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Introduction

Renal vein thrombosis (RVT) is characterized by thrombotic occlusion of one or both renal veins.  Although associated with malignancy, trauma, and hypercoagulable disorders, it most frequently arises in patients with nephrotic syndrome, particularly those with membranous nephropathy.  Acute RVT is usually symptomatic, whereas chronic RVT is typically asymptomatic and detected incidentally.

Pathophysiology and risk factors

The primary driver of RVT is hypercoagulability, which also predisposes to deep vein thrombosis and pulmonary embolism (PE).  In nephrotic syndrome, the leading cause of RVT, the following 3 key mechanisms are thought to contribute to thrombotic risk:

  • Urinary loss of natural anticoagulant proteins (eg, protein C).
  • Increased hepatic synthesis of procoagulant factors (eg, fibrinogen).
  • Increased platelet activity (eg, increased thromboxane A2 synthesis).

These changes tilt the hemostatic system toward thrombosis.  In addition, hemoconcentration in the postglomerular circulation (due to fluid loss at the glomerulus) further increases the likelihood of RVT.

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