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• W2010455909 abstract "Dear Sir, Suggested mechanisms for recombinant erythropoietin (EPO)-induced hypertension in end-stage renal disease (ESRD) patients include increased peripheral vascular resistance secondary to increased whole blood viscosity, and failure of an elevated cardiac output to decrease in response to increased hematocrit [1]. In addition, a pressor effect by EPO on vascular smooth muscle has been postulated, either directly [2], or indirectly via local activation of the renin-angiotensin system in tissues [3], or through the release of endothelin-1 [4]. However, most clinical explorations of EPO-induced hypertension focused exclusively on long-term sustained hypertension, and not on blood pressure measured immediately after the injection of EPO. To explore the time course of EPO-induced hypertension, we conducted a prospective 4-week study (12 dialysis treatments) in 90 randomly selected EPO-treated ESRD patients on hemodialysis and investigated the relation between the dose of EPO and (a) predialysis blood pressure, and (b) postdialysis blood pressure measured 30 min after the intravenous administration of EPO. From the record of each subject, we extracted their EPO dose, cause of ESRD, and number and dose of currently prescribed antihypertensive medications. All information was confirmed with the patient, and mean hematocrit was calculated from four weekly measurements. Conventional dialysis was performed using modified cellulose acetate dialyzers, a bicarbonate bath, with a dialysate sodium concentration of 140 mEq/l, and a dialysate calcium concentration of 3.5 mEq/l. All subjects received EPO intravenously thrice weekly at the end of each session and the dose of EPO was not altered during the study. The study group consisted of 43 men and 47 women including 61 African Americans, 16 Whites, 10 Hispanics, and 3 Asians. Their mean age was 58 ± 15 years. The mean thrice weekly dose of EPO was 55 ± 32 U/kg body weight. Predialysis systolic blood pressure was 144 ± 15 mm Hg, and mean predialysis diastolic blood pressure was 81 ± 7.8 mm Hg. Postdialysis systolic blood pressure was 130 ± 16 mm Hg, and mean postdialysis diastolic blood pressure was 77 ± 7 mm Hg. Of the 90 subjects 49 (54.4%) were receiving at least one antihypertensive medication, daily. The dose of EPO correlated significantly with postdialysis systolic blood pressure (r = 0.25; p = 0.01), as well as postdialysis diastolic blood pressure (r = 0.3; p = 0.004). Neither predialysis systolic blood pressure (r = 0.1; p = 0.34), nor predialysis diastolic blood pressure (r = 0.13; p = 0.22) correlated significantly with the dose of EPO (table 2). Selecting postdialysis systolic blood pressure as the outcome variable, multiple regression analysis revealed direct correlations with dose of EPO (p = 0.05) (table 1). With postdialysis diastolic blood pressure as the outcome variable, a significant association was noted with the dose of EPO (p = 0.007) (table 2). In both analyses elevation in blood pressure was more likely in those taking antihypertensive medication (tables 1, 2). Our key finding is that in hemodialysis patients who received intravenous EPO at the end of each dialysis session, there was a relation between the dose of EPO and postdialysis blood pressure but not with predialysis blood pressure. Our results support and extend recent findings by other investigators of a vasopressor effect of EPO on blood vessel smooth muscle, either directly [2], or through the release of endothelin-1 [4]. Additional evidence in support of a direct pressor effect of EPO, is the finding in a study of three groups of hemodialysis patients in whom anemia was treated by different methods, that only the EPO-treated group manifested hypertension [5]. Furthermore, it appears that the incidence of EPO-associated hypertension is higher with intravenous EPO than with subcutaneously administered EPO [6, 7]. The limitation to our study is that we did not document blood pressure immediately before the administration of EPO. Nevertheless, our results indicate that, in addition to the long-term effect on blood pressure that results from EPO administration, there is an immediate effect that is dose dependent. Whether a relationship exists between these two pathogenetic sequences need to be clarified. We emphasize that in the search for mechanism underlying EPO-induced hypertension, the focus should not be limited to the exploration of long-term sustained hypertension." @default.
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• W2010455909 title "Erythropoietin-Induced Elevation in Blood Pressure Is Immediate and Dose Dependent" @default.
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• W2010455909 doi "https://doi.org/10.1159/000045103" @default.
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