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

Citation
I. Stefanidis et al., Influence of hematocrit on hemostasis in continuous venovenous hemofiltration during acute renal failure, KIDNEY INT, 56, 1999, pp. S51-S55
Citations number
21
Categorie Soggetti
Urology & Nephrology","da verificare
Journal title
KIDNEY INTERNATIONAL
ISSN journal
00852538 → ACNP
Volume
56
Year of publication
1999
Supplement
72
Pages
S51 - S55
Database
ISI
SICI code
0085-2538(199911)56:<S51:IOHOHI>2.0.ZU;2-U
Abstract
Background Hematocrit plays a major role in primary hemostasis by influenci ng blood viscosity and platelet adhesion. During continuous venovenous hemo filtration (CVVH), it is suspected that an increased hematocrit is accompan ied by an activation of hemostasis and frequently leads to thromboses in th e extracorporeal system. In order to examine this hypothesis, we studied th e influence of hematocrit on hemostasis during CVVH. Methods. Fourteen patients (8 men and 6 women, mean age 65 +/- 10 years) wi th acute renal failure undergoing CVVH were prospectively enrolled. Polysul fone hemofilters (AV 600(R); Fresenius, Oberursel, Germany) were used in al l of the patients; blood flow rates were adjusted to 120 ml/min. No blood p roducts and coagulation-related medication, except unfractionated heparin, were applied. Study exclusion criteria included a history of thromboembolis m and artificial heart valves. Hemostasis activation markers (fibrinopeptid e A, thrombin-antithrombin III complex, beta-thromboglobulin, platelet rete ntion) and hematocrit values were determined before and at three-day interv als during the course of CVVH treatment. Results. The mean hematocrit value ((X) over bar +/- SEM) was 29 +/- 1% (ra nge, 22 to 35%). Patients with hematocrit values of less than 30% (N = 7) w ere compared with patients with higher hematocrit values (>30%, N = 7). The patients with a lower hematocrit (<30%) showed a stronger activation of he mostasis during CVVH when compared with those with a higher hematocrit (>30 %), as indicated by a tendency toward higher values for fibrinopeptide A (2 5 +/- 8 vs. 14 +/- 5 ng/ml, P = 0.35), thrombin-antithrombin III complex (1 5 +/- 4 vs. 10 +/- 2 ng/ml, P = 0.66), and a higher beta-thromboglobulin/cr eatinine 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. Conc erning hemostasis activation, hematocrit values between 30 and 35% may be s uitable for patients on CVVH.