SummaryA case of renal tubular acidosis is reported.The prominent clinical feature in this case was recurrent attacks of paralysis due to hypokaliemie.Laboratory data showed hyperchloraemic acidosis and hypophosphataemie associated to hypokaliaemie. Ammonie production and acidification of urine were markedly impaired.Biological studies permitted to draw the following conclusions :a) Infusion of glucose and ingestion of NH4Cl lowered plasma potassium to paralytic level.b) Renal threshold of bicarbonate was markedly reduced.c) Excessive urinary loss of potassium was much more obvious at low plasma level of potassium than when normal plasma potassium was restored.d) Hyperphosphaturie seemed to be directly related to potassium depletion.e) KCl administration greatly increased urinary output of calcium and magnesium.