Clinical and experimental nephrology · 2008
Is there a role for endothelin-1 in the hemodynamic changes during hemodialysis?
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El-Shafey E M, El-Nagar G F, Selim M F, El-Sorogy H A, Sabry A A
Аннотация
BACKGROUND: The etiology of hemodialysis (HD)-induced hypotension and hypertension remains speculative. There is mounting evidence that endothelin-1 (ET-1) may play a vital role in these hemodynamic changes. We examined the possible role of intradialytic changes of ET-1 in the pathogenesis of hypotension and rebound hypertension during HD.
METHODS: The present study included 45 patients with end-stage renal disease (ESRD) on regular HD. They were divided according to their hemodynamic status during HD into three groups (group I had stable intradialytic hemodynamics, group II had dialysis-induced hypotension, and group III had rebound hypertension during HD). In addition, 15 healthy volunteers were included as a control group. Pulse and blood pressure were monitored before, during (every half hour), and after HD session. ET-1 level was measured at the beginning, middle, and end of HD. ET-1 was measured in the control group for comparison.
RESULTS: Pre-dialysis levels of ET-1 were significantly higher in dialysis patients compared to the controls (P < 0.001); however, they were comparable in the three HD groups. The post-dialysis ET-1 level was not changed significantly in group I compared with predialysis values (14.49 +/- 2.04 vs. 14.33 +/- 2.23 pg/ml; P = NS), while the ET-1 concentration decreased significantly in group II and increased in group III in comparison to predialysis values (8.56 +/- 1.44 vs. 11.75 +/- 2.51; 16.39 +/- 3.12 vs. 11.93 +/- 2.11 pg/ml, respectively; P < 0.001).
CONCLUSION: Altered ET-1 levels may be involved in the pathogenesis of rebound hypertension and hypotension during HD.
METHODS: The present study included 45 patients with end-stage renal disease (ESRD) on regular HD. They were divided according to their hemodynamic status during HD into three groups (group I had stable intradialytic hemodynamics, group II had dialysis-induced hypotension, and group III had rebound hypertension during HD). In addition, 15 healthy volunteers were included as a control group. Pulse and blood pressure were monitored before, during (every half hour), and after HD session. ET-1 level was measured at the beginning, middle, and end of HD. ET-1 was measured in the control group for comparison.
RESULTS: Pre-dialysis levels of ET-1 were significantly higher in dialysis patients compared to the controls (P < 0.001); however, they were comparable in the three HD groups. The post-dialysis ET-1 level was not changed significantly in group I compared with predialysis values (14.49 +/- 2.04 vs. 14.33 +/- 2.23 pg/ml; P = NS), while the ET-1 concentration decreased significantly in group II and increased in group III in comparison to predialysis values (8.56 +/- 1.44 vs. 11.75 +/- 2.51; 16.39 +/- 3.12 vs. 11.93 +/- 2.11 pg/ml, respectively; P < 0.001).
CONCLUSION: Altered ET-1 levels may be involved in the pathogenesis of rebound hypertension and hypotension during HD.