Intrarenal Determinants of Sodium Retention in Mild Heart Failure

Abstract

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 P.O.). 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.

Dietary Sodium Intake in Heart Failure

“…Natriuretic peptide levels were affected inconsistently among studies; levels did not change significantly with dietary sodium modification in 4 studies using very low to moderate dietary sodium restriction, 34,36 -38 decreased in 2 studies with a moderate-to-high sodium diet, 35,39 and increased in 3 studies with a low-sodium diet. 40 -42 Levels of neurohormones, such as PRA, norepinephrine, angiotensin-II, and urinary aldosterone, increased with dietary sodium restriction regardless of degree of restriction.…”

“…Two studies by Volpe and colleagues 35,36 concluded that moderate-to-high sodium intake had no hemodynamic effects on NYHA I to II patients Only consensus opinion of experts, case studies, or standard of care; FairϭBenefits exceed the harms but quality of evidence is not as strong; 1ϩ ϭ well-conducted meta-analysis, systemic reviews, or randomized controlled trials with low risk of bias. NYHA indicates New York Heart Association.…”

“…Concomitant fluid intake was described in some studies and it varied, whereas adherence to the recommended amount of fluid was either not reported or subjectively assessed. Earlier studies discontinued HF medications before randomization, 33,35,36 and later studies did not consistently have patients on optimal medical therapy. Hemodynamic changes varied in these studies in response to a restricted sodium diet; however, statistically significant adverse neurohormonal changes were consistently noted.…”

Worsening of proteinuria caused by combination therapy of hypertonic saline and low-dose furosemide for treatment of acute decompensated heart failure with overt diabetic nephropathy

“…Sodium loading increases renal plasma flow (RPF) and GFR in mild heart failure patients [6]. GFR is determined mainly by filtration pressure and filtration coefficient.…”

The cardiorenal syndrome

“…Volpe et al (9) described the effects of increased sodium intake on GFR, renal plasma fl ow and renal vascular resistance in mild asymptomatic HF. In both normal and mild heart failure subjects, the increased sodium intake (250 mmol/day vs. 100 mmol/day) caused GFR and renal plasma fl ow and fi ltered load of sodium to increase signifi cantly and renal vascular resistance to drop but, while the fractional clearance of water, excretion of potassium and sodium increased in normal subjects, it was signifi cantly reduced in the mild CHF group.…”