THE PATHOGENESIS OF HYPER-CHLOREMIC METABOLIC-ACIDOSIS ASSOCIATED WITH KIDNEY-TRANSPLANTATION

The mechanism of persistent hyperchloremic metabolic acidosis developing after kidney transplantation was investigated in 6 patients. In 5 patients in whom acidosis failed to lower the urine pH below 5.5, an infusion of sodium sulfate also failed to lower the urine pH. Neutral phosphate infusion failed to increase the urine minus blood (U-B) carbon dioxide tension (pCO2) difference normally in these patients. This abnormal response to both maneuvers indicates the presence of a tubular defect for distal hydrogen ion secretion. In the remaining patient, spontaneous acidosis lowered the urine pH below 5.5 and increased the U-B pCO2 normally with the administration of phosphate; this demonstrates that this patient''s distal capacity for hydrogen secretion was intact. The plasma aldosterone level was low in this patient, and thus he had the acidification defect characteristic of aldosterone deficiency. Hyperkalemia developed in 2 patients; both were aldosterone-deficient, and they had a low fractional K excretion in response to stimulation with sodium sulfate or acetazolamide. In all but 1 patient, who lost his kidney to accelerated rejection, chronic rejection developed. Homogeneous deposition of complement (C3) along the tubular basement membrane was found in 3 patients. Apparently a secretory type of distal renal tubular acidosis can be an early sign of the immunologic process that leads to chronic rejection.