Effect of synthetic human atrial natriuretic peptide (102-126) in nephrotic syndrome

Effect of synthetic human atrial natriuretic peptide (102-126) in nephrotic syndrome. Synthetic human ANP (102-126) or vehicle was intravenously administered to eight patients with non-edematous nephrotic syndrome to study its effect on protein and sodium excretion. ANP was given in ascending doses, each dose for one hour, two to three days apart. Four patients received 0.03, 0.10 and 0.45 µg/kg/min of ANP, and four received 0.015, 0.06 and 0.20 µg/kg/min. Natriuresis increased at all doses; by 179 ± 13.6% (mean ± SEM; P < 0.05) at 0.015 µg/kg/min and by 660 ± 71.5% (P < 0.01) at 0.20 µg/kg/min. Urinary albumin excretion increased by 138 ± 30.1% (P < 0.05) at 0.015 µg/kg/min of ANP and by 534 ± 132% (P < 0.01) at 0.20 µg/kg/min. Immunoglobulin G excretion increased proportionally to albumin excretion. Hematocrit and serum albumin concentration increased after ANP. In each patient the percent reduction of plasma volume calculated from the effect on serum albumin was smaller than the hemocon-centration calculated from the effect on hematocrit, suggesting a loss of albumin from the intravascular compartment. This could not be accounted for by the increased glomerular filtration of albumin. Blood pressure and effective renal plasma flow decreased and filtration fraction increased after ANP. Plasma renin was suppressed at lower doses of ANP but was stimulated, together with plasma noradrenaline, at higher doses. Basal plasma ANP levels were normal and rose at the lowest dose to levels slightly above the physiological range. Thus, ANP appears to increase the transcapillary filtration of intravascular protein in the glomerulus and possibly elsewhere in the body. In non-edematous patients with nephrotic syndrome the proteinuric and natriuric effects of ANP were already seen at low doses. Endogenous ANP may therefore have similar effects in these patients