A Clinical Study on the Angiotensin I-Converting Enzyme in Human Urine

Urinary angiotensin I-converting enzyme (ACE) excretion was determined in 5 normal subjects and 37 hypertensive patients, of whom 31 had essential hypertension, 5 had chronic glomerulonephritis and 1 had renovascular hypertension.Urinary ACE excretion was 229.6± 73.9 units/day (mean ± S.D.) in the normal subjects, 244.6 ± 227.0 units/day in the patients with essential hypertension, 380.0 ± 177.3 units/day in the patients with chronic glomerulonephritis, and 324.0 units/day in the patient with renovascular hypertension. Renin activity and aldosterone concentration in plasma were 1.53 ± 0.88 ng/ml/h and 10.1 ± 5.5ng/dl in the normal subjects, 0.87 ± 0.55 ng/ml/h and 7.3 ± 5.7ng/dl in the patients with essential hypertension, 1.54 ± 1.85ng/ml/h and 4.1 ± 2.4ng/dl in the patients with chronic glomerulonephritis, and 12.1ng/ml/h and 25.5 ng/dl in the patient with renovascular hypertension, respectively. There was no significant relationship between urinary ACE excretion and plasma renin activity or plasma aldosterone concentration in either the normal subjects or the hypertensive patients. Urinary sodium excretion was 148.4 ± 27.1mEq/day in the normal subjects, 148.2 ± 58.2 mEq/day in the patients with essential hypertension, 175.5 ± 30.9 mEq/day in the patients with chronic glomerulonephritis, and 120.5mEq/day in the patient with renovascular hypertension. There was a significant correlation between urinary sodium excretion and urinary ACE excretion in the hypertensive patients (r=0.70, p<0.001), while there was no significant correlation between urinary ACE excretion and urinary potassium or creatinine excretion (r =0.19 for urinary potassium excretion; r= 0.13 for urinary creatinine excretion).From these results, it is suggested that urinary ACE, which may originate from the kidney, plays a possible role in sodium excretion in cooperation with the renal kallikreinkinin system in hypertensive patients.