title: Complete correction of renal anemia by recombinant human erythropoietin.
abstract: The target-hematocrit (Hct) for the correction of renal anemia by recombinant human erythropoeitin (rhEPO) therapy is discussed controversially. A normalization of the Hct that could lead to a further improvement of the patients status, is often rejected, because of possible side effects as a result of an increase in blood viscosity. Hemodialysis (HD) induces an acute hemoconcentration due to ultrafiltration that might influence these risk factors negatively and therefore conflict with the normalization of Hct. The aim of this study was to investigate the changes in rheological and biochemical parameters in chronic HD patients with a normal initial Hct before hemodialysis. Results in 39 patients are given as mean +/- SD before/after HD: Hct 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) 19.9 +/- 0.6/20.1 +/- 0.6 (p < 0.01), red blood cell (RBC) elongation (%) 60.97 +/- 3.67/60.99 +/- 3.73, RBC aggregation index AI0 0.52 +/- 0.12/0.50 +/- 0.12, AI4 0.52 +/- 0.14/0.51 +/- 0.12, plasma viscosity 1.74 +/- 0.14/1.92 +/- 0.20 (p < 0.001), whole blood viscosity (WBV), etaabs.100(mPas) 5.91 +/- 0.78/6.80 +/- 1.2 (p < 0.001), etaabs.0.01(mPas) 75.81 +/- 35.48/167.656 +/- 98.686 (p < 0.05), ultrafiltration (FM) 2.1 +/- 1.1. The biochemical parameters protein, albumin, IgG, IgA, IgM, cholesterol, transferrin and fibrinogen are significantly increased after HD. The hemoconcentration during HD is associated with a significant increase in WBV, mainly associated with the increase in Hct (r = 0.83), but not exceeding the normal range compared to healthy controls. The increase in plasma viscosity is correlated mainly with an increase in protein (r = 0.80), albumin (r = 0.74), and fibrinogen (r = 0.54). No significant changes in RBC aggregation and deformability were observed during the HD session. In conclusion, from the rheological point of view it is unlikely that the normalization of the Hct will contribute to an increased risk in access thrombosis or thromboembolic events in HD patients.
authors.affiliation: Medical Clinic, Department of Nephrology and Intensive Care Medicine, Humboldt University, Berlin, Germany.
authors.forename: K
authors.initials: K
authors.lastname: Ludat
authors.forename: M
authors.initials: M
authors.lastname: Paulitschke
authors.forename: E
authors.initials: E
authors.lastname: Riedel
authors.forename: H
authors.initials: H
authors.lastname: Hampl
mesh_terms: D000740:Anemia / Q000097:blood* / Q000188:drug therapy* / Q000209:etiology; D004921:Erythropoietin / Q000627:therapeutic use*; D005260:Female; D018056:Hemorheology; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000150:complications* / Q000628:therapy; D008297:Male; D008875:Middle Aged; D011994:Recombinant Proteins; D012074:Remission Induction; D006435:Renal Dialysis
chemical_list: D011994:Recombinant Proteins; D004921:Erythropoietin