated defect of uric acid postsecretory reabsorption in seven patients, impaired reabsorption at both pre- and postsecretory site in one case and enhanced tubular secretion of uric acid in two patients. This study indicates that different defects of uric acid transport in nephron are the frequent cause of hyperuricosuria in patients with recurrent calcium nephrolithiasis.

The study involved 30 patients treated with nifedipine in daily dose of 30 mg for 7 days. Calcium, magnesium, phosphate, oxalate, and uric acid levels in the urine were measured. It was found that nifedipine significantly decreased oxaluria urinary excretion of calcium, magnesium, phosphate, and uric acid remained unchanged following nifedipine therapy. Results may suggest that nifedipine may exert an influence on renal stone formation.

An effect of cimetidine on parathyroid glands functioning in healthy subjects was evaluated. Serum calcium, phosphate, and magnesium concentrations together with renal excretion++ of these ions in healthy subjects as well as cAMP excretion++ in selected individuals were determined before and following intravenous administration of cimetidine (Altratmet Lek Ljublijana) in total dose of 500 mg (50 mg injected rapidly as a bolus following with 450 mg in an intravenous infusion during 60 minutes). No significant changes in serum calcium, phosphates, and magnesium concentrations were noted. Renal clearance of calcium and magnesium remained unchanged whereas renal phosphate excretion++ increased from 10.69 +/- 4.9 mL/min to 15.1 +/- 5.41 mL/min (p less than 0.02). Excretion++ of 3.5 cAMP increased from 2.65 +/- 2.19 nM/min to 5.16 +/- 2.0 nM/min (p less than 05). The obtained results do not exclude stimulating effect of intravenous cimetidine on parathyroid glands. Cimetidine given intravenously in the bleeding gastric or duodenal ulcers in the course of the primary hyperparathyroidism+ may decrease serum phosphate levels due to increased exretion of this ion with the urine.

In 11 epileptics treated with DPH for 10-20 years a significant fall was observed in the serum levels of calcium, phosphates, and ionic index, with a significant rise in the serum magnesium concentration. No detectable changes were observed in the radiological appearance of bones and alkaline phosphates activity was within normal range. In two cases histological examinations demonstrated signs of osteomalacia. The authors postulate the necessity of monitoring selected parameters of calcium metabolism in patients on long-term treatment with diphenylhydantoin.

Daily calcium, oxalates, magnesium, citrates and creatinine excretion with the urine was determined in 36 patients with calcium renal stones and in 25 healthy individuals. Then, risk index according to Tiselius was calculated. It was found that daily calcium excretion is significantly higher and daily citrates excretion is significantly lower in patients with calcium renal stones. Daily excretion of oxalates, magnesium and creatinine with the urine did not differ in both groups. Risk index according to Tiselius was two-fold higher in patients suffering from urolithiasis than in healthy individuals (p greater than 0.001) and better illustrated the tendency to stone formation than the analysis of metabolic disorders.