HERBERT W. JOHNSON, M.D., F.A.C.P.
Renal acidosis resulting from tubular insufficiency without glomerular insufficiency is a relatively uncommon entity.1-14 It is accompanied frequently by calcification and stone formation in the kidney and occasionally by osteomalacia. The relative roles of hypercalciuria, systemic acidosis, and parathyroid activity in the pathogenesis of these complications are not certain, although Albright and colleagues postulated that parathyroid hyperplasia develops secondary to the renal loss of calcium. The primary disturbance, however, is clearly a failure of the kidney to excrete acid in a normal manner.
The excretion of acid and the conservation of base is one of the major functions of the
JOHNSON HW. RENAL TUBULAR HYPERCHLOREMIC ACIDOSIS WITH BONE DISEASE: A CASE REPORT1. Ann Intern Med. ;54:1273–1280. doi: 10.7326/0003-4819-54-6-1273
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Published: Ann Intern Med. 1961;54(6):1273-1280.
Endocrine and Metabolism, Nephrology.
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