Sodium reabsorption and distribution of Na+/K+-ATPase during postischemic injury to the renal allograft

Background A loss of proximal tubule cell polarity is thought to activate t ubuloglomerular feedback, thereby contributing to glomerular filtration rat e depression in postischemic acute renal failure (ARF). Methods. We used immunomicroscopy to evaluate the segmental distribution of Na+/K+-ATPase in tubules of recipients of cadaveric renal allografts. Frac tional excretion (FE) of sodium and lithium was determined simultaneously. Observations were made on two occasions: one to three hours after graft rep erfusion (day 0) and again on post-transplant day 7. An inulin clearance be low or above 25 ml/min on day 7 was used to divide subjects into groups wit h sustained (N = 15) or recovering (N = 16) ARF, respectively. Results. In sustained ARF, the fractional excretion of sodium (FENa) was 40 +/- 6% and 11 +/- 5%, and the fractional excretion of lithium (FELi) was 7 6 +/- 5% and 70 +/- 2% on days 0 and 7, respectively. Corresponding finding s in recovering ARF were 28 +/- 2% and 6 +/- 2% for the FENa and 77 +/- 4% and 55 +/- 3% (P < 0.05 vs, sustained) for FELi.Na+/K+-ATPase distribution in both groups was mainly basolateral in distal straight and convoluted tub ule segments and collecting ducts. However, Na+/K+-ATPase was poorly retain ed in the basolateral membrane of proximal convoluted and straight tubule s egments in sustained and recovering ARF on both days 0 and 7. Conclusions. We conclude that loss of proximal tubule cell polarity for Na/K+-ATPase distribution is associated with enhanced delivery of filtered Na + to the macula densa for seven days after allograft reperfusion. Whether a n ensuing activation of tubuloglomerular feedback is an important cause of glomerular filtration rate depression in this form of ARF remains to be det ermined.