The role of renin and aldosterone in the salt retention of edema

The response of plasma renin and aldosterone to five days of excessive sodium intake was determined in patients with congestive heart failure, cirrhosis and nephrosis. In eight patients with congestive heart failure, four had elevated plasma renin and aldosterone levels, 11.4 ± 0.5 ng/ml/hour and 21.9 ± .8 ng/100 ml, respectively, after a 3.9 ± 0.5 kg weight gain and a cumulative sodium retention of 501 ± 78 meq, but four had a similar weight gain, 3.8 ± 1 kg, and sodium retention, 488 ± 108 meq, without elevated plasma renin and aldosterone levels. In patients with cirrhosis, six had persistent hypersecretion of renin, 8.4 ± 2.3 ng/ml/hour, and plasma aldosterone, 17.7 ± 2.2 ng/100 ml, after a 6.1 ± 0.8 kg weight gain and 881 ± 104 meq sodium retention, but five gained 5.4 ± 1.5 kg weight and retained 794 ± 211 meq sodium with normal suppression of renin and aldosterone. In 10 patients with the nephrotic syndrome, eight maintained elevated plasma renin and aldosterone levels during a 6.5 ± 0.8 kg weight gain and 874 ± 99 meq sodium but two retained similar amounts of sodium with suppression of plasma renin and aldosterone. In all studies, there was no correlation between the response of plasma renin and aldosterone to sodium intake and glomerular filtration rate, urinary sodium excretion, blood pressure or serum protein concentration. These studies indicate that edema associated with cardiac, renal or hepatic disease can occur without increased aldosterone secretion. We postulate that increased renin secretion is needed in some edematous patients to maintain arterial blood pressure, but the secondary increase in aldosterone which occurs is not the primary cause of the sodium retention.