Tubular dysfunction following kidney transplantation.

摘要: After transplantation the kidney is subjected to rejection and other deleterious factors including ischemic damage, acute tubular necrosis, use of cyclosporine A (CsA) or FK506. As a result, damage may be generalized with azotemia as its hallmark. These syndromes cause profound changes in acid base balance level certain blood electrolytes minerals. general rule, renal acidosis (RTA) that appears early following disappears spontaneously predominantly sequela failure. On hand, defects occurring late posttransplant period are often due chronic CsA-induced nephrotoxicity. Secondary hyperparathyroidism, urinary tract infection obstructive uropathy also play contributory role pathogenesis RTA. Chronic RTA interfere bone metabolism at times lead nephrocalcinosis nephrolithiasis. Therefore, if condition prolonged, supplement bicarbonate should given for no reason than protect skeleton. these patients develop either hyperkalemia hypokalemia, treatment potassium supplements potassium-sparing diuretics carried out caution under constant surveillance. Furthermore, magnesium replacement advisable hypomagnesemia by decreased proximal reabsorption becomes clinically evident. Tubular dysfunction occur even maintained glomerular filtration rate induce number clinical problems deterioration graft function.