Leucocytes were used to study cellular sodium (NaWBC) and potassium (KWBC) content and sodium transport (sodium flux rate, FR and sodium pump rate constant, RC). In the first part of this work, a method was developed for reliable counting of the cells, thus avoiding weighing and permitting more estimations of cation content on a given volume of blood. This allowed identification of methodological factors which altered NaWBC. After isolation, an incubation of at least 30 minutes was required before NaWBC became stable. Intermittent gentle resuspension of the cells during incubation gave the lowest values for NaWBC. Mixing by inversion, or centrifugation at 200g for 6 minutes significantly increased NaWBC. Sodium transport was assessed by measuring the increase in NaWBC during a 20 minute incubation with ouabain. The rise was linear over this time and equal to FR. FR divided by baseline Na equalled RC. Ethanol used as a solvent for ouabain was found to affect sodium influx at concentrations > 17 mmol/l. Using these methods, no effects of age or sex were found on NaWBC, FR or RC, but KWBC was higher in females (p = 0.05). These methods were then used to investigate suggestions that chronic renal failure (CRF) in man is associated with release of a circulating sodium pump inhibitor which raises intracellular sodium. In 14 CRF patients who had never been dialysed, NaWBC was raised compared with controls (p< 0.001) but this could not be attributed to reduced RC. In 15 continuous ambulatory peritoneal dialysis (CAPD) patients, NaWBC was less than in the undialysed group (p = 0.05), due to a better matching of FR and RC. In the CAPD group only, NaWBC correlated with plasma urea (p = 0.005) and creatinine (p = 0.031) concentrations. Eighteen regular haemodialysis patients were studied immediately before and after a standard haemodialysis (HD). NaWBC (p = 0.078), FR (p = 0.006) and RC (p = 0.071) were lower at the end of dialysis. No correlations were found between these changes and measures of the biochemical or volume changes produced by HD. Simultaneous measurements in erythrocytes (RBC) showed opposing abnormalities in sodium content. In undialysed patients, sodium was low compared with controls and CAPD patients. HD was associated with a rise in NaRBC. These studies provided evidence in opposition to the theory that intracellular sodium is raised in patients with CRF due to the presence of a volume-related circulating sodium pump inhibitor. The presence of very different abnormalities in RBC and WBC questions the assumption that changes in sodium transport in either of these cell types can be extrapolated to more relevant but less accessible cells.