**2.1.4 Renal transplantation and venous thromboembolism**

In renal transplantation, few studies had evaluated the risk of venous thromboembolism, the largest one used the United States Renal Data System database to study 28,924 patients receiving a kidney transplant, the rate of VTE occurring 1.5 to 3 years after transplantation was 2.9 episodes/1,000 person-years. Estimated glomerular filtration rate less than 30 mL/min/1.73 m2 versus higher at the end of the first year after renal transplantation was associated with significantly increased risk for later venous thromboembolism (adjusted hazard ratio, 2.05; 95% confidence interval, 1.08 to 3.89). Patients with severe chronic kidney disease, after renal transplantation should be regarded as high risk for late venous tromboembolism, which is a potentially preventable cause of death in this population (Abbott, 2004).

A prospective study of a cohort of 578 patients with renal transplantation, reports 9.1 % incidence of deep vein thrombosis of the lower limbs, 39.5% were asymptomatic and the diagnosis was made during routine ultrasound examination. Those patients, who experience venous thromboembolism, were at high risk of recurrence after thromboprophylaxis withdrawal (Poli, 2006).

Co-morbilities like diabetes mellitus could increase the risk of venous thromboembolism, in a prospective study the frequency of deep vein thrombosis during the first 3 weeks after kidney transplantation has been evaluated using the combination of thermography and strain-gauge plethysmography for objective diagnosis. 83 consecutive

Venous Thromboembolism in Neonates, Children and

**2.2.2 Decrease endogenous anticoagulants** 

increased urinary loss.(Vaziri, 1984).

**2.2.4 Reduced fibrinolysis** 

present unknow (Lisman, 2005).

both(Lobo, 2007).

**2.2.3 Platelet activation and aggregation** 

Patients with Chronic Renal Disease – Special Considerations 45

In the nephrotic syndrome the hypercoagulable state is distinguished by an increase in coagulation factors (V, VIII and fibrinogen) a decrease in the levels of antitrombin III and S Proteins, an increase in alpha 2 antiplasmin activity and exaggerated platelet adhesiveness and aggregation. This prothrombotic state may be aggravated by additional rheological

The lower level of antithrombin III in patients with nephrotic syndrome is probably due to

P-selectin is a marker of platelet activation and is increased in nephrotic syndrome patients. Platelet aggregation increases because of hypoalbuminemia that result in an increase

Fibrin cloths with reduced permeability, increased clot stiffness and reduced fibrinolysis susceptibility may predispose to thrombosis. Using permeability and turbidity studies in 22 end stage renal disease patients and 24 healthy controls. Fibrin clots made from plasma of patients with chronic renal disease were found to be less permeable, less compactable and

Another study in 33 patiens in long term haemodialysis has demonstrated unfavorably altered clot properties that may be associated with increase cardiovascular mortality (Unaas, 2008) There are studies that demonstrates that individuals with reduced fibrinolytic potential as measured by plasma based assays , have an increased risk of developing a first venous thrombosis. Whether this hypofibrinolytic state determined by genetic or adquired factors or a combination of them and which proteins are evolved is at

In conclusion, chronic kidney disease patients presents a pro-thrombotic state that increases the risk of venous thromboembolism and comprises alteration of platelet functions, coagulation factors, endogenous anticoagulants and fibrinolytic system, many

Anticoagulants are widely used to prevent and treat venous thromboembolism, these drugs are often used in patients with renal impairment. Renal impairment is at the same time, a risk factor for bleeding and thrombosis during anticoagulant therapy and may influence the

The available anticoagulants for the treatment of thromboembolism are heparins, the Factor X inhibitor fondaparinux, warfarin and the new anticoagulants Factor X inhibitors and direct thrombin inhibitors. Most of the antithrombotics are eliminated primarily by the kidneys , so dosing in patients with several renal impairment may require dosage reduction or increase frequency of monitoring for bleeding and thromboembolism complications or

factors (immobilization, diuretic therapy, etc.) (Keusch, 1989; Adams, 2008).

avalaibility of thromboxane a-2 that is a potent platelet agonist (Jackson, 1982).

less susceptible to fibrinolysis than clots from controls (Siǿland, 2007).

mechanism are still unknown and opens a potential field for investigation.

balance between the safety and efficacy of such drugs (Harder, 2011).

**2.3 Treatment of venous thromboembolism in chronic renal disease patients** 

patients were included, 33 with juvenile diabetes mellitus. The overall frequency of thrombosis was 24.1%, diabetes mellitus being a significant risk factor (Bergqvist, 1985).

Epidemiological studies have attempted to define risk in terms of modifiable (drugs, dialysis modality, surgical procedure) and no modifiable (age, diabetes mellitus, vascular anomalies, factor or identify changes in coagulation or fibrinolysis) promoting a more thrombotic state. Most recently the evolution of thrombophilia research has established the potential for inherited hypercoagulability to predispose to acute allograft thrombosis. Inheritance of the factor V Leiden (FVL), prothrombin G20210A mutation, or the presence of antiphospholipid antibodies may increase the risk of renal allograft thrombosis certain 3 fold in selected patients. Patients with end-stage renal disease due to systemic lupus erythematosus appear at particularly high risk of thrombosis, especially if they have either antiphospholipid antibodies or detectable β2-glycoprotein-1. (Irish, 2004).
