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American Journal of Clinical Nutrition, Vol 4, 523-528, Copyright © 1956 by The American Society for Clinical Nutrition, Inc.

Kaliopenic Nephropathy

JEROME W. CONN M.D.1 and ROBERT D. JOHNSON M.D.1

1 From the Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan

Kaliopenic nephropathy must be recognized as an established clinical and pathologic entity. It can be induced experimentally by diets deficient in potassium. It is reproducible by repeated administration of large doses of desoxycorticosterone and preventable when supplementary potassium is given in such desoxycorticosterone experiments.

In man, the syndrome is observed most frequently in the potassium-deficient state associated with chronic intestinal disease. It is also present in primary aldosteronism, the renal manifestations of which are analagous to DOC-induced "diabetes insipidus" in animals.

A decreased tubular capacity to reabsorb water, not influenced by administered pitressin, is the most distinctive functional abnormality encountered in kaliopenic nephropathy. While other renal functions, too, may be impaired, hyposthenuria is disproportionately severe. Histologically, the lesion is limimited to tubular cells and is characterized by diffuse hydropic vacuolarization. This anatomic lesion is observed in chronic hypokalemia in man whether the latter is produced by long-standing diarrhea on the one hand, or by an aldosterone-secreting cortical tumor on the other.

In most instances both the functional and anatomic abnormalities appear to be slowly reparable after replacement of the potassiumn deficit. It is likely, however, that in some cases so much damage has occurred during chronic kaliopenia that functional recovery is impossible.




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