ENHANCED URINARY-EXCRETION OF ALBUMIN IN CONGESTIVE-HEART-FAILURE - EFFECT OF ACE-INHIBITION

Urinary excretion of albumin and beta-2-microglobulin were measured in 13 patients with congestive heart failure, NYHA class II-IV, before and after Captopril treatment for 4 weeks, and in 13 healthy control subjects. The urinary excretion of albumin was enhanced in heart failure patients compared to control subjects (12.0-mu-g min-1 vs 2.8-mu-g min-1; medians, P<0.01), whereas beta-2-microglobulin excretion was normal. No significant change in urinary excretion of albumin was observed after captopril. Using Spearmann's test the urinary excretion of albumin was correlated to the NYHA class (Px=0.681, p<0.05, plasma renin (Px=0.886, p<0.01) and plasma angiotensin II (Px=0.5840, p<0.05). Correlations with atrial natriuretic peptide (rho=0.412, p=0.153) and aldosterone (Px=0.487, P=0.106) did not reach significance. By multiple linear regression analysis only plasma renin activity was correlated to albumin excretion. In conclusion, patients with congestive heart failure had an increased urinary excretion of albumin. It is suggested that the enhanced transglomerular passage of albumin in congestive heart failure is partly due to an increased intrarenal angiotensin II generation, but elevated plasma level of atrial natriuretic Peptide and increased renal venous pressure may also be important pathogenetic factors.