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A prospective randomized, double-blind, double-dummy study investigated the effects of two angiotensin converting enzyme (ACE) inhibitors on urinary albumin excretion in nondiabetic patients with mild to moderate essential hypertension. At the end of a 4-week placebo run-in period, 36 patients were randomly allocated to receive a 12-week course of treatment with quinapril (10, 20, or 40 mg) once daily or captopril (25, 50, or 75 mg) twice daily. Seventeen patients in each group completed the study. The mean change in mean blood pressure for patients taking quinapril (mean dose 32 mg/24 h) was -5 mm Hg (P = .002), and for patients taking captopril (mean dose 132 mg/24 h), -9 mm Hg (P = .002). The baseline urinary albumin excretion rate in both groups was (mean +/- EEM) 57 +/- 7 micrograms/min. Fifteen patients in the quinapril group and 12 patients in the captopril group had baseline albumin excretion rates of more than 20 micrograms/min. Mean urinary albumin excretion decreased in patients treated with quinapril from 55 to 33 micrograms/min (mean decrease 22 micrograms/min, 95% confidence interval [CI], 1 to 43 micrograms/min; P = .031) and with captopril from 59 to 41 micrograms/min (mean decrease 18 micrograms/min, 95% CI, 3 to 32 micrograms/min; P = .025). No significant modifications were observed in serum lipid concentrations, serum and urinary electrolytes, and magnesium or phosphorus metabolism. Mean urinary calcium excretion decreased in the quinapril-treated group (from 219 to 188 mg/24 h; P = .023) but not in the captopril group (from 264 to 267 mg/24 h).(ABSTRACT TRUNCATED AT 250 WORDS)

Purpose: The renal excretion of uric acid is usually diminished in primary gout with respect to increased serum urate levels. To determine whether the renal excretion of uric acid precursors, hypoxanthine and xanthine, is also abnormal in primary gout, the concentrations of these purines were measured in plasma and 24-hour urine samples in normal subjects, in patients with primary gout and uric acid underexcretion, and in patients with enzyme deficiencies that are known to result in over-production of uric acid., Subjects and Methods: Three groups of subjects were studied: Group I consisted of 10 ambulatory healthy normal men; Group II consisted of 15 patients in whom primary gout was diagnosed; and Group III consisted of 10 patients with various enzyme defects known to produce an excessive synthesis of uric acid. In each subject, plasma and 24-hour urinary uric acid, hypoxanthine, xanthine, and creatinine concentrations were measured and the mean of three consecutive determinations was used. The fractional excretion of purine compounds was calculated from a formula. Hypoxanthine phosphoribosyltransferase, adenine phosphoribosyltransferase, and hemoglobin were also measured in each subject., Results: Plasma hypoxanthine and xanthine were increased in the two groups of patients compared with the control subjects. Urinary hypoxanthine and xanthine levels were reduced in gouty patients compared with control subjects, whereas levels were increased in patients with uric acid overproduction. A positive correlation was found between the renal clearances of uric acid, hypoxanthine, and xanthine., Conclusion: The results indicate that the renal excretion of hypoxanthine and xanthine is severely impaired in most patients with primary gout.

Monitoring of plasma oxypurinol has been proposed to prevent allopurinol side effects. An 89-year-old man developed a severe desquamative rash, fever, eosinophilia, hepatocellular injury and renal failure after allopurinol administration. Eight hours after the last dose, plasma allopurinol was undetectable and plasma oxypurinol was 50 mumol/l. This is the first case in which severe allopurinol hypersensitivity occurred despite a simultaneous plasma oxypurinol concentration within recommended levels (below 100 mumol/l).