To investigate the status of the Na + concentration and ionic fluxes in red cells of human subjects with dialyzed chronic uremia, the authors measured the Na +-K + pump activity as well as Na +-K + cotransport (CoT), Na +-Li + countertransport (CTT) and Na + passive permeability in erythrocytes from 37 normal subjects and 23 chronic uremic patiens receiving maintenance hemodialysis. The mean intracellular Na + concentration [Na +]i value in the pre-dialytic group was significantly lower than that in control subjects (p<.0001), but tended to recover to the normal value of [Na +]i in the post-dialytic group. The mean intracellular K + concentration value in the post-dialytic group was significantly higher than that of the control group (p<.001), but not significantly different from that of the pre-dialytic group. It was found that the Na +-K + pump activity of erythrocytes in the pre- and post-dialytic groups markedly decreased over that of the normal control group with statistical significance (p<.0001, respectively). The Na +-K + pump activity in the post-dialytic group, however, tended to recover, but not significantly. The rate constant for ouabain-sensitive Na + efflux in the post-dialytic group was significantly decreased over that of the normal controls (p<.05). The authors observed a significant decrease of the Na + CoT value (p<.001 respectively) and rate constant for Na + CoT (p<.05, respectively) in the patients with pre- and post-dialytic uremia vs. that of normal subjects. Also, the authors observed a marked decrease of the Na +-Li + CTT value in the patients in the pre- and post-dialytic groups than that of the control subjects (p<.05, respectively). Passive Na + permeability in the patients with pre-dialytic uremia was decreased markedly compared to the normal subjects (p<10 −5), but its value in the post-dialytic group tended to recover to the normal value. In conclusion, our studies demonstrate that another possible mechanism of inhibition of the Na +-K + pump in pre- dialytic uremia might then be a secondary adaptive response of the cell to maintain normal intracellular ion concentration and transmembrane ion gradients in the face of the reduced [Na +]i due to decreased passive Na + permeability.