Effect of hydrochlorothiazide and indapamide on renal handling of uric acid in patients with essential hypertension

Abstract

Background High serum uric acid is a frequent finding in patients with essential hypertension, It is partly caused by antihypertensive therapy. Thiazides diminish renal excretion of uric acid and increase the incidence of hyperuricemia. Indapamide, thiazide-like diuretic has diiferent metabolic profile but little is known about its effect on uric acid excretion. The aim of the study was to compare the effect of hydrochlorothiazide and indapamide on plasma uric acid and tubular transport of urate in nephron in hypertensive patients.
Methods Thirty six patients with mild to moderate essential hypertension were studied. Twenty of them received hydrochlorothiazide in dose 25 mg/day and sixteen were treated with indapamide in dose 2,5 mg/day as monotherapy. Patients were kept on normal sodium and purine diet. Plasma uric acid (Pua) was measured and pharmacological tests with pirazynamide and benzbromarone were performed before and after 3 to 5 weeks of diuretic treatment. Based on these tests uric acid clearance and fractional excretion as well as presecretory reabsorption, tubular secretion and postsecretory reabsorption of uric acid were calculated.
Results and conclusions Hydrochlorothiazide increases plasma uric acid and decreases its renal excretion in hypertensive patients. Both diminished tubular secretion and accelerated postsecretory reabsorption of uric acid are responsible for hypcruricaemic action of hydrochlorothiazide. Indapamide does not change neither plasma uric acid nor its renal handling. It seems that in patients with essential hypertension and gout indapamide is the diuretic of choice.