Renal vein thrombosis usually results from local and systemic hypercoagulability due to nephrotic syndrome associated with membranous nephropathy (most often), minimal change disease, or membranoproliferative glomerulonephritis. The risk of thrombosis due to nephrotic syndrome appears to be proportional to the severity of the hypoalbuminemia. Overly aggressive diuresis or prolonged high-dose corticosteroid treatment may contribute to thrombosis of the renal vein in patients with these conditions.
Other causes include
Less common causes are related to reduced renal vein blood flow and include malignant renal tumors that extend into the renal veins (typically renal cell carcinoma), extrinsic compression of the renal vein or inferior vena cava (eg, by vascular abnormalities, tumor, retroperitoneal disease, ligation of the inferior vena cava, aortic aneurysm), oral contraceptive use, trauma, dehydration, and, rarely, thrombophlebitis migrans and cocaine abuse.
Usually, onset of renal dysfunction is insidious. However, onset may be acute, causing renal infarction with nausea, vomiting, flank pain, gross hematuria, and decreased urine output.
Renal vein thrombosis should be considered in patients with renal infarction or any unexplained deterioration in renal function, particularly in patients with the nephrotic syndrome or other risk factors.
The traditional diagnostic test of choice and the standard is venography of the inferior vena cava; this test is diagnostic, but it may mobilize clots. Because of the risks of conventional venography, magnetic resonance venography and Doppler ultrasonography are being used increasingly. Magnetic resonance venography can be done if glomerular filtration rate (GFR) > 30 mL/minute. Doppler ultrasonography sometimes detects renal vein thrombosis but has high false-negative and false-positive rates. Notching of the ureter due to dilated collateral veins is a characteristic finding in some chronic cases.
CT angiography provides good detail with high sensitivity and specificity and is fast but requires administration of a radiocontrast agent, which may be nephrotoxic. Serum electrolytes and urinalysis are done and confirm deterioration of renal function.
Microscopic hematuria is often present. Proteinuria may be in the nephrotic range.
If no cause is apparent, testing for hypercoagulability disorders should be initiated (see Overview of Thrombotic Disorders). Renal biopsy is nonspecific but may detect a coexisting renal disorder.
The underlying disorder should be treated.
Treatment options for renal vein thrombosis include anticoagulation with heparin, thrombolysis, and catheter-directed or surgical thrombectomy. Long-term anticoagulation with low molecular weight heparin or oral warfarin should be started immediately if no invasive intervention is planned. Anticoagulation minimizes risk of new thrombi, promotes recanalization of vessels with existing clots, and improves renal function. Anticoagulation should be continued for at least 6 to 12 months and, if a hypercoagulability disorder (eg, persistent nephrotic syndrome) is present, indefinitely.
Use of a percutaneous catheter for thrombectomy or thrombolysis is currently recommended. Surgical thrombectomy is rarely used but should be considered in patients with acute bilateral renal vein thrombosis and acute kidney injury who cannot be treated with percutaneous catheter thrombectomy and/or thrombolysis.
Nephrectomy is done only if infarction is total (in certain cases) or if the underlying disorder warrants it.
The most common cause of renal vein thrombosis is nephrotic syndrome associated with membranous nephropathy.
Consider renal vein thrombosis in patients with renal infarction or any unexplained deterioration in renal function, particularly those who have the nephrotic syndrome or other risk factors.
Confirm the diagnosis with vascular imaging, usually magnetic resonance venography (if GFR > 30 mL/minute) or Doppler ultrasonography.
Treat the underlying disorder and initiate anticoagulation, thrombolysis, or thrombectomy.