Atrial natriuretic factor in the acute nephritic and nephrotic syndromes

Because the role of systemic hormones in the pathophysiology of edema in acute renal disease remains incompletely understood, we compared the levels of atrial natriuretic factor (ANF) and plasma renin activity (PRA) in patients with acute glomerulonephritis (AGN), nephrotic syndrome (NS), and normal individuals during salt deprivation and salt loading. Sixteen patients with AGN (10 males) and nine patients with NS and hypoalbuminemia (7 males) were studied on admission, and after recovery (12 AGN patients) or remission (4 NS patients). Eighteen normal controls were each studied after five days on a low (20 mEq Na/day), regular (120 mEq Na/day) and high (300 mEq Na/day) dietary salt intake. Patients with AGN and NS had comparable edema (AGN 2.8 ± 0.53 kg; NS 3.36 ± 0.47 kg; SE) and urinary Na excretion (mean ± SEM: AGN 0.97 ± 0.11 mEq/hr; NS 1.06 ± 0.16 mEq/hr), but AGN patients had five times higher ANF (AGN 27.2 ± 4.06 fmol/ml; NS 5.51 ± 1.02 fmol/ml; P < 0.001) and six times lower PRA ng/liter · sec levels (AGN 0.187 ± 0.047; NS 1.144 ± 0.222; P < 0.001) than NS patients. The degree of edema was correlated with ANF levels in AGN patients (P < 0.001) but not in NS patients. There was a strong exponential negative correlation (r = -0.773, P < 0.0001) between ANF and PRA, in which AGN patients and Na-restricted controls were located in the opposite ends of the volume sensing-response, and NS patients in the middle, alongside controls with regular Na intake. Our studies suggest that intrarenal mechanisms are responsible for Na retention in AGN as well as in NS, but AGN patients have a compensatory hormonal response related to the degree of fluid retention, while volume-sensing receptors in hypoalbuminemic NS patients are neither actively stimulated nor suppressed, probably due to increased transudation of fluid out of the capillaries.