Spontaneous remission of the defect in urinary acidification after cadaver kidney homotransplantation.

Abstract

Abstract Six patients who had previously been shown to have a defect in urinary acidification after cadaver kidney homotransplantation were followed up for a mean period of 15 months (range 14-16 months). During this period their ability to lower urinary pH was largely restored to normal and mean absolute titratable acid excretion increased twofold. There was a slight decline in mean absolute ammonia excretion. The capacity to acidify the urine and excrete titratable acid improved despite a reduction by about a third in mean glomerular filtration-rate secondary to chronic rejection. These findings suggest that neither the immune reaction of the host-versus-graft nor chronic exposure to immunosuppressive drugs have a major causal role in the aetiology of the defect in urinary acidification occasionally seen after kidney transplantation. It would seem that the severe acute tubular necrosis after cadaver kidney homotransplantation is responsible for this tubular dysfunction.