CONSIDERATIONS ON THE SODIUM RETENTION IN NEPHROTIC SYNDROME

Renin-angiotensin-aldosterone system, plasma atrial natriuretic peptid e (PANP), and blood volume (BV) have been investigated in 20 nephrotic patients with normal renal function and with (group 1; n = 12) or wit hout (group 2; n = 8) sodium retention. Patients of group 1 had a plas ma albumin (PALB) concentration < 1.7 g/dl, low BV and PANP levels, a reduced fractional excretion of lithium (FELi), and high plasma angiot ensin II levels. Patients of group 2 had PALE > 1.7 g/dl, and the othe r parameters were normal. The spontaneous intake of dietary sodium was lower in group 1 than in group 2. In all patients the BV was directly correlated with PALE, and the plasma renin activity (PRA) was inverse ly correlated with both BV and PALE. A nonlinear inverse relationship was present between plasma aldosterone (PALD) levels and fractional ex cretion of sodium (FENa). The acute expansion of the BV in patients of group 1 normalized PRA, PALD, PAII, FENa, and FELi and increased PANP . The administration of spironolactone to the patients of both groups had variable effects on FENa, did not modify PRA and PALD, and reduced body weight, PANP, and FELi, thus suggesting that the reduction of BV induced by the drug increased the proximal reabsorption of sodium. Th ree additional patients who had sodium retention, PALE of 2.3-2.4 g/dl , normal PRA and PALD, elevated urinary excretion of aldosterone, and a slightly low PANP showed a spontaneous normalization of urinary aldo sterone and PANP associated with natriuresis and weight loss, but ther eafter urinary aldosterone increased, PANP decreased, and the sodium r etention began again. Our data suggest that in nephrotic patients with severe hypoalbuminemia, contraction of BV plays a major role in promo ting the sodium retention through the activation of compensatory hormo nal mechanisms. On the other hand, when PALE is not severely reduced, the patients have normal BV, but they are very sensitive to small chan ges of BV which are better evidenced by modifications of the urinary e xcretion of aldosterone and PANP rather than by the profiles of PRA an d PALD.