1. The defect in sodium conservation shown by patients with advanced chronic renal failure has been studied during the administration of diazoxide.
2. All nine patients showed a reduction in urinary sodium concentration to levels substantially lower than those which can normally be produced in such patients even with prolonged sodium depletion. Seven patients produced a nearly sodium-free urine. In all patients this effect could be reversed by the administration of high doses of frusemide. The fall in urinary sodium concentration was associated with a sustained fall in creatinine clearance in only two cases.
3. One patient with salt-losing renal disease showed a more modest fall in sodium concentration on treatment with diazoxide.
4. It is concluded that since the defect in sodium conservation shown by patients with chronic renal failure can be corrected without diminishing the osmotic load, it cannot be solely due to the effect of the osmotic diuresis upon residual functioning nephrons. It is suggested that the distal tubular transport mechanism for sodium is saturated by the increased delivery of sodium from the proximal tubule.