Does Increasing Haemoglobin (Hb) or Haematocrit (Hct) Have a Pressor Effect in Dialysis Patients?

Recombinant Human Erythropoietin and Its Effects on Macro- and Microcirculation during Normovolemia

“…Similar findings were reported by Neff et al [46] who increased the Hct of anemic dia lyzed patients by serial blood transfusion to at least 40% within 6-12 weeks, and saw an increase in the peripheral vascular resistance and a decrease in cardiac index, while MAP increased [46]. Williams et al [47], increas ing the Hct with an average value of 8% in a large and varied dialysis population, did not find an increase in predialysis blood pres sures within 1 week after the blood transfu sion. More detailed hemodynamic investiga tions unfortunately were not performed in this study [47], Obviously, not all rHuEpo-treated pa tients develop hypertension, despite an in crease in SVR, and it has been reported that individuals prone to hypertension had rela tively high pre-and posttreatment cardiac output levels as compared to other patients treated with rHuEpo, but remaining normotensive [45,48], In general, cardiac index and stroke volume decrease during the cor rection of anemia by rHuEpo therapy, whereas SVR increases.…”

“…Williams et al [47], increas ing the Hct with an average value of 8% in a large and varied dialysis population, did not find an increase in predialysis blood pres sures within 1 week after the blood transfu sion. More detailed hemodynamic investiga tions unfortunately were not performed in this study [47], Obviously, not all rHuEpo-treated pa tients develop hypertension, despite an in crease in SVR, and it has been reported that individuals prone to hypertension had rela tively high pre-and posttreatment cardiac output levels as compared to other patients treated with rHuEpo, but remaining normotensive [45,48], In general, cardiac index and stroke volume decrease during the cor rection of anemia by rHuEpo therapy, whereas SVR increases. Whether the MAP will rise depends on the rate of increment in Hct, the ultimate Hct level achieved, the preexistence of hypertension and last but not least on the actual fluid status.…”

Cardiovascular Effects of Increasing Hemoglobin in Chronic Renal Failure

“…Interestingly, in the same study the authors recorded blood pressure in CAPD patients within the first year of dialysis when hemoglobin rose spontaneously from 8.5 to 10.7 g/dl. Blood pressure surprisingly decreased, although there was no sign of a change in the hydration status of the patients [6], Nonetheless, most studies on the hemodynamic effects of correction of renal anemia by r-huEPO gave similar results to the report of Neff et al [5]. Table l summarizes the results of 12 studies published after 1989 on cardiac output [7][8][9][10][11][12][13][14][15][16][17][18].…”

“…However, when Neff et al [5] corrected anemia by the use of blood transfusions cardiac output was reduced but, sur prisingly, blood pressure became even more elevated because of a marked increase in peripheral resistance. At least as far as blood pressure is concerned, these results could not be reproduced by Williams et al [6], although the individual development of vascular resistance and cardiac output was not measured in this study. When they administered blood transfusions to anemic hemodialysis patients the mean arterial blood pressure was stable.…”

Beyond Anemia: The Clinical Impact of the Physiologic Effects of Erythropoietin

“…As hypertension and polycythemia had long been known to accompany each other (105) the finding was not surprising. However, it is now clear that the increase in Hct alone does not produce hypertension (106); erythrocytosis seen in the spontaneous hypertensive rat model is preceded by hypertension (107). Administration of rHuEPO has been reported to increase systemic vascular resistance and decrease cardiac output (108), perhaps a result of increased endothelin (109), angiotensin (110), impaired endothelium‐dependent relaxation (111), altered calcium homeostasis in vascular smooth muscle cells (112), or serotonin release from platelet dysfunction (112,113).…”