By replacing normal water intake with 0–9% saline solution on a continuing basis, animals are protected against acute is chœmic tubular necrosis. Last‐minute plasma volume expansion does not provide this protection. To see whether the protection is intrinsic to the kidney or merely involves the host, kidneys were transplanted syngeneically from salt‐drinking rats to water‐drinking rats, and vice versa, and the recipients were injected with glycerol to produce myohœmoglobinuric renal failure. The kidneys transplanted from water‐drinking animals did not develop failure in the salt‐drinking animals, but those from salt drinkers did develop failure in the water drinkers. Therefore overhydration of the recipient by continuous salt loading is important in preventing acute tubular necrosis in renal tr