INCREASED NA/H ANTIPORT ACTIVITY AND ABUNDANCE IN UREMIC RED-BLOOD-CELLS

Alterations in red blood cell sodium (Na) transport have been described in chronic renal failure. This study examines the possible impact of uremia on two ouabain-insensitive pathways, the Na/H antiporter and the Cl-/NaCO3- anion exchanger. The V.. of Na/H antiporter measured as Na influx driven by outward H gradient in acid loaded red blood cells was significantly higher in uremic red blood cells versus controls (60.5 +/- 16.5 vs. 24.5 +/- 5.4 mmol/liter cells/hr, P < 0.025). This increase in activity was associated with an increased abundance of the Na/H antiporter as determined by immunologic analysis using an affinity purified polyclonal antibody to the human NHE-1 isoform of the antiporter. By contrast, the activity of the anion exchanger measured as the DIDS-sensitive lithium (Li) influx was similar in uremic versus control red blood cells (2.10 +/- 0.18 vs. 2.14 +/-0.20 mmol/liter cells/hr). These experiments, when considered in conjunction with prior studies showing normal Na/Li countertransport in uremia indicate that there is a selective increase in the number of functional Na/H antiporters in uremic red blood cells and that Na/Li countertransport measurements may not be a valid marker for Na/H antiporter activity in red blood cells in patients requiring dialysis for end-stage renal failure.