The sodium-conserving ability of 46 patients with renal disease of varying etiology was observed during rigid sodium restriction and mineralocorticoid administration. Glomerular filtration rate (inulin clearance) was used to estimate the number of residual nephrons. The patients were divided into two groups: (1) predominantly glomerular disease (glomerulonephritis, amyloidosis, diabetic nephropathy, lupus nephritis), (2) predominantly tubular disease (pyelonephritis, gouty nephropathy, polycystic disease, renal tubular acidosis, nephrocalcinosis, multiple myeloma). With few exceptions, patients with glomerular lesions showed sodium wasting only when the glomerular filtration rate was severely reduced (less than one-fifth normal). On the other hand, a higher proportion of the patients with tubular lesions showed sodium wasting with minimal to moderate reductions in glomerular filtration rate. Thus, the sodium-wasting abnormality in the first group appeared to be related principally to the increased osmotic load per residual nephron, whereas an additional tubular defect in the reabsorption of sodium may have played a significant role in certain patients within the second group.