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Renal Tubular Acidosis After Kidney Transplantation: Natural History and Significance

D. R. WILSON, M.D., F.R.C.P.(C); and A. A. SIDDIQUI, M.D., F.R.C.P.(C)
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Presented in part January 1971, Annual Meeting of the Royal College of Physicians and Surgeons of Canada, Ottawa, Canada.

Grant support: grant PR 226, Department of Health of the Province of Ontario; Dr. Siddiqui was supported by the Medical Research Council of Canada.

▸ Requests for reprints should be addressed to D. R. Wilson, M.D., Division of Nephrology, Toronto General Hospital, Toronto, Ontario M5G IL7, Canada.

Toronto, Canada

Ann Intern Med. 1973;79(3):352-359. doi:10.7326/0003-4819-79-3-352
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Thirty-two patients whose renal allografts have been functioning for 1 to 3 years have been followed and repeatedly tested for urine acidification. In the first 1 to 2 months after transplantation a variety of defects—distal renal tubular acidosis (complete or incomplete), proximal bicarbonate-wasting renal tubular acidosis, or reduced ammonia excretion—were seen; these may be related to factors such as secondary hyperparathyroidism, malnutrition, acute tubular necrosis, and acute rejection. Long-term studies indicated that proximal renal tubular acidosis and reduced ammonia excretion usually disappeared. Distal renal tubular acidosis (incomplete), however, was associated with the features of chronic rejection (proteinuria, hypertension, decreased creatinine clearance) and was present in 43% of patients followed for 1 to 3 years. Distal renal tubular acidosis in long-standing renal allografts is probably the result of immunologic mechanisms and may be the functional equivalent of the interstitial infiltrate and fibrosis that are present in kidneys affected by chronic rejection.





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