Intrarenal Determinants of Sodium Retention in Mild Heart Failure: Effects of Angiotensin-Converting Enzyme Inhibition

The onset and the mechanisms leading to Na retention in incipient congestive heart failure (CHF) have not been systematically investigated. To investigate renal Na handling in the early or mild stages of CHF, Na balance and renal clearances were assessed in 10 asymptomatic patients with idiopathic or ischemic dilated cardiomyopathy and mild heart failure (HF) off treatment (left ventricular ejection fraction, 29.7 +/- 2%) and in 10 matched normal subjects during a diet containing 100 mmol/d of NaCl and after 8 days of high salt intake (250 mmol/d). Six patients were studied again after 6 weeks of treatment with enalapril (5 mg/d PO). At the end of the high salt diet, in patients with mild HF the cumulative Na balance exceeded by 110 mmol that of normal subjects (F = 3.86, P < .001). During high salt intake, renal plasma flow and glomerular filtration rate were similarly increased in both normal subjects and mild HF patients. In spite of comparable increases of filtered Na in the two groups, fractional excretion of Na, fractional clearance of free water, and fractional excretion of K (indexes of distal delivery of Na) increased in normal subjects and were reduced in patients with mild HF. During enalapril treatment, in the mild HF patients the cumulative Na balance was restored to normal; furthermore, enalapril significantly attenuated the abnormalities in the distal delivery of Na. Our results indicate that a defective adaptation of Na reabsorption in the proximal nephron is associated with Na retention in response to increased salt intake in the early or mild stages of HF. These abnormalities of renal Na handling are largely reversed by enalapril. (Hypertension. 1997;30[part 1]:168-176.)