renal vein thrombosis - new york university.pptVIP

Renal vein thrombosis Patients with the nephrotic syndrome are at increased risk of developing venous and arterial thromboembolism, particularly RVT The mechanism of thromboembolism in nephrotic syndrome and optimal diagnostic and anticoagulant management strategies remain controversial Prevalence of renal vein thrombosis according to underlying disease in nephrotic syndrome A retrospective study involving 298 patients with mean follow up of 10 years showed annual incidences of VTE and ATE of 1.02% and 1.48% respectively Risks of both VTE and ATE were particularly high within the first 6 months of NS (annual incidences 9.85% and 5.52% respectively) Clinical features RVT may be unilateral or bilateral and may extend into the inferior vena cava RVT most often has an insidious onset and produces no symptoms referable to the kidney Acute RVT is usually due to trauma, severe dehydration or a generalized hypercoagulable state It typically presents with symptoms of renal infarction, including flank pain, microscopic or gross hematuria, a marked elevation in serum lactate dehydrogenase, and an increase in renal size on radiographic study Bilateral RVT may present with acute renal failure Pathogenesis Increased platelet aggregation Thrombocytosis, decreased red blood cell deformability, and increased von Willebrand factor levels in NS favor platelet transport towards the vessel wall and increase platelet adhesion Hypoalbuminemia results in increased availability of normally albumin-bound arachidonic acid, leading to increased formation of thromboxane A2 in platelets, a stimulus for platelet aggregation Elevated levels of LDL cholesterol may increase platelet aggregation Activation of the coagulation system Patients with nephrotic syndrome demonstrate urinary loss of plasma proteins that include factors IX, X, and XII, prothrombin, antithrombin, and α2-antiplasmin In contrast, proteins of higher molecular weight, including factor V, factor VIII, von Willebrand facto