Viscosity, an important determinant of microcirculatory hemodynamics, is related to hematocrit (HCT), and may be altered by renal failure or its treatment. To assess these factors, we studied the effect of dialysis on the viscosity of whole blood, plasma, and reconstituted 70% HCT blood of eight continuous ambulatory peritoneal dialysis (CAPD) and nine hemodialysis (HD) patients under steady shear flow conditions at different shear rates, before and after dialysis, compared with nine normal subjects. The density of the red blood cells (RBCs), a marker of cell hydration, was measured in HD patients by a nonaqueous differential floatation technique. Whole blood viscosity was higher in controls than patients, and correlated with HCT before treatment (P < 0.05) at shear rates of 11.5 to 230 s−1 in HD patients, and 23 to 230 s−1 in all end-stage renal disease (ESRD) patients. In contrast, whole blood viscosity correlated with HCT in CAPD patients only at the lowest shear rates (2.3 and 5.75 s−1, P < 0.05). Plasma viscosity was higher in CAPD patients than both HD patients before treatment and controls (P < 0.05, analysis of variance [ANOVA]), despite lower plasma total protein, albumin, and similar fibrinogen concentration compared with HD patients. When all samples were reconstituted to 70% HCT, CAPD patients had higher whole blood viscosity than control subjects'. The high HCT blood viscosity of the ESRD patients was higher than control subjects' at capillary shear rates, suggesting increased RBC aggregation and decreased RBC deformability in patients with renal disease. Whole blood viscosity increased concomitantly with ultrafiltration during HD treatment, and was similar in control subjects and HD patients after treatment, although patients had lower HCT than the controls (P < 0.001). Plasma viscosity was higher in HD patients after dialysis compared with controls, due to increased plasma protein concentration. The density profile of the erythrocytes increased after HD, and their median density increased linearly as a function of the ultrafiltered volume. We conclude that uremia per se significantly alters blood viscosity, independently of HCT. Patients with ESRD treated with CAPD have higher plasma viscosity despite lower plasma protein concentration, and higher whole blood viscosity at increased HCT levels. Alterations in total plasma protein and fibrinogen concentration, and the effect of ultrafiltration on these parameters, may play critical roles in determining hyperviscosity in patients treated with HD. Changes in RBC surface area to volume ratio and increased RBC density, and hence internal viscosity, as well as elevated plasma protein levels, may induce RBC aggregation. These cellular alterations may affect microcirculatory hemodynamics and predispose patients with ESRD to coagulation abnormalities. © 1992, National Kidney Foundation. All rights reserved. All rights reserved.
