Complete correction of renal anemia by recombinant human erythropoietin

The target-hematocrit (Hct) For the correction of renal anemia by recombina nt human erythropoeitin (rhEPO) therapy is discussed controversially. A nor malization of the Hct that: could lead to a further improvement of the pati ents status, is often rejected, because of possible side effects as a resul t of an increase in blood viscosity. Hemodialysis (HD) induces an acute hem oconcentration due to ultrafiltration. that might influence these risk fact ors negatively and therefore conflict with the normalization of Hct. The ai m of this study was to investigate the changes in rheological and biochemic al parameters in chronic HD patients with a normal initial Hct before hemod ialysis, Results in 39 patients are given as mean +/- SD before/after HD: H ct 0.42 +/- 0.05/0.45 +/- 0.05 (p < 0.001), hemoglobin (g/dI) 13.3 +/- 1.0/ 14.4 +/- 1.3 (p < 0.001), MCV (fl) 99.3 +/- 5.7/99.1 +/- 5.5, MCHC (mM/l) 1 9.9 +/- 0.6/20.1 +/- 0.6 (p < 0.01), red blood cell (RBC) elongation (%) 60 .97 +/- 3.67/60.99 +/- 3.75, RBC aggregation index AI(0) 0.52 +/- 0.12/0.50 +/- 0.12, AI(4) 0.52 +/- 0.14/0.51 +/- 0.12, plasma viscosity 1.74 +/- 0.1 4/1.92 +/- 0.20 (p < 0.001), whole blood viscosity (WBV), eta(abs.100)(mPas ) 5.91 +/- 0.78/6.80 +/- 1.2 (p < 0.001), eta(abs.0.01)(mPas) 75.81 +/- 35. 48/167.656 +/- 98.656 (p < 0.05), ultrafiltration (FM) 2.1 +/- 1.1. The bio chemical parameters protein, albumin, IgG, IgA, IgM, cholesterol, transferr in and fibrinogen are significantly increased after HD. The hemoconcentrati on during HD is associated with a significant increase in WBV, mainly assoc iated with the increase in Hct (r = 0.83), but not exceeding the; normal ra nge compared to healthy controls. The Increase in plasma viscosity is corre lated mainly with an increase in protein (r = 0.80), albumin (r = 0.74), an d fibrinogen (r = 0.54). No significant changes in RBC aggregation and defo rmability were observed during the I-FD session. In conclusion, from the rh eological point of view it is unlikely that the normalization of the Hct wi ll contribute to an increased risk in access thrombosis or thromboembolic e vents in IID patients.