D. R. WILSON, M.D., F.R.C.P.(C); A. A. SIDDIQUI, M.D., F.R.C.P.(C)
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.
D. R. WILSON, A. A. SIDDIQUI. Renal Tubular Acidosis After Kidney Transplantation: Natural History and Significance. Ann Intern Med. 1973;79:352–359. doi: 10.7326/0003-4819-79-3-352
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Published: Ann Intern Med. 1973;79(3):352-359.
Nephrology, Renal Replacement Therapy.
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