POSTISCHEMIC INJURY, DELAYED FUNCTION AND NA+ K+-ATPASE DISTRIBUTION IN THE TRANSPLANTED KIDNEY/

We evaluated the postischemic renal injury in 22 patients undergoing r enal transplantation. Renal tissue obtained 45 to 60 minutes after rep erfusion of the allograft was stained with specific antibodies against the partial derivative subunit of Na+/K+-ATPase, fodrin and ankyrin. The distribution of each cytoskeletal protein was analyzed by laser co nfocal microscopy. Subsequent allograft function was assessed on two o ccasions, 1 to 3 and 36 hours post-reperfusion, respectively. Recipien ts were divided into two groups: those who achieved a normal GFR on po st-transplant day 3 (group 1, N = 12) and those with persistent hypofi ltration (group 2, N = 10). Patients of both groups exhibited impaired sodium reabsorption and isosthenuria one to three hours postoperative ly, but these abnormalities persisted on day 3 only in group 2 subject s with persistent hypofiltration. Abnormalities of Na+/K+-ATPase, anky rin and fodrin were confined to proximal tubule cells and were marked only in the subjects of group 2. They consisted of redistribution of e ach cytoskeletal protein from the basolateral membrane to the cytoplas m. We conclude that postischemic injury to a renal allograft results i n a loss of polarity of proximal tubule cells. We propose that ensuing impairment of proximal sodium reabsorption could activate tubuloglome rular feedback, thereby contributing to the protracted hypo-filtration that characterizes this form of postischemic, acute renal failure.