In order to study the tubular mechanism for salt retention in acute proliferative glomerulonephritis, clearance and micropuncture experiments were performed on nine volume-expanded dogs before and after injection of sheep anti-dog glomerular basement membrane (GBM) antibodies (nephrotoxic sera [NTS]). Histologic sections obtained two hours after NTS injection following completion of the functional studies demonstrated infiltration of glomerular tufts by polymorphonuclear leukocytes, swelling of both glomerular endothelial and mesangial cells and the mesangial matrix, and linear anti-GBM antibody deposits along the glomerular capillaries. There was an almost immediate reduction in glomerular filtration rate (GFR), filtration fraction, urine flow and absolute and fractional sodium excretion; arterial blood pressure and renal plasma flow were not significantly altered. Micropuncture studies revealed no change in fractional sodium reabsorption in the proximal tubule despite a fall in single nephron GFR. A proportional reduction in single nephron and kidney GFR coupled with an unchanged intrarenal distribution of blood flow following NTS suggests a relatively uniform effect on both superficial and deep nephrons. In contrast to the well-preserved glomerulotubular balance in the proximal tubule, fractional distal sodium reabsorption was significantly increased as reflected by the decreased fractional urinary sodium excretion. We conclude that salt retention and low fractional urinary sodium excretion observed in acute glomerulonephritis could be primarily due to reduced distal delivery of sodium which leads to increased fractional sodium reabsorption in the nephron segments distal to the proximal convoluted tubule.