Hemostasis in renal disease: Pathophysiology and management

A prospective study was designed to evaluate disorders of hemostasis and levels of anticardiolipin antibodies (ACL) in 30 patients with severe leptospirosis and acute renal failure (ARF) (ARF was defined as serum creatinine > or = 1.5 mg/dL). The patients had been admitted to the Walter Cantídio University Hospital, São José Infectious Diseases Hospital and General Hospital of Fortaleza, Ceará, from August 1999 to July 2001. They all were male, with a mean age of 32 ± 14 years and with clinical and laboratory diagnoses of ARF leptospirosis. The time elapsed between onset of symptoms and the first hemorrhagic manifestation was 9 ± 4 days. Bleeding was observed in 86% of the patients. Laboratory tests showed significantly high levels of urea (181 ±95 mg/dl), fibrinogen, (515 ± 220 mg/dl), prothrombin time (13.3 ± 0.9 seconds) and low platelet counts (69 ± 65x10³/mm³) on admission. There was no elevation in activated partial thromboplastin time or thrombin time. Levels of IgM and IgG ACL concentrations were significantly increased (p < 0.05) in leptospirosis patients when compared to control patients (28.5 ± 32.4 vs. 11.5 ± 7.9MPL U/ml and 36.7 ± 36.1 vs. 6.5 ± 2.5 GPL U/ml), respectively. Vasculitis, thrombocytopenia and uremia should be considered important factors for the pathogenesis of hemorrhagic disturbances and the main cause of death in severe leptospirosis.

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“…Uremic bleeding appears to correlate most closely with prolongation of bleeding time, due primarily to platelet dysfunction 6,9 .…”

Section: Discussionmentioning

confidence: 99%

Evaluation of hemostasis disorders and anticardiolipin antibody in patients with severe leptospirosis

Daher

Neto

Ramirez

2002

Rev. Inst. Med. trop. S. Paulo

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“…The bleeding diathesis of uraemia seems mainly related to functional impairment of platelets [1]; the incidence of bleeding, however, is apparently declining at present. On the other hand, the tendency towards thrombosis (particularly of the arteriovenous shunt) is a frequent and major problem in dialysis [1]. Thrombotic complications have an increased incidence in patients suffering from uraemia [2] and may represent the predominant cause of mortality [3].…”

Section: Introductionmentioning

confidence: 99%

Red blood cells may contribute to hypercoagulability in uraemia via enhanced surface exposure of phosphatidylserine

Bonomini¹,

Sirolli²,

Merciaro³

et al. 2004

Nephrology Dialysis Transplantation

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Background. The exposure of phosphatidylserine (PS) on the outer leaflet of the erythrocyte membrane may have several pathophysiological consequences, including the development of a procoagulant phenotype, a finding that seems relevant to the thrombotic risk seen in many disorders. Methods. Because PS externalization increases in erythrocytes from patients suffering from chronic uraemia, which is frequently associated with a prothrombotic state, the possible relationship between erythrocyte PS exposure, erythrocyte procoagulant activity and plasma levels of several haemostatic markers was studied in a group of haemodialysed patients. Results. Uraemic erythrocytes displayed increased procoagulant activity, which proved to be correlated directly with erythrocyte PS exposure. Pre-incubation of uraemic erythrocytes with annexin V, a protein with high affinity and specificity for PS, strongly inhibited in vitro thrombin generation induced by erythrocytes as compared with untreated red cells. Thrombin generation and activation of fibrinolysis were found to occur in uraemic patients, as substantiated by increased plasma levels of markers for thrombin generation (prothrombin fragment F1.2 and thrombinantithrombin complex) and fibrinolysis (D-dimer and plasmin-antiplasmin complex), respectively. Significant correlations between prothrombin fragment F1.2 and D-dimer suggested that hyperfibrinolysis was secondary to thrombin generation. Correlations were also found between erythrocyte PS levels and plasma levels of haemostatic markers, including prothrombin fragment F1.2 (P ¼ 0.007), thrombin-antithrombin complex (P ¼ 0.00009), plasmin-antiplasmin complex (P ¼ 0.0009) and D-dimer (P ¼ 0.005).Conclusions. Our study suggests that increased PS exposure may cause a pathological erythrocyte procoagulant phenotype, which may be a factor inducing a hypercoagulable state in uraemia.

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“…49,50 Another mechanism by which erythrocytes modulate hemostasis is the rheological effect of red cells on the margination of platelets. 51 Under normal circumstances, red cell flow is maximal at the centre of a vessel, tending to push platelets towards the periphery of the vessel lumen, thereby optimizing their interaction with injured endothelium and promoting hemostasis. In rabbit arterioles, platelet numbers are highest near the vessel wall 52 and platelets align themselves with their equatorial plane parallel to the vessel wall as they move closer toward the periphery of the vessel.…”

Section: Blood Components and Alterations Of Hemostasis 1 Red Cellsmentioning

confidence: 99%

Massive transfusion and coagulopathy: pathophysiology and implications for clinical management

Hardy

Moerloose

Samama

2006

Can J Anesth/J Can Anesth

192

108

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Purpose:To review the pathophysiology of coagulopathy in massively transfused, adult and previously hemostatically competent patients in both elective surgical and trauma settings, and to recommend the most appropriate treatment strategies. Methods:Medline was searched for articles on "massive transfusion," "transfusion," "trauma," "surgery," "coagulopathy" and "hemostatic defects." A group of experts reviewed the findings. Principal findings:Coagulopathy will result from hemodilution, hypothermia, the use of fractionated blood products and disseminated intravascular coagulation. The clinical significance of the effects of hydroxyethyl starch solutions on hemostasis remains unclear. Maintaining a normal body temperature is a first-line, effective strategy to improve hemostasis during massive transfusion. Red cells play an important role in coagulation and hematocrits higher than 30% may be required to sustain hemostasis. In elective surgery patients, a decrease in fibrinogen concentration is observed initially while thrombocytopenia is a late occurrence. In trauma patients, tissue trauma, shock, tissue anoxia and hypothermia contribute to the development of disseminated intravascular coagulation and microvascular bleeding. The use of platelets and/or fresh frozen plasma should depend on clinical judgment as well as the results of coagulation testing and should be used mainly to treat a clinical coagulopathy. Conclusions:Coagulopathy associated with massive transfusion remains an important clinical problem. It is an intricate, multifactorial and multicellular event. Treatment strategies include the maintenance of adequate tissue perfusion, the correction of hypothermia and anemia, and the use of hemostatic blood products to correct microvascular bleeding.

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Hemostasis in renal disease: Pathophysiology and management

Cited by 138 publications

References 116 publications

Evaluation of hemostasis disorders and anticardiolipin antibody in patients with severe leptospirosis

Evaluation of hemostasis disorders and anticardiolipin antibody in patients with severe leptospirosis

Red blood cells may contribute to hypercoagulability in uraemia via enhanced surface exposure of phosphatidylserine

Massive transfusion and coagulopathy: pathophysiology and implications for clinical management

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