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.

Bivalirudin versus Unfractionated Heparin for Prevention of Hemofilter Occlusion During Continuous Renal Replacement Therapy

“…A procoagulant state can be related to tissue factor expression, endothelial cell activation, alterations in protein C and S, and inhibition of fibrinolysis. 2 This procoagulant process can be increased by the extracorporeal dialysis circuit due to further activation of the tissue factor pathway, turbulent blood flow, blood-air interface, or contact activation after exposure of the blood to foreign surfaces of the hemofilter circuit. [3][4][5] However, excessive anticoagulation in these patients can lead to bleeding.…”

Prefilter Bivalirudin for Preventing Hemofilter Occlusion in Continuous Renal Replacement Therapy

“…The blood flow, hemofiltration, and dialysate rates remained at 150 mUrnin, 2000 mUh, and 0 mLth, respectively. Five hemofilters were evaluated throughout the 109 hours ofCRRT (ICU days [16][17][18][19][20]. Filter occlusion occurred at 8,28,26, and 13 hours, with last known filter still non occluded at 34 hours (Table 1).…”

Effect of Erythropoietin on Activity of Plasma Proteolytic Systems during Experimental Renal Failure

“…Treatment with erythropoietin led to partial recovery of fi brin formation and fi brinolysis. Under analytical in vitro conditions, 30-min incubation of whole blood from healthy donors with erythropoietin in doses of 1.9-30.0 U/liter was followed by a dose-dependent inhibition of the fi brin formation system and activation of fi brinolysis.Dysregulation of plasma proteolytic systems of fi brin formation and fi brinolysis and the anticoagulant system can serve as a key pathogenetic factor for thrombohemorrhagic complications in renal failure of different genesis [4,13]. Erythropoietin (EPO) is a glycoprotein (molecular weight 30.4 kDa) responsible for proliferation, differentiation, and inhibition of apoptosis in glycoprotein-sensitivebone marrow erythroid lineage cells.…”

“…Dysregulation of plasma proteolytic systems of fi brin formation and fi brinolysis and the anticoagulant system can serve as a key pathogenetic factor for thrombohemorrhagic complications in renal failure of different genesis [4,13]. Erythropoietin (EPO) is a glycoprotein (molecular weight 30.4 kDa) responsible for proliferation, differentiation, and inhibition of apoptosis in glycoprotein-sensitivebone marrow erythroid lineage cells.…”