In a patient with renal amyloidosis secondary to chronic urinary tract infection with nephrotic syndrome, polyuric acute renal failure developed after reduction from a high to a normal dietary intake of sodium and was reversed by salt replacement therapy. As documented by functional and morphological studies, the patient had a marked defect of tubular sodium reabsorption at the proximal site and along the ascending limb of Henle's loop, a distal tubular unresponsiveness to aldosterone, and severe tubulointerstitial damage in the medulla. We propose that the sodium dietary reduction in conjunction with severe tubular dysfunction and hypovolemia due to nephrotic syndrome is responsible for this unused form of polyuric acute prerenal failure.