Vascular changes in hemodialysis patients in response to recombinant human erythropoietin

• Published in: Kidney international Vol. 36; no. 5; pp. 878 - 882
• Main Authors: London, Gérard M., Zins, Brigitte, Pannier, Bruno, Naret, Catherine, Berthelot, Jean-Michel, Jacquot, Christian, Safar, Michel, Drueke, Tilman B.
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.11.1989; Nature Publishing
• Subjects: Adult; Anemia - drug therapy; Anemia - etiology; Biological and medical sciences; Blood Viscosity - drug effects; Erythropoietin - therapeutic use; Female; Hemodynamics - drug effects; Hormones. Endocrine system; Humans; Male; Medical sciences; Myocardial Contraction - drug effects; Pharmacology. Drug treatments; Recombinant Proteins - therapeutic use; Renal Dialysis; Uremia - complications; Uremia - therapy; Human; Cardiac performance; Urinary system disease; Intravenous administration; Erythropoietin; Anemia; Hemodialysis; Hemopathy; Glycoprotein hormone; Biological activity; Extrarenal dialysis; Chemotherapy; Blood vessel; Renal failure; Circulatory system; Recombinant protein; Hemodynamics
• ISSN: 0085-2538; 1523-1755
• DOI: 10.1038/ki.1989.274

Vascular changes in hemodialysis patients in response to recombinant human erythropoietin. The partial correction of anemia with recombinant human erythropoietin (rHuEpo) is frequently associated with an increase in arterial pressure and could oppose the beneficial effect of anemia correction on myocardial function. In order to analyze the influence of rHuEpo therapy on the vessels and the heart, we performed systemic and regional hemodynamics studies in 11 hemodialysis patients before and 10 to 35 weeks after initiation of rHuEpo therapy, when hemoglobin concentration was 6.8 ± 0.9 and 10.6 ± 0.66 g/dl (mean ± SD), respectively. The mean arterial pressure remained unchanged during this period (88 ± 21 vs. 88 ± 15mm Hg). Echocardiography study showed that rHuEpo treatment led to a decrease in left ventricular end-diastolic diameter (4.9 ± 0.5 vs. 5.1 ± 0.6 cm; P < 0.03), left atrial diameter (3.22 ± 0.30 vs. 3.43 ± 0.33; P < 0.03), and left ventricular mass index (109.8 ± 30.6 vs. 133 ± 30.8 g/m2; P < 0.05). Left ventricular ejection volume decreased from 86 ± 24 to 75 ± 19ml (P < 0.03) and heart rate from 76 ± 9 to 70 ± 10 beats/min (P < 0.05). Cardiac index decreased from 4715 ± 700 to 3635 ± 444ml/min/m2 (P < 0.01) and peripheral resistances rose from 1480 ± 162 to 1943 ± 250 dynes · sec · cm-5 · m2 (P < 0.01). Fractional ejection and mean circumferential fiber shortening remained unchanged. The treatment with rHuEpo did not change the aortic diameters. Aortic distensibility (pulse wave velocity, PWV) decreased (aortic PWV rose from 804 ± 262 to 907 ± 252 cm/sec) but not significantly (P = 0.08). Forearm and calf blood flow decreased during rHuEpo treatment (4.6 ± 1.4 vs. 6.3 ± 1 and 3.2 ± 1.2 vs. 4.4 ± 1.6ml/mn/100ml; P < 0.01) while the forearm and calf arterial resistances increased (P < 0.01). Correction of anemia with rHuEpo induced a significant decrease in forearm and calf venous distensibility. In the lower limb, we observed a significant increase in venous tone (with a slope of pressure-volume relationship increasing from 21 ± 11 to 26 ± 14mm Hgml 100ml (P < 0.01), and in the forearm a significant increase in minimal occluding pressure from 3.4 ± 2.10 to 5.7 ± 3.7mm Hg (P < 0.01). Our data indicate that correction of renal anemia with rHuEpo can normalize the heart function and induce modifications of arteriolar and venous circulations.