Renal Vein Thrombosis

Updated: Mar 01, 2023
  • Author: Huong K Truong, MD, RPVI; Chief Editor: Vincent Lopez Rowe, MD, FACS  more...
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Practice Essentials

Renal vein thrombosis (RVT) most commonly occurs in patients with nephrotic syndrome (defined as urinary protein loss >3 g/day, hypoalbuminemia, hypercholesterolemia, and edema) due to the loss of antithrombin III (ATIII)  in the urine, which in turn leads to an increase in hypercoagulability. [1]  Other common causes of RVT include malignancies (eg, renal cell carcinoma [RCC]), instrumentation to the area, and any hypercoagulable state. These hypercoagulable states can be transient (eg, from pregnancy, oral contraceptives, or traumatic injury) or chronic (eg, from factor V Leidensystemic lupus erythematosus [SLE], or deficiency of protein C or S). [2]

Treatment of RVT depends on the severity of symptoms but is typically managed with therapeutic anticoagulation to prevent potential thromboembolic complications. Intravenous (IV) unfractionated heparin (UFH) is often the first-line agent in the acute hospital setting, before transition to warfarin or a novel oral anticoagulant (NOAC) such as rivaroxaban or apixaban. [3, 4]  In severe cases (eg, bilateral RVT with impending renal failure), thrombolysis or mechanical thrombectomy can be performed. In the most severe cases, in which RVT has caused capsular rupture of the kidney, urgent nephrectomy is performed to stop life-threatening hemorrhage.



In general, the fundamental principles of thrombosis apply to RVT, and any pathologic condition contributing to an aspect of the Virchow triad (endothelial disruption, stasis, hypercoagulability) will increase the risk that RVT will develop. [5] The left renal vein is three times more likely to be involved than the right renal vein, probably because of its greater length.



The most common etiology of RVT is the hypercoagulability resulting from nephrotic syndrome, with membranous nephropathy being the most common pathology. Membranous nephropathy is idiopathic in most cases, but it can also be caused by membranoproliferative glomerulonephritis, minimal change disease, rapidly progressive glomerulonephritis, amyloid, focal sclerosis, or lupus nephritis. RVT tends to be more common in patients with a primary nephropathy than in those with a secondary nephropathy.

Initially, nephrotic syndrome was believed to be a consequence of RVT; however, the following observations showed that this belief was mistaken:

  • Experimentally induced RVT causes only mild proteinuria
  • RVT in the absence of nephrotic syndrome has been reported in the surgical literature
  • Nephrotic syndrome 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; therefore, nephrotic syndrome is not a direct result of RVT but rather a potential cause of RVT

In nephrotic syndrome, lower-molecular-weight proteins such as ATIII are lost in the urine, and this leads to hypercoagulability. Additionally, low oncotic pressure gradients may lead to hemoconcentration, which can further contribute to hypercoagulability. Other specific aspects of the underlying nephropathy not listed above may also cause systemic hypercoagulability.

Tumors (most commonly RCC) have a tendency to invade the renal vein and cause RVT. If the tumor is large, it can extend into the inferior vena cava (IVC). Extrinsic compression from mass effect may also cause a prothrombotic environment, even without direct invasion of the vein.

Other systemic diseases or processes associated with RVT include but are not limited to the following:

  • ATIII deficiency
  • Protein C or S deficiency
  • Pregnancy or estrogen therapy
  • Factor V Leiden
  • SLE
  • Severe dehydration in infants or neonates
  • Surgical manipulation or intraluminal instrumentation
  • Extrinsic compression (eg, from lymph nodes, tumor, retroperitoneal fibrosis/adenopathy, or aortic aneurysms)
  • Trauma
  • Steroid administration

In cases of hypercoagulability resulting from systemic causes, thrombosis typically begins in the arcuate and intralobular venules and propagates outward. In cases resulting from extrinsic compression or instrumentation, thrombosis typically begins in the main renal vein or its primary tributaries.



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 ranging from 5% to 62%. Other studies have shown that RVT may develop in as many as 20% of patients with nephrotic syndrome, though it is often subclinical. 

Age is a factor in RVT. For example, membranous nephropathy, which is most commonly associated with RVT, is also the most common cause of nephrotic syndrome in adults. RVT peaks in the fourth through sixth decades of life and rarely affects children. In infants, more than 80% of cases of RVT are diagnosed within the first month of life, typically resulting from severe dehydration, prolonged hypotension, inherited coagulable states, or some combination thereof. RVT from RCC typically affects older age groups but can also occur at any age with a history of malignancy, surgical instrumentation, or extrinsic compression.

No sex-specific data are available for the frequency of RVT. Theoretically, however, membranous nephropathy has a male-to-female ratio of 2:1; therefore, a male preponderance may exist for RVT. 

Currently, there is little evidence to suggest that RVT has any a predilection for certain races or ethnicities.



The prognosis of patients with RVT is predicated on several factors, including the following:

  • Unilateral or bilateral at presentation
  • Extent of venous collateralization and recanalization
  • Cause of the underlying thrombosis (most important)

Unilateral RVT will have a better prognosis than bilateral RVT. Sufficient collateralization and recanalization can slow and prevent the development of renal dysfunction. 

Usually, however, morbidity and mortality are secondary to the effects of the underlying condition causing RVT (eg, nephrotic syndrome, malignancy, [9] trauma, or a hypercoagulable disorder). The prognosis of any glomerular disease may be worsened by the superimposition of an acute RVT, but it is unclear whether the slow development of chronic RVT accelerates renal functional loss.

In RVT secondary to malignant etiology, morbidity and mortality result from either thromboembolism or the cancer itself and may act as a signal of dissemination of the malignancy. In the setting of transplantation, RVT may lead to loss of the graft. When morbidity and mortality are directly caused by sequelae of RVT, they are typically due to thromboembolism resulting in caval thrombosis and pulmonary embolism (PE) or to renal dysfunction or failure. In severe cases where RVT causes capsular distention and rupture, morbidity is secondary to life-threatening retroperitoneal hemorrhage.