Influence of hematocrit on hemostasis in continuous venovenous hemofiltration during acute renal failure.

Kidney international. Supplement Pub Date : 1999-11-01
I Stefanidis, B Heintz, D Frank, P R Mertens, H P Kierdorf
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Abstract

Background: Hematocrit plays a major role in primary hemostasis by influencing blood viscosity and platelet adhesion. During continuous venovenous hemofiltration (CVVH), it is suspected that an increased hematocrit is accompanied by an activation of hemostasis and frequently leads to thromboses in the extracorporeal system. In order to examine this hypothesis, we studied the influence of hematocrit on hemostasis during CVVH.

Methods: Fourteen patients (8 men and 6 women, mean age 65+/-10 years) with acute renal failure undergoing CVVH were prospectively enrolled. Polysulfone hemofilters (AV 600; Fresenius, Oberursel, Germany) were used in all of the patients; blood flow rates were adjusted to 120 ml/min. No blood products and coagulation-related medication, except unfractionated heparin, were applied. Study exclusion criteria included a history of thromboembolism and artificial heart valves. Hemostasis activation markers (fibrinopeptide A, thrombin-antithrombin III complex, beta-thromboglobulin, platelet retention) and hematocrit values were determined before and at three-day intervals during the course of CVVH treatment.

Results: The mean hematocrit value (mean +/- SEM) was 29+/-1% (range, 22 to 35%). Patients with hematocrit values of less than 30% (N = 7) were compared with patients with higher hematocrit values (>30%, N = 7). The patients with a lower hematocrit (<30%) showed a stronger activation of hemostasis during CVVH when compared with those with a higher hematocrit (>30%), as indicated by a tendency toward higher values for fibrinopeptide A (25+/-8 vs. 14+/-5 ng/ml, P = 0.35), thrombin-antithrombin III complex (15+/-4 vs. 10+/-2 ng/ml, P = 0.66), and a higher beta-thromboglobulin/creatinine ratio (0.62+/-0.17 vs. 0.48+/-0.12, P = 0.8).

Conclusion: Contrary to our hypothesis, hematocrit values of more than 30% are not accompanied by an increased hemostasis activation during CVVH. Concerning hemostasis activation, hematocrit values between 30 and 35% may be suitable for patients on CVVH.

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急性肾功能衰竭持续静脉-静脉血液滤过中红细胞压积对止血的影响。
背景:红细胞压积通过影响血液黏度和血小板粘附在原发性止血中起重要作用。在持续静脉静脉血液滤过(CVVH)期间,怀疑红细胞压积增加伴随着止血的激活,并经常导致体外系统血栓形成。为了检验这一假设,我们研究了红细胞压积对CVVH期间止血的影响。方法:前瞻性纳入14例(8男6女,平均年龄65+/-10岁)行CVVH的急性肾功能衰竭患者。聚砜血液过滤器(av600;费森尤斯,Oberursel,德国)在所有患者中使用;血流速率调整为120 ml/min。除未分离肝素外,未使用血液制品和凝血相关药物。研究排除标准包括血栓栓塞史和人工心脏瓣膜。在CVVH治疗前和治疗过程中每隔三天检测止血激活标志物(纤维蛋白肽A、凝血酶-抗凝血酶III复合物、β -血栓球蛋白、血小板保留)和红细胞压积值。结果:平均红细胞压积值(平均+/- SEM)为29+/-1%(范围为22 ~ 35%)。将红细胞比容值小于30%的患者(N = 7)与红细胞比容值较高的患者(>30%,N = 7)进行比较。红细胞比容值较低的患者(30%),纤维蛋白肽a (25+/-8 vs. 14+/-5 ng/ml, P = 0.35)、凝血酶-抗凝血酶III复合物(15+/-4 vs. 10+/-2 ng/ml, P = 0.66)和β -血栓球蛋白/肌酐比值较高(0.62+/-0.17 vs. 0.48+/-0.12, P = 0.8)的数值倾向较高。结论:与我们的假设相反,在CVVH期间,超过30%的红细胞压积值并不伴随着止血激活的增加。关于止血激活,血细胞比容值在30 - 35%之间可能适合于CVVH患者。
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Alport syndrome. New strategies to prevent cardiovascular risk in chronic kidney disease. Proceedings of the Sixth International Conference on Hypertension and the Kidney. February 2008. Madrid, Spain. Prevention of Renal Disease in the Emerging World: Toward Global Health Equity. Proceedings of the Bellagio Conference, March 16-18, 2004, Italy. The in vitro biocompatibility performance of a 25 mmol/L bicarbonate/10 mmol/L lactate-buffered peritoneal dialysis fluid. Proceedings of the Third International Conference on Hypertension and the Kidney, February 2002, Madrid, Spain.
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