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

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 tubuloglomerular feedback, thereby contributing to glomerular filtration rate 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. Fractional excretion (FE) of sodium and lithium was determined simultaneously. Observations were made on two occasions: one to three hours after graft reperfusion (day 0) and again on post-transplant day 7. An inulin clearance below or above 25 ml/min on day 7 was used to divide subjects into groups with sustained ( N = 15) or recovering ( N = 16) ARF, respectively. Results In sustained ARF, the fractional excretion of sodium (FE Na ) was 40 ± 6% and 11 ± 5%, and the fractional excretion of lithium (FE Li ) was 76 ± 5% and 70 ± 2% on days 0 and 7, respectively. Corresponding findings in recovering ARF were 28 ± 2% and 6 ± 2% for the FE Na and 77 ± 4% and 55 ± 3% ( P Li . Na + /K + -ATPase distribution in both groups was mainly basolateral in distal straight and convoluted tubule segments and collecting ducts. However, Na + /K + -ATPase was poorly retained in the basolateral membrane of proximal convoluted and straight tubule segments 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 an ensuing activation of tubuloglomerular feedback is an important cause of glomerular filtration rate depression in this form of ARF remains to be determined.