TITLE

Short stature, hyperkalemia and acidosis: A defect in renal transport of potassium

AUTHOR(S)
Spitzer, Adrian; Edelmann, Jr., Chester M.; Goldberg, Lee D.; Henneman, Philip H.
PUB. DATE
January 1973
SOURCE
Kidney International;Jan1973, Vol. 3 Issue 1, p251
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
An eleven-year-old boy presented with short stature, hyperkalemia. and metabolic acidosis. No endocrine cause for a short stature could be demonstrated. Renal function, as assessed by inulin and PAH clearances, concentrating and diluting capacity, and ability to acidify the urine and lo excrete net acid, was normal. No defect was detected in adrenal secretion of, or renal responsiveness to, aldosterone. A low renal threshold for bicarbonate was documented which apparently explained the acidosis. However, correction of the acidosis by administration of sodium bicarbonate did not influence the hyperkalemia, making it unlikely that an abnormality in bicarbonate reabsorption was the primary defect. Chlorothiazide induced a fall in serum potassium and a rise in serum bicarbonate to normal levels. During bicarbonate loading the rates of excretion of potassium in urine were consistently below those observed in control subjects. It appeared, therefore, that the patient had a primary abnormality in potassium excretion. The resulting hyperkalemia caused urinary loss of bicarbonate and systemic acidosis. Correction of both the acidosis and hyperkalemia by chronic administration of chlorothiazide and sodium bicarbonate has resulted in resumption of normal growth.
ACCESSION #
18287660

 

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