Renal Vein Thrombosis

Updated: Aug 27, 2020
  • Author: Igor A Laskowski, MD; Chief Editor: Vincent Lopez Rowe, MD  more...
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Although renal vein thrombosis (RVT) has numerous etiologies, it occurs most commonly in patients with nephrotic syndrome (ie, >3 g/day protein loss in the urine, hypoalbuminemia, hypercholesterolemia, edema). [1]

The syndrome is responsible for a hypercoagulable state. The excessive urinary protein loss is associated with decreased antithrombin III, a relative excess of fibrinogen, and changes in other clotting factors; all lead to a propensity to clot. Numerous studies have demonstrated a direct relation between nephrotic syndrome and both arterial and venous thromboses. Why the renal vein is susceptible to thrombosis is unclear. [2]

The renal vein may also contain thrombus after invasion by renal cell cancer. Other less common causes include renal transplantation, Behçet syndrome, hypercoagulable states, and antiphospholipid antibody syndrome.



Hypercoagulability is the fundamental process involved in both arterial and venous renal thrombosis. In the setting of malignant invasion of the vein by cancer, the presence of the tumor cells elicits thrombosis of the renal vein only. It may also occur as the result of blunt trauma to the abdomen or back. In infants, RVT can be associated with dehydration. [3, 4, 5]



In patients who are nephrotic, the most common underlying nephropathy associated with RVT is membranous nephropathy. The tumor association for RVT is renal cell carcinoma (RCC). However, most cases of membranous nephropathy are idiopathic.

RVT also may be the result of nephrotic syndrome from membranoproliferative glomerulonephritis, minimal change disease, rapidly progressive glomerulonephritis, amyloid, focal sclerosis, or lupus nephritis. RVT is more common in patients with primary nephropathy than in those with secondary nephropathy.

Findings relative to the causative disease may be present (eg, systemic lupus erythematosus [SLE], antiphospholipid antibody syndrome, cancer [6] ).

Theories for the putative relation between nephrotic syndrome and RVT have evolved. Initially, nephrotic syndrome was believed to be a consequence of RVT. However, this presumed sequence was found to be incorrect, for reasons including the following:

  • Experimentally induced RVT causes only mild proteinuria
  • RVT in the absence of nephrotic syndrome has been reported in the surgical literature
  • Nephrotic patients with RVT who have undergone histologic evaluation show evidence of an identifiable glomerulopathy
  • RVT is known to occur after the onset of nephrotic syndrome; thus, nephrotic syndrome is not a direct result of RVT but, rather, leads to RVT

SLE has also been associated with RVT. In general, patients with lupus and documented RVT have membranous lupus nephritis (World Heath Organization class V). Generally, thrombophlebitis and circulating anticoagulants (anticardiolipin antibodies) are believed to be much less important than nephrotic syndrome as predisposing factors of RVT in SLE.

RVT is an uncommon but definite problem in neonates. [7, 8] A possible association exists between RVT and the factor V Leiden mutation in this age group.

Other diseases or situations that have been associated with RVT include the following:

  • Protein C or S deficiency
  • Antiphospholipid antibody syndrome [9]
  • Pregnancy or estrogen therapy
  • Renal vein invasion by malignant cells
  • Post renal transplantation [10, 11]
  • Extrinsic compression (eg, lymph nodes, tumor, retroperitoneal fibrosis, aortic aneurysm)

Aside from RCC, the other associations are uncommon. Trauma, ingestion of oral contraceptive agents, dehydration (infants), and steroid administration also have been associated with RVT.



The prevalence of RVT in the United States has been difficult to establish. Studies have shown a high degree of variability in the presence of RVT among patients with nephrotic syndrome, with reported rates of 5-62%.

Age is a factor in RVT only insofar as is the case with any age-related risk of glomerular disease. For example, membranous nephropathy, the lesion most associated with RVT, is the most common cause of nephrotic syndrome in adults, but it is rare in children. Membranous nephropathy peaks in the fourth through sixth decade, thus making RVT more likely in this specific age group. However, exact incidence or prevalence figures are not available. RVT from RCC occurs in older age groups.

No specific numbers are available for the respective frequencies of RVT in the two sexes. Theoretically, however, membranous nephropathy, the disease most commonly associated with RVT, has a male-to-female ratio of 2:1; therefore, a male preponderance may exist for RVT.

No race-related predilection for RVT exists.



The morbidity and mortality of RVT are usually secondary to the effects of nephrotic syndrome (including arterial thrombosis), renal dysfunction or failure, or the complications resulting from thromboembolism.

If the etiology of the RVT is malignancy, morbidity and mortality are a result of either thromboembolism or the cancer itself. RVT that is secondary to cancer may signal dissemination of the malignancy. In the setting of transplantation, RVT may lead to loss of the graft. If the RVT eventuates from the other causes discussed, thromboembolism is the source of complications.

The prognosis of any glomerular disease may be worsened by superimposition of acute RVT, but it is unclear whether the slow development of chronic RVT accelerates renal functional loss.