In six patients with nephrotic syndrome of various aetiology, the increase in absolute and fractional sodium excretion (FENa) after a bolus injection of 100 micrograms alpha-human atrial natriuretic peptide (ANP) was not different from the effect in normal healthy subjects at comparable sodium levels. Glomerular filtration rate rose in normals as well as in patients. In two patients, however, baseline sodium excretion was very low and the natriuretic response to ANP was proportionally blunted. The high baseline sodium reabsorption and blunted response to ANP may be explained as due either to an intrinsic renal defect or to a circulatory hypovolaemia. The finding of a low plasma ANP in these two patients, however, suggests involvement of a hypovolaemic component.