AJP - Renal Physiology, Vol 252, Issue 5 785-F793, Copyright © 1987 by American Physiological Society
Na+-K+ pump in chronic renal failure
D. Kaji and K. Thomas
This review summarizes the evidence for the defect in Na+-K+ pump in
chronic renal failure, considers the role of various factors in causing
this defect, and discusses the clinical implications thereof. Intracellular
Na is elevated in erythrocytes, leukocytes, and muscle cells from some
patients with chronic renal failure (CRF). Recent evidence suggests that
this elevation of cell Na may be, in large part, a consequence of decreased
number of Na+-K+ pump units per cell. Maintenance dialysis over a period of
weeks ameliorates the defect in intracellular Na+, and this improvement is
contemporaneous with an increase in the number of Na+-K+ pump sites per
cell. In erythrocytes with normal cell Na+, acute hemodialysis increases
the rate of Na+ and K+ transport. Many factors such as the presence of
retained toxic metabolite or circulating inhibitor in the uremic plasma, or
biochemical changes produced by acute hemodialysis, may explain this
finding. In cells with high cell Na+, the pump-mediated K+ transport is
normalized at the expense of a raised cell Na+. The decreased muscle
membrane potential in uremic subjects has been attributed to a decreased
activity of Na+-K+ pump. Enzymatic Na+-K+-ATPase activity of the uremic
erythrocyte, leukocyte, sarcolemma, and intestines is also decreased. We
discuss the role of hormonal abnormalities and circulating inhibitors,
which may cause an acute inhibition of the pump and of other factors such
as K+ depletion, which may cause more chronic alterations. The implications
of alteration of Na+ and K+ pump transport and raised cell Na+ on other
non-pump-mediated transport pathways are discussed.(ABSTRACT TRUNCATED AT
250 WORDS)
