1. We have studied Na+/K+ pump activity in vivo in three groups of subjects: patients with chronic renal failure not receiving maintenance dialysis, patients being treated by either haemodialysis or continuous ambulatory peritoneal dialysis, and matched control subjects.
2. To do this we have measured the changes in plasma and intraerythrocytic rubidium concentrations after an oral load of rubidium chloride, having previously shown that changes in the disposition of rubidium measured in this way reflect changes in the activity of the Na+/K+ pump in vivo.
3. Erythrocyte rubidium uptake was significantly reduced both in ten patients with chronic renal failure not receiving maintenance dialysis and in 12 patients being treated by haemodialysis, when compared with 31 healthy control subjects. In contrast, erythrocyte rubidium uptake was not altered in 13 patients treated by continuous ambulatory peritoneal dialysis. There was also a significantly reduced rate constant for erythrocyte rubidium uptake in patients with undialysed chronic renal failure (0.66 h−1) and in those treated by haemodialysis (0.78 h−1), whereas in patients treated by continuous ambulatory peritoneal dialysis the rate constant for erythrocyte rubidium uptake was not significantly different from control values (1.36h−1 and 1.41 h−1, respectively).
4. These findings are consistent with a reversal of the inhibition of erythrocyte Na+/K+ pump activity in vivo found in chronic renal failure by continuous ambulatory peritoneal dialysis, but not by haemodialysis. This difference may be due to the failure of haemodialysis to clear a circulating inhibitor of Na+, K+-ATPase or to the rapid re-accumulation of such an inhibitor after haemodialysis. Alternatively, it could be due to a dialysable inhibitor of potassium efflux, with a secondary reduction in the activity of the Na+/K+ pump.
5. Neither continuous ambulatory peritoneal dialysis nor haemodialysis reversed the abnormal disposition of rubidium in the plasma found in undialysed patients. This suggests that the putative inhibitor which accumulates in chronic renal failure does not affect cation transport in all tissues of the body, and that abnormalities of cation transport in chronic renal failure may be due to more than one mechanism.