Renal tubular acidosis after cadaver kidney homotransplantation

Studies on mechanism
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      In the case cited, renal tubular acidosis developed after cadaver renal homotransplantation. Prior glomerulonephritis with uremia and hypertensive encephalopathy necessitated bilateral nephrectomy and chronic dialysis. No clinical or morphologic features of renal tubular acidosis were present in the recipient or donor, who died of hepatic failure.
      The studies performed included induced metabolic acidosis, phosphate infusion, acetazolamide administration and bicarbonate loading. Discontinuation of 3.6 gm. sodium bicarbonate orally per day led to marked reduction in arterial blood pH (7.32), pCO2 (27 mm. Hg) and bicarbonate (16 mEq. per L.). Net hydrogen ion excretion was only 22.4 μEq. per minute. Neutral phosphate infusion increased serum phosphorus to 10.3 mg. per cent and raised excretion from 14.7 to 63.3 μM per minute, but titratable acidity increased only 12.8 μEq. per minute. Intravenously administered acetazolamide did not change urine volume or bicarbonate reabsorption and when given orally (15 mg. per kg.) bicarbonate excretion increased only from 27.6 to 46.9 μEq. per minute. Intravenous bicarbonate loading increased bicarbonate excretion from 37.5 to 153 μEq. per minute as the percentage reabsorption of bicarbonate decreased. Phosphate clearance was 15 ml. per minute when the creatinine clearance was 45 ml. per minute. However, glycosuria (1.0 to 1.5 gm. per 24 hours) occurred without hyperglycemia and 24 hour alpha amino nitrogen excretion was 1,360 mg.
      It is concluded that a high concentration gradient between luminal fluid and peritubular blood could not be obtained. Evidence for impaired tubular hydrogen ion production, which in turn suggested decreased carbonic anhydrase activity and diminished renal ammonia production, was found in this patient with multiple tubular defects.
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