The pathogenesis of hyperchloremic metabolic acidosis associated with kidney transplantation

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