title: Hemostasis activation markers in acute renal failure.
abstract: Fibrinopeptide A and thrombin-antithrombin III complex were used respectively as markers for in vivo thrombin formation and beta-thromboglobulin as a marker for platelet activation. In cases of acute renal failure (ARF) a heightened plasma concentration in the hemostasis activation markers may occur, because of a renal elimination disturbance, without a previous activation of the hemostasis. In order to check the validity of fibrinopeptide A, thrombin-antithrombin III complex and beta-thromboglobulin as markers for the hemostasis activation in cases of ARF we examined 32 patients prior to renal replacement therapy. A significant rise in fibrinopeptide A (x +/- SD: 34 +/- 22 ng/mL, ref < 3.0), thrombin-antithrombin III complex (19 +/- 15 ng/mL, ref 1.0-4.0) and beta-thromboglobulin (149 +/- 58 U/mL, ref 10-40) was found. None of the parameters examined showed a correlation to the serum creatinine. A correlation was observed respectively between fibrinopeptide A (r = 0.34, p < .05), beta-thromboglobulin (r = 0.39, p < .05) and the beta-thromboglobulin/creatinine coefficient (0.50 +/- 0.30, r = 0.72, p < .001) on the one side and the thrombin-antithrombin III complex on the other. A greater rise in the concentration of all parameters in patients with disseminated intravascular coagulation (DIC) was established, in contrast to patients without DIC (fibrinopeptide A: 44 +/- 31 vs. 32 +/- 20 ng/mL, beta-thromboglobulin: 169 +/- 57 vs. 144 +/- 60 U/mL, thrombin-antithrombin III complex 40 +/- 21 vs. 14 +/- 7 ng/mL, p < .05). Fibrinopeptide A and beta-thromboglobulin/creatinine coefficient in combination with the thrombin-antithrombin III complex can be employed as markers for the activation of hemostasis in cases of ARF there is no direct relationship between restricted kidney function in ARF and the plasma concentration of these markers, which behave similarly in spite of their varying elimination patterns.
authors.affiliation: Medical Clinic II, University Hospital, Aachen, Germany.
authors.forename: I
authors.initials: I
authors.lastname: Stefanidis
authors.forename: D
authors.initials: D
authors.lastname: Frank
authors.forename: N
authors.initials: N
authors.lastname: Maurin
mesh_terms: D058186:Acute Kidney Injury / Q000097:blood* / Q000628:therapy; D000990:Antithrombin III / Q000032:analysis*; D016022:Case-Control Studies; D003404:Creatinine / Q000097:blood; D004211:Disseminated Intravascular Coagulation / Q000097:blood; D005260:Female; D005344:Fibrinopeptide A / Q000032:analysis*; D006440:Hemofiltration; D006487:Hemostasis; D006801:Humans; D007668:Kidney / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D010447:Peptide Hydrolases / Q000032:analysis*; D006435:Renal Dialysis; D001620:beta-Thromboglobulin / Q000032:analysis*
chemical_list: C046193:antithrombin III-protease complex; D001620:beta-Thromboglobulin; D005344:Fibrinopeptide A; D000990:Antithrombin III; D003404:Creatinine; D010447:Peptide Hydrolases