Hematology

Renal vein thrombosis and hypercoagulable state in nephrotic syndrome

Renal vein thrombosis and hypercoagulable state in nephrotic syndrome
Author
Jai Radhakrishnan, MD, MS, MRCP, FACC, FASN
Section Editor
Richard J Glassock, MD, MACP
Deputy Editor
Alice M Sheridan, MD
Last literature review version 19.3: Fri Sep 30 00:00:00 GMT 2011 |This topic last updated: Fri Feb 12 00:00:00 GMT 2010 (More)

INTRODUCTION — Patients with the nephrotic syndrome are at increased risk for venous thrombosis, particularly deep vein and renal vein thrombosis (DVT and RVT) [1-4] . Pulmonary embolization (mostly asymptomatic) is relatively common, and there are case reports of cerebral venous thrombosis [1-4] . Arterial thromboses (eg, limb and cerebral) also occur with higher frequency than in the general population [4-7] .

This topic will review the epidemiology and pathogenesis of hypercoagulability in the nephrotic syndrome, and the clinical features and treatment of renal vein thrombosis in adults. Overviews of the nephrotic syndrome and causes of venous thrombosis are discussed separately. (See "Overview of heavy proteinuria and the nephrotic syndrome" and "Overview of the causes of venous thrombosis".)

EPIDEMIOLOGY — The incidences of both venous and arterial thrombosis are much higher in patients with nephrotic syndrome compared to estimates in the general population [7] . This issue was examined in a retrospective study of 298 (predominantly adult) patients who presented with the nephrotic syndrome and were followed for a mean period of 10 years [7] . In this study, the absolute risk of venous thrombosis was 1.02 percent per year, which is eight times higher than the age- and sex-matched annual incidence reported in the Worcester DVT study [7,8] . (See "Overview of the causes of venous thrombosis", section on 'VTE and atherosclerotic disease'.) The absolute risk of arterial thrombosis was 1.48 percent per year, also approximately eight times that observed in a general population [9] . The risk of both venous and arterial thrombosis was greatest within the first six months of diagnosis (with annual incidences of 9.85 and 5.52 percent, respectively) [7] .

In a retrospective review of 326 children with the nephrotic syndrome, 9 percent experienced 38 thromboembolic episodes over a median period of 3.7 years. Older age and severity of proteinuria were predictive of a thromboembolic event. Central vein catheters were associated with nearly half of these events [10] .

The risk of thrombosis varies among the causes of nephrotic syndrome. The risk is highest with membranous nephropathy followed by membranoproliferative glomerulonephritis (MPGN) and minimal change disease [11,12] . The risk of thrombosis may also be related to the severity and duration of the nephrotic state [7,9,11]  and appears to be particularly increased with serum albumin concentrations ≤2.0 g/dL (20 g/L) [4,11,13-15] .

Renal vein thrombus — There is wide variability in the reported rate of RVT, probably related to the selection of patients for study (eg, degree of nephrotic syndrome, symptomatic or asymptomatic thrombosis, since RVT is often clinically silent) and methods of detection (since the sensitivities of the available tests differ).

The prevalence of RVT in patients with the nephrotic syndrome ranges from 5 to over 60 percent [1-4,16] . In studies of consecutive or unselected patients without membranous nephropathy who underwent venography, the prevalence of RVT ranges from 10 to 50 percent, most frequently due to minimal change disease, MPGN, and focal segmental glomerulosclerosis (FSGS) [4] . By comparison, a higher prevalence has been noted in patients with membranous nephropathy (20 to 60 percent) [4,11,12,17-19] . In the largest available prospective series of 151 patients with nephrotic syndrome (mean serum albumin 2.1 to 2.4 g/dL [21 to 24 g/L] and protein excretion 5 to 5.8 g/day), RVT was detected in 33 patients overall (22 percent) and in 20 of 69 patients with membranous nephropathy (29 percent) [11] .

Deep vein thrombosis — DVT of the extremities is the most commonly observed thromboembolic event in patients with nephrotic syndrome [20,21] . This was illustrated in a review of discharge diagnoses from nonfederal short stay hospitals in the United States from 1979 to 2005 in which 925,000 patients had a diagnosis of nephrotic syndrome [20] . Among the nephrotic patients, 14,000 (1.5 percent) were diagnosed with DVT while fewer than 5000 had RVT. The relative risk of DVT was significantly increased (1.72) in nephrotic compared to nonnephrotic patients.

Pulmonary embolism — Pulmonary embolism (PE) has been described in nephrotic patients with or without an evident DVT or RVT [1,4,11-14,17,18,22] . The estimated prevalence of asymptomatic PE in patients with the nephrotic syndrome ranges from 12 to over 30 percent, as illustrated in the following findings:

 

  • In a study of 151 consecutive nephrotic patients, 94 underwent ventilation-perfusion lung scan (V/Q scan) [11] . PE was present in 12 patients (13 percent): five had a PE associated with chronic or acute RVT, and seven had an isolated PE.
  • In a series of 89 nephrotic patients with a serum albumin concentration <2.0 g/dL (20 g/L), 19 (21 percent) had a high probability V/Q scan and, in an additional 25 patients with low or intermediate probability scans, arteriography demonstrated PE in 10 (11 percent of the total population) [13] .

 

The risk of symptomatic PE also appears to be increased. In the review cited above of discharge diagnoses from nonfederal short stay hospitals in the United States, there was a significant 39 percent increased in PE risk in nephrotic compared to nonnephrotic patients [20] .

PATHOGENESIS — The underlying cause of the hypercoagulable state in patients with nephrotic syndrome is not well understood. Studies evaluating measures of hemostasis activation, such as the plasma level of fibrinopeptide A, which is cleaved from fibrinogen by thrombin, suggest that even asymptomatic nephrotic patients have evidence of ongoing subclinical coagulation [23] . A variety of hemostatic abnormalities have been described, including decreased levels of antithrombin and plasminogen (due to urinary losses), increased platelet activation, hyperfibrinogenemia, inhibition of plasminogen activation, and the presence of high molecular weight fibrinogen moieties in the circulation [2,4,24-27] .

An additional possibility is that immune-complex injury in the glomerulus may result in increased procoagulant activity that is sufficient to have a systemic effect [23] . There may also be an effect on the venous circulation of the kidney.

The tendency to form thrombi at the renal vein in the nephrotic syndrome may be due in part to the loss of fluid across the glomerulus [4] . The ensuing hemoconcentration in the postglomerular circulation, which is worsened by diuretic therapy, may promote thrombus formation in patients who are already hypercoagulable.

RENAL VEIN THROMBOSIS — Spontaneous renal vein thrombosis is rare in ambulatory subjects who are not nephrotic or without an underlying renal malignancy [28,29] . Among 218 patients who presented with renal vein thrombosis in a single center study, 143 individuals had a malignancy (111 with renal cell carcinoma) and 43 patients had the nephrotic syndrome [29] .

Some reported additional causes include trauma (including kidney biopsy), oral contraceptives, hypovolemia (especially in infants), and inherited procoagulant defects [28,30] . These patients are not nephrotic, which demonstrates the important point that nephrotic syndrome is a cause, not the result, of RVT.

Clinical features — RVT may be unilateral or bilateral and may extend into the inferior vena cava. RVT is more often chronic, but acute RVT can occur and has a more dramatic presentation.

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Chronic renal vein thrombosis — RVT most often has an insidious onset and produces no symptoms referable to the kidney [11,17,18] . In this setting, a pulmonary embolus is usually the only clinical clue to the presence of renal or other deep vein thrombosis. Abnormal ventilation-perfusion scans of the lungs indicative or suggestive of pulmonary emboli have been found in as many as 10 to 30 percent of patients with chronic RVT, most of whom are asymptomatic [1,4,11-14,17,18] . (See 'Pulmonary embolism' above.)

It has been suggested that a chronic RVT in patients with nephrotic syndrome may lead to increased proteinuria or progressively worsening kidney function. However, this has never been clearly documented [17] . Furthermore, in a case report of a patient with unilateral RVT and nephrotic syndrome due to membranous nephropathy, bilateral ureteral catheterization studies showed no difference in protein excretion or creatinine clearance between the two kidneys [31] .

Acute renal vein thrombosis — Acute RVT is most often due to trauma, severe dehydration (especially in infants), or a generalized hypercoagulable state. It is an uncommon complication of the nephrotic syndrome [1] . (See "Overview of the causes of venous thrombosis".)

Acute RVT typically presents with symptoms of renal infarction, including flank pain, microscopic or gross hematuria, a marked elevation in serum lactate dehydrogenase (without change in transaminases), and an increase in renal size on radiographic study [1] . Bilateral RVT may present with acute renal failure.

Significant proteinuria is a rare complication of acute RVT in patients without underlying nephrotic syndrome [11,32] . In a case report, a previously healthy individual with bilateral RVT presented acutely with lower abdominal and flank pain and proteinuria (2.3 g over 24 hours); both the thrombus and proteinuria disappeared after two courses of urokinase followed by intravenous heparin [32] . Subsequent examination of renal biopsy tissue via light microscopy, immunofluorescence, and electron microscopy was normal.

Diagnosis and screening — Although the gold standard diagnostic test for RVT is selective renal venography (picture 1), less invasive procedures, including spiral computed tomography (CT) with contrast, magnetic resonance imaging (MRI), and Doppler ultrasonography, are increasingly being used [4,16,33-37] . Institutional expertise is important in choosing a noninvasive test since false negative and false positive results have been reported [4,16,35,37] .

Routine screening for RVT is not recommended in patients with nephrotic syndrome, even in those at high-risk for RVT (eg, membranous nephropathy associated with protein excretion above 10 g/day and/or a serum albumin concentration below 2 g/dL [20 g/L] ) [2] . There are two problems with screening: there is no proven benefit to diagnosing occult disease, and a patient with a negative study may develop RVT at a later time, requiring sequential studies [2] .

It is also not particularly useful to evaluate for RVT in a patient who experiences an overt embolic event (such as a pulmonary embolus) for the following reasons:

 

  • It cannot be proven that the pulmonary embolus originated in the renal veins, since a DVT in the lower extremities may have coexisted.
  • In situ pulmonary thrombosis (not an embolus) may occur in patients with severe nephrotic syndrome and profound hypoalbuminemia.
  • Most important, a patient with nephrotic syndrome who has developed a thromboembolic event will be treated with anticoagulants whether or not an RVT is present.

 

Taking all of these factors into consideration, it is rarely necessary to image the renal veins for a thrombus in patients with the nephrotic syndrome. An important exception occurs in the rare patient suspected of having acute, complete RVT (eg, signs or symptoms of a renal infarct), which will be accompanied by acute renal failure if it is bilateral. Although a selective renal venogram is the gold standard diagnostic test and has the additional advantage of permitting a simultaneous therapeutic procedure, we suggest an initial noninvasive evaluation with CT angiography.

A separate issue is whether chronic bilateral RVT might be a cause of a rising serum creatinine or increasing proteinuria and, if so, whether anticoagulation might be beneficial. There are no data to support this hypothesis [17] . Opinions of experts vary as to whether or not patients with marked and progressive nephrotic syndrome or a slowly rising serum creatinine should undergo an imaging procedure to screen for RVT.

TREATMENT — There are no randomized trials to guide optimal therapy of hypercoagulability in nephrotic syndrome. There are two aspects to therapy of the hypercoagulable state in the nephrotic syndrome that must be considered: anticoagulation to prevent thromboembolic events (including RVT, DVT, and PE) and dissolution or removal of the thrombus with thrombolytic therapy or thrombectomy, which are primarily considered in patients with acute RVT.

Prevention of thromboembolism — There are three issues that must be addressed for prevention of thromboembolism in patients with the nephrotic syndrome: prophylactic anticoagulation, anticoagulation for asymptomatic RVT, and anticoagulation after a symptomatic thromboembolic event. The goals of anticoagulation are to minimize the formation of new thrombi and promote recanalization of the existing thrombus.

Prophylactic anticoagulation — The likelihood of benefit from prophylactic anticoagulation is strongly dependent upon the incidence of thrombotic events and the risks of anticoagulation. (See "Therapeutic use of warfarin", section on 'Bleeding' and "Therapeutic use of warfarin", section on 'Other complications'.)

No prospective controlled clinical study has compared the risks associated with undiagnosed RVT with the risk of long-term anticoagulation to evaluate the potential benefits of prophylactic anticoagulation. In the one available prospective uncontrolled study, 30 patients with nephrotic syndrome (14 with membranous, 13 with focal segmental glomerulosclerosis, median serum albumin 1.7 mg/dL [17 g/L] and median protein excretion of 9 g/day) were treated with low molecular weight heparin for a median of 13 months [38] . Patients had no thromboses at baseline, as assessed by Doppler ultrasound of the renal and lower extremity veins and V/Q scan of the lungs, and reassessment every three months demonstrated no thromboses throughout follow-up.

In the absence of convincing data, we suggest not routinely providing prophylactic anticoagulation to asymptomatic patients with the nephrotic syndrome who do not have another reason for anticoagulation (eg, atrial fibrillation).

Experts differ as to the ability to identify patients at high risk who might benefit from prophylactic oral anticoagulation [39] . There is general agreement that patients with membranous nephropathy, massive proteinuria, and a serum albumin below 2.0 g/dL (20 g/L) represent the highest risk group. Some would prophylactically anticoagulate all such patients, some require an additional risk factor (eg, atrial fibrillation), and some do not prescribe prophylactic anticoagulation.

We provide prophylactic anticoagulation to patients with nephrotic syndrome who have massive proteinuria, a serum albumin below 2.0 g/dL (20 g/L), and an additional risk factor for thrombosis (eg, a prior idiopathic thromboembolic event; immobilization; severe heart failure; morbid obesity; or abdominal, orthopedic or gynecologic surgery). Patients who achieve remission of nephrotic syndrome should have anticoagulation discontinued after six months following remission if there is no other indication for anticoagulation. (See "Overview of the causes of venous thrombosis".)

In any patient, the potential benefit from chronic warfarin therapy must be weighed against the patient's risk of a bleeding complication. (See "Therapeutic use of warfarin", section on 'Bleeding'.)

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Anticoagulation for asymptomatic RVT — Asymptomatic RVT is detected in one of two ways: during screening, which we do not recommend, and during imaging for some other reason.

There are no randomized trials or definitive observational studies that have evaluated the role of anticoagulation in patients with nephrotic syndrome who have an asymptomatic RVT, but case series report treating such patients [11,17] . Possible benefits include prevention of DVT or PE, while the major risk is bleeding [11] .

An example of the difficulty in determining the proper approach comes from a poll of eight experts that we conducted. All would treat an asymptomatic RVT if it were discovered, although some with reluctance. However, only two recommend screening for RVT and only during the baseline evaluation for membranous nephropathy.

Anticoagulation therapy should thus be provided to patients with an incidentally discovered RVT, unless contraindicated.

Anticoagulation for a thromboembolic event — Patients with a symptomatic RVT (eg, acute RVT or with an associated thromboembolic event) or a thromboembolic event in the absence of RVT are treated the same as patients who have a DVT or PE. Treatment typically consists of anticoagulation, initially with unfractionated or low molecular weight heparin and then warfarin [39,40] . Some patients with nephrotic syndrome are partially resistant to heparin therapy due to severe antithrombin deficiency. (See "Treatment of lower extremity deep vein thrombosis" and "Therapeutic use of heparin and low molecular weight heparin", section on 'Heparin resistance'.)

Duration of anticoagulation — Warfarin therapy is given for a minimum of 6 to 12 months. However, most experts feel that warfarin should be continued for as long as the patient remains nephrotic [1,2] . The recommendation for prolonged therapy is similar to that in other hypercoagulable states such as an idiopathic DVT or a thromboembolic event in patients with antiphospholipid syndrome. (See "Treatment of lower extremity deep vein thrombosis", section on 'Idiopathic VTE' and "Treatment of the antiphospholipid syndrome", section on 'Duration of warfarin use'.)

The goal INR is 2.0 to 3.0. This level of anticoagulation is associated with a modest increase in risk of bleeding; a higher bleeding risk, compared with less intense therapy, is observed particularly among the elderly.

Inferior vena cava filters — In patients with pulmonary embolism and documented renal vein thrombosis with contraindications to anticoagulation, suprarenal IVC filters have occasionally been used and are thought to be relatively safe [41] .

Direct therapy of RVT

Fibrinolytic therapy and catheter thrombectomy — Systemic fibrinolysis has been used in patients with RVT, but carries the risk of bleeding, including intracranial bleeding, and is not recommended [42-44] . (See "Fibrinolytic (thrombolytic) agents in acute ST elevation myocardial infarction: Therapeutic use", section on 'Risks'.)

Successful outcomes have been reported using local thrombolytic therapy with or without extraction catheter thrombectomy in nephrotic patients with acute RVT [45-48] . The potential efficacy of this approach was illustrated in a report of six patients (five of whom had proteinuric renal disease, but level of proteinuria or serum albumin not reported) with acute RVT who had percutaneous catheter thrombectomy followed by local thrombolysis for a mean of 22 hours [46] . Renal venous flow was restored in all patients, and the mean serum creatinine declined post-procedure from 3.3 to 1.9 mg/dL (292 to 168 µmol/L). At two years, kidney function was stable, and there were no further episodes of RVT.

We favor local thrombolytic therapy with or without thrombectomy in patients who have signs of acute RVT.

Surgery — Surgical thrombectomy should be considered only in the rare patient with acute bilateral RVT and acute renal failure who cannot be treated with percutaneous thrombectomy and/or thrombolysis [49] .

SUMMARY AND RECOMMENDATIONS — Patients with the nephrotic syndrome are at increased risk for arterial and venous thrombosis, particularly deep vein thrombosis (DVT) and renal vein thrombosis (RVT). The estimated prevalence of RVT ranges from 5 to 60 percent and is described most commonly in patients with membranous nephropathy. RVT may be unilateral or bilateral, may extend into the inferior vena cava, and may be associated with pulmonary embolism. (See 'Epidemiology' above.)

The risk of thrombosis appears to be proportional to the severity of the nephrotic syndrome, being particularly increased with serum albumin concentrations below 2.0 g/dL (20 g/L).

Most RVT develop insidiously and are asymptomatic. There is no clear evidence that chronic RVT leads to increased proteinuria or worsening kidney function. In contrast, acute RVT presents with signs of renal infarction. (See 'Clinical features' above.)

Diagnosis — The gold standard for the diagnosis of RVT is an inferior vena cavagram with selective renal venography. However, more typically, the diagnosis is made by spiral CT scanning with contrast, magnetic resonance imaging, or Doppler ultrasonography, with the choice of test based upon institutional expertise. (See 'Diagnosis and screening' above.)

We suggest not routinely screening for RVT in patients with the nephrotic syndrome (Grade 2C). In addition, we do not screen nephrotic patients with worsening nephrotic syndrome or slowly rising serum creatinine. (See 'Diagnosis and screening' above.)

In patients suspected of having acute, complete RVT because of signs or symptoms of a renal infarct or, if bilateral, acute renal failure, we suggest obtaining renal CT angiography to evaluate for both arterial and venous occlusion (Grade 2B). (See 'Acute renal vein thrombosis' above and "Diagnosis and treatment of renal infarction", section on 'Treatment'.)

Therapy — Data on prophylactic or therapeutic anticoagulation with warfarin (or other vitamin K antagonist) for RVT are limited. The decision to treat and choice of therapy must be individualized based upon the risks of anticoagulation, and presence of associated thromboemboli (eg, DVT or PE), or acute renal failure. (See 'Prophylactic anticoagulation' above.)

 

  • We suggest not providing routine prophylactic anticoagulation to patients with nephrotic syndrome (Grade 2C).
  • There is general agreement that patients with membranous nephropathy, massive proteinuria, and a serum albumin below 2.0 g/dL (20 g/L) represent the highest risk group for thromboembolism. However, this risk is also increased in patients with other causes of nephrotic syndrome who meet these criteria. In such patients, we suggest prophylactic anticoagulation if there is an additional risk factor for thrombosis (eg, a prior idiopathic thromboembolic event; immobilization; severe heart failure; morbid obesity; or abdominal, orthopedic or gynecologic surgery) (Grade 2C). (See 'Prophylactic anticoagulation' above and "Overview of the causes of venous thrombosis".)
  • We suggest anticoagulation therapy in patients with an incidentally discovered RVT (Grade 2C).
  • We recommend anticoagulation in patients with nephrotic syndrome who have had a nonrenal thromboembolic event or acute RVT (Grade 1B). (See 'Anticoagulation for a thromboembolic event' above.)
  • We suggest thrombolytic therapy with or without catheter thrombectomy in patients with acute RVT (Grade 2C). (See 'Fibrinolytic therapy and catheter thrombectomy' above.)
  • When anticoagulation is given, we suggest that warfarin be continued for as long as the patient remains nephrotic, with a minimum duration of 6 to 12 months (Grade 2C). The goal INR is 2.0 to 3.0.

 

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