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The Role of Defective Renal Tubular Sodium Reabsorption and Secondary Hyperaldosteronism in Its Pathogenesis

S. J. FLEISHMAN, M.B.; B. SENIOR, M.B.; M. M. SUZMAN, M.D.; for Submitted

AMA Arch Intern Med. 1959;104(4):613-618.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

In 1946, Albright et al.¹ described the disorder of "renal acidosis resulting from tubular insufficiency without glomerular insufficiency." Since then a number of reports and reviews of this condition have appeared under a variety of titles, such as renal acidosis, renal hyperchloremic acidosis, and renal tubular acidosis.^2-6

The clinical features may be polyuria and polydipsia; the presence of renal calculi, muscular weakness, paralysis, or cramps due to hypokalemia, and bone pains resulting from osteomalacia. The diagnosis depends upon the presence of a systemic acidosis, manifested by a low blood pH, hyperchloremia and a low CO₂ content, and the excretion of a dilute urine that is alkaline or only slightly acid. A striking contrast exists between the degree of systemic acidosis and the high urinary pH. Hypokalemia is usually present. Nephrocalcinosis and osteomalacia are frequently encountered.

Theories regarding the etiology and pathogenesis of renal tubular acidosis include infection, . . . [Full Text PDF of this Article]

Author Affiliations
(Witwatersrand), M.R.C.P. (Edin.); (Witwatersrand), M.R.C.P. (Lond.); (Dunelm), F.R.C.P. (Lond.); Johannesburg, South Africa

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