eMedicine Specialties > Vascular Surgery > Medical Topics

Renal Vein Thrombosis: Treatment & Medication

Author: Igor A Laskowski, MD, Assistant Professor of Surgery, Section of Vascular Surgery, New York Medical College, Westchester Medical Center
Coauthor(s): Louis Schwing, MD, Consulting Staff, Department of Internal Medicine, Carle Clinic Associates
Contributor Information and Disclosures

Updated: Sep 17, 2009

Treatment

Medical Care

  • Treatment of nephrotic syndrome: Measures may include steroids and immune-suppression therapy. Treatment of underlying renal cell cancer includes surgery for early-stage disease.
  • Symptomatic treatment includes diuretics and angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin II receptor blockers (ARBs) to decrease proteinuria from nephrotic syndrome. If a combination of ACEIs and ARBs lowers protein excretion more than either alone, they should be used together. Decreasing protein loss in the urine decreases hypercoagulability.
  • Anticoagulation with warfarin has been recommended in some studies for prophylaxis against pulmonary embolism. Treat hypercholesterolemia according to accepted national guidelines (ie, using appropriate low-density lipoprotein targets for primary or secondary prevention).
  • A recent study by Bianchi suggests that atorvastatin decreases the rate of progression of kidney disease, proteinuria, and hypercholesterolemia.6

Surgical Care

  • Surgical treatment for renal vein thrombosis (RVT) is rarely used today.
  • Surgery has been used in the presence of bilateral renal vein thrombosis (RVT) or if pulmonary emboli have occurred and anticoagulation is contraindicated.7 Inferior vena caval filters may be used in this instance.
  • Surgery may be necessary for renal vein thrombosis (RVT) of renal cell cancer, particularly for cure of malignancy.
  • Hypernephroma or renal cell cancer is unique in that intraluminal tumor extends into the renal vein and inferior vena cava (IVC) and sometimes extends into the right atrium. In such cases, radical nephrectomy and removal of the tumor from the IVC and right atrium affords the chance of cure. This is not distant metastasis; rather, this is tumor extension within the renal vein and IVC.

Consultations

  • Consult a nephrologist and interventional radiologist (only when medical therapy does not prevent pulmonary emboli).
  • A surgeon (urologist) can assist in the staging and potential surgery for renal cell carcinoma (early-stage disease).
  • A combined team that consists of a urologist, vascular surgeon, cardiac surgeon, transplant surgeon, or a combination thereof works together in complex cases of renal cancer with extension into renal vein, IVC, and right atrium.

Diet

  • Many nephrologists recommend normal protein intake for patients with nephrotic syndrome.
  • Protein restriction may be used with benefit in patients who are nephrotic who do not spill massive amounts of protein (approximately 10 g or more over 24 h) or in those who have chronic renal failure.8

Activity

Activity is allowed as tolerated.

Medication

Reduction in proteinuria is essential in the treatment of renal vein thrombosis (RVT) in patients who are nephrotic. The current standard is ACE inhibition and/or ARBs. Pulmonary emboli from renal vein thrombosis (RVT) should be diagnosed and treated exactly as they are when resulting from other sources (ie, heparin, warfarin). If renal vein thrombosis (RVT) is associated with pulmonary emboli, anticoagulation must be continued as long as nephrotic syndrome is present.

The indicators for thrombolysis in the setting of renal vein thrombosis (RVT) are unclear. No data are available comparing thrombolytic therapy with anticoagulation. In pulmonary embolic disease from other causes, thrombolytics are indicated in the setting of pulmonary hypertension (as found during examination or discovered by echocardiography).

Warfarin, ARBs, and ACEIs are unsafe in pregnancy. Patients with renal vein thrombosis (RVT) in pregnancy are treated best with heparin alone.

Angiotensin-converting enzyme inhibitors

These agents reduce urine protein excretion by decreasing glomerular hydraulic pressure. Decrease efferent arteriolar constriction, thereby decreasing the pressure, resulting in the filtration of protein. The filtered protein, per se, is injurious to the kidney.


Benazepril (Lotensin)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. This increases levels of plasma renin and reduces aldosterone secretion. In kidney, the drug decreases glomerular hydraulic pressure, thereby decreasing filtration of protein.

Adult

20-40 mg/d PO qd or divided bid; make dose adjustments based on effects at times of peak (2-6 h after dosing) and trough
Start with lowest dose and titrate to highest level to decrease proteinuria
Use appropriate practice guidelines for target blood pressures (eg, if RVT is occurring in a patient with diabetes, target blood pressure is 130/80 mm Hg

Pediatric

Not established

NSAIDs may reduce hypotensive effects of benazepril; ACEIs may increase digoxin, lithium, and allopurinol levels; rifampin decreases benazepril levels; probenecid may increase benazepril levels; the hypotensive effects of ACEIs may be enhanced when given concurrently with diuretics

Documented hypersensitivity; prior serious adverse event; angioedema

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Decreased coronary perfusion in aortic stenosis possible; renal failure in high-grade renal vascular disease may occur; may cause angioedema, anaphylactoid reactions, neutropenia, renal failure, hepatic failure, and cough; caution in infants susceptible to adverse hemodynamic effects


Captopril (Capoten)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. This increases levels of plasma renin and reduces aldosterone secretion. In kidney, the drug decreases glomerular hydraulic pressure, thereby decreasing filtration of protein.

Adult

12.5-25 mg PO bid/tid; may increase by 12.5-25 mg/dose q1-2wk; not to exceed 50 mg tid
Start with lowest dose and titrate to highest level to decrease proteinuria

Pediatric

Not established

NSAIDs may reduce hypotensive effects of captopril; ACEIs may increase digoxin, lithium, and allopurinol levels; rifampin decreases captopril levels; probenecid may increase captopril levels; the hypotensive effects of ACEIs may be enhanced when given concurrently with diuretics

Documented hypersensitivity; prior serious adverse event; angioedema

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Decreased coronary perfusion in aortic stenosis possible; renal failure in high-grade renal vascular disease may occur; may cause angioedema, anaphylactoid reactions, neutropenia, renal failure, hepatic failure, and cough; caution in infants susceptible to adverse hemodynamic effects


Enalapril (Vasotec)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. This increases levels of plasma renin and reduces aldosterone secretion. In kidney, the drug decreases glomerular hydraulic pressure, thereby decreasing filtration of protein.

Adult

2.5-5 mg/d PO (increase as necessary)
Dosing range: 10-40 mg/d PO divided q12-24h
Start with lowest dose and titrate to highest level to decrease proteinuria

Pediatric

Not established

NSAIDs may reduce hypotensive effects of enalapril; ACEIs may increase digoxin, lithium, and allopurinol levels; rifampin decreases enalapril levels; probenecid may increase enalapril levels; the hypotensive effects of ACEIs may be enhanced when given concurrently with diuretics

Documented hypersensitivity; prior serious adverse event; angioedema

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Decreased coronary perfusion in aortic stenosis possible; renal failure in high-grade renal vascular disease may occur; may cause angioedema, anaphylactoid reactions, neutropenia, renal failure, hepatic failure, and cough; caution in infants susceptible to adverse hemodynamic effects


Fosinopril (Monopril)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. This increases levels of plasma renin and reduces aldosterone secretion. In kidney, the drug decreases glomerular hydraulic pressure, thereby decreasing filtration of protein.

Adult

10 mg/d PO initially; may increase to 20-40 mg/d
Start with lowest dose and titrate to highest level to decrease proteinuria

Pediatric

Not established

NSAIDs may reduce hypotensive effects of fosinopril; ACEIs may increase digoxin, lithium, and allopurinol levels; rifampin decreases fosinopril levels; probenecid may increase fosinopril levels; the hypotensive effects of ACEIs may be enhanced when given concurrently with diuretics

Documented hypersensitivity; prior serious adverse event; angioedema

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Decreased coronary perfusion in aortic stenosis possible; renal failure in high-grade renal vascular disease may occur; may cause angioedema, anaphylactoid reactions, neutropenia, renal failure, hepatic failure, and cough; caution in infants susceptible to adverse hemodynamic effects


Lisinopril (Zestril, Prinivil)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. This increases levels of plasma renin and reduces aldosterone secretion. In kidney, the drug decreases glomerular hydraulic pressure, thereby decreasing filtration of protein.

Adult

10 mg/d PO; increase 5-10 mg/d at 1- to 2-wk intervals; not to exceed 40 mg
Start with lowest dose and titrate to highest level to decrease proteinuria

Pediatric

Not established

NSAIDs may reduce hypotensive effects of lisinopril; ACEIs may increase digoxin, lithium, and allopurinol levels; rifampin decreases lisinopril levels; probenecid may increase lisinopril levels; the hypotensive effects of ACEIs may be enhanced when given concurrently with diuretics

Documented hypersensitivity; prior serious adverse event; angioedema

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Decreased coronary perfusion in aortic stenosis possible; renal failure in high-grade renal vascular disease may occur; may cause angioedema, anaphylactoid reactions, neutropenia, renal failure, hepatic failure, and cough; caution in infants susceptible to adverse hemodynamic effects


Moexipril (Univasc)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. This increases levels of plasma renin and reduces aldosterone secretion. In kidney, the drug decreases glomerular hydraulic pressure, thereby decreasing filtration of protein.

Adult

3.75-7.5 mg PO qd initially; may increase gradually to 7.5-30 mg/d PO divided q12-24h; not to exceed 60 mg/d
Start with lowest dose and titrate to highest level to decrease proteinuria

Pediatric

Not established

NSAIDs may reduce hypotensive effects of moexipril; ACEIs may increase digoxin, lithium, and allopurinol levels; rifampin decreases moexipril levels; probenecid may increase moexipril levels; the hypotensive effects of ACEIs may be enhanced when given concurrently with diuretics

Documented hypersensitivity; prior serious adverse event; angioedema

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Decreased coronary perfusion in aortic stenosis possible; renal failure in high-grade renal vascular disease may occur; may cause angioedema, anaphylactoid reactions, neutropenia, renal failure, hepatic failure, and cough; caution in infants susceptible to adverse hemodynamic effects


Perindopril (Aceon)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. This increases levels of plasma renin and reduces aldosterone secretion. In kidney, the drug decreases glomerular hydraulic pressure, thereby decreasing filtration of protein.

Adult

4 mg PO qd; may increase dose; not to exceed 16 mg PO divided q12-24h
Start with lowest dose and titrate to highest level to decrease proteinuria

Pediatric

Not established

NSAIDs may reduce hypotensive effects of perindopril; ACEIs may increase digoxin, lithium, and allopurinol levels; rifampin decreases perindopril levels; probenecid may increase perindopril levels; the hypotensive effects of ACEIs may be enhanced when given concurrently with diuretics

Documented hypersensitivity; prior serious adverse event; angioedema

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Decreased coronary perfusion in aortic stenosis possible; renal failure in high-grade renal vascular disease may occur; may cause angioedema, anaphylactoid reactions, neutropenia, renal failure, hepatic failure, and cough; caution in infants susceptible to adverse hemodynamic effects

Angiotensin receptor blockers

These agents reduce urine protein excretion by decreasing glomerular hydraulic pressure.


Candesartan (Atacand)

Blocks vasoconstrictor and aldosterone-secreting effects of angiotensin II. May induce more complete inhibition of renin-angiotensin system than ACEIs, does not affect response to bradykinin, and is less likely to be associated with cough and angioedema. Use in patients unable to tolerate ACEIs.

Adult

16 mg/d PO initially; not to exceed 32 mg/d
Start with lowest dose and titrate to highest level to decrease proteinuria

Pediatric

Not established

May increase digoxin, lithium, and allopurinol levels; probenecid may increase candesartan levels; coadministration with diuretics, increase hypotensive effects; NSAIDs may reduce hypotensive effects of candesartan; may increase risk of hyperkalemia if taken concurrently with potassium supplements or other potassium-sparing diuretics

Documented hypersensitivity; prior serious adverse event; angioedema

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal impairment (serum creatinine >3.5), valvular stenosis, or severe congestive heart failure; watch for serum potassium; caution in infants susceptible to adverse hemodynamic effects


Eprosartan (Teveten)

Blocks vasoconstrictor and aldosterone-secreting effects of angiotensin II. May induce more complete inhibition of renin-angiotensin system than ACEIs, does not affect response to bradykinin, and is less likely to be associated with cough and angioedema. Use in patients unable to tolerate ACEIs.

Adult

400-800 mg PO divided q12-24h
Start with lowest dose and titrate to highest level to decrease proteinuria

Pediatric

Not established

May increase digoxin, lithium, and allopurinol levels; probenecid may increase eprosartan levels; coadministration with diuretics, increase hypotensive effects; NSAIDs may reduce hypotensive effects of eprosartan; may increase risk of hyperkalemia if taken concurrently with potassium supplements or other potassium-sparing diuretics

Documented hypersensitivity; prior serious adverse event; angioedema

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal impairment (serum creatinine >3.5), valvular stenosis, or severe congestive heart failure; watch for serum potassium; caution in infants susceptible to adverse hemodynamic effects


Irbesartan (Avapro)

Blocks vasoconstrictor and aldosterone-secreting effects of angiotensin II. May induce more complete inhibition of renin-angiotensin system than ACEIs, does not affect response to bradykinin, and is less likely to be associated with cough and angioedema. Use in patients unable to tolerate ACEIs.

Adult

150-300 mg PO qd
Start with lowest dose and titrate to highest level to decrease proteinuria

Pediatric

Not established

May increase digoxin, lithium, and allopurinol levels; probenecid may increase irbesartan levels; coadministration with diuretics, increase hypotensive effects; NSAIDs may reduce hypotensive effects of irbesartan; may increase risk of hyperkalemia if taken concurrently with potassium supplements or other potassium-sparing diuretics

Documented hypersensitivity; prior serious adverse event; angioedema

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal impairment (serum creatinine >3.5), valvular stenosis, or severe congestive heart failure; watch for serum potassium; caution in infants susceptible to adverse hemodynamic effects


Losartan (Cozaar)

Blocks vasoconstrictor and aldosterone-secreting effects of angiotensin II. May induce more complete inhibition of renin-angiotensin system than ACEIs, does not affect response to bradykinin, and is less likely to be associated with cough and angioedema. Use in patients unable to tolerate ACEIs.

Adult

25-100 mg PO divided q12-24h
Start with lowest dose and titrate to highest level to decrease proteinuria

Pediatric

Not established

May increase digoxin, lithium, and allopurinol levels; probenecid may increase losartan levels; coadministration with diuretics, increase hypotensive effects; NSAIDs may reduce hypotensive effects of losartan; may increase risk of hyperkalemia if taken concurrently with potassium supplements or other potassium-sparing diuretics

Documented hypersensitivity; prior serious adverse event; angioedema

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal impairment (serum creatinine >3.5), valvular stenosis, or severe congestive heart failure; watch for serum potassium; caution in infants susceptible to adverse hemodynamic effects


Telmisartan (Micardis)

Blocks vasoconstrictor and aldosterone-secreting effects of angiotensin II. May induce more complete inhibition of renin-angiotensin system than ACEIs, does not affect response to bradykinin, and is less likely to be associated with cough and angioedema. Use in patients unable to tolerate ACEIs.

Adult

20-80 mg PO qd
Start with lowest dose and titrate to highest level to decrease proteinuria

Pediatric

Not established

May increase digoxin, lithium, and allopurinol levels; probenecid may increase telmisartan levels; coadministration with diuretics, increase hypotensive effects; NSAIDs may reduce hypotensive effects of telmisartan; may increase risk of hyperkalemia if taken concurrently with potassium supplements or other potassium-sparing diuretics

Documented hypersensitivity; prior serious adverse event; angioedema

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal impairment (serum creatinine >3.5), valvular stenosis, or severe congestive heart failure; watch for serum potassium; caution in infants susceptible to adverse hemodynamic effects


Valsartan (Diovan)

Prodrug that produces direct antagonism of angiotensin II receptors. Displaces angiotensin II from AT1 receptor and may lower blood pressure by antagonizing AT1-induced vasoconstriction, aldosterone release, catecholamine release, arginine vasopressin release, water intake, and hypertrophic responses. May induce more complete inhibition of renin-angiotensin system than ACEIs, does not affect response to bradykinin, and is less likely to be associated with cough and angioedema. For use in patients unable to tolerate ACEIs.

Adult

80-320 mg PO qd
Start with lowest dose and titrate to highest level to decrease proteinuria

Pediatric

Not established

May increase digoxin, lithium, and allopurinol levels; probenecid may increase valsartan levels; coadministration with diuretics, increase hypotensive effects; NSAIDs may reduce hypotensive effects of valsartan; may increase risk of hyperkalemia if taken concurrently with potassium supplements or other potassium-sparing diuretics

Documented hypersensitivity; prior serious adverse event; angioedema

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal impairment (serum creatinine >3.5), valvular stenosis, or severe congestive heart failure; watch for serum potassium; caution in infants susceptible to adverse hemodynamic effects

More on Renal Vein Thrombosis

Overview: Renal Vein Thrombosis
Differential Diagnoses & Workup: Renal Vein Thrombosis
Treatment & Medication: Renal Vein Thrombosis
Follow-up: Renal Vein Thrombosis
Multimedia: Renal Vein Thrombosis
References
Further Reading
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References

  1. Reimold EW, Wittel RA. Renal venous thrombosis in children: changes in management. South Med J. Oct 1983;76(10):1277-84. [Medline].

  2. Dutta TK, Venugopal V. Venous thromboembolism: the intricacies. J Postgrad Med. Jan-Mar 2009;55(1):55-64. [Medline].

  3. Dauger S, Michot C, Garnier A, Hurtaud-Roux MF. [Neonatal renal venous thrombosis in 2008]. Arch Pediatr. Feb 2009;16(2):132-41. [Medline].

  4. Decoster T, Schwagten V, Hendriks J, Beaucourt L. Renal colic as the first symptom of acute renal vein thrombosis, resulting in the diagnosis of nephrotic syndrome. Eur J Emerg Med. Apr 20 2009;[Medline].

  5. Basterrechea Iriarte F, Sota Busselo I, Nogués Pérez A. [Evolution of imaging in renal vein thrombosis in the newborn]. An Pediatr (Barc). Nov 2008;69(5):442-5. [Medline].

  6. Bianchi S, Bigazzi R, Caiazza A, et al. A controlled, prospective study of the effects of atorvastatin on proteinuria and progression of kidney disease. Am J Kidney Dis. Mar 2003;41(3):565-70. [Medline].

  7. Jaako Dardashti V, Bekassy ZD, Ljung R, Gelberg J, Wingren P, Simonsen O, et al. Successful thrombolysis of neonatal bilateral renal vein thrombosis originating in the IVC. Pediatr Nephrol. Mar 24 2009;[Medline].

  8. Maroni BJ. Protein restriction in the pre-end-stage renal disease (ESRD) patient: who, when, how, and the effect on subsequent ESRD outcome. J Am Soc Nephrol. Dec 1998;9(12 Suppl):S100-6. [Medline].

  9. Babu SC, Manoni T, Shah PM. Malignant renal tumor with extension to the inferior vena cava. The American Journal of Surgery. 1998;176:137 -139.

  10. Borrello JA. Renal MR angiography. Magn Reson Imaging Clin N Am. Feb 1997;5(1):83-93. [Medline].

  11. Irish AB, Green FR, Gray DW, et al. The factor V Leiden (R506Q) mutation and risk of thrombosis in renal transplant recipients. Transplantation. Aug 27 1997;64(4):604-7. [Medline].

  12. Kim HS, Fine DM, Atta MG. Catheter-directed thrombectomy and thrombolysis for acute renal vein thrombosis. J Vasc Interv Radiol. May 2006;17(5):815-22. [Medline].

  13. Markowitz GS, Brignol F, Burns ER, et al. Renal vein thrombosis treated with thrombolytic therapy: case report and brief review. Am J Kidney Dis. May 1995;25(5):801-6. [Medline].

  14. Meehan SM, Limsrichamrern S, Manaligod JR, et al. Platelets and capillary injury in acute humoral rejection of renal allografts. Hum Pathol. Jun 2003;34(6):533-40. [Medline].

  15. Nickolas TL, Radhakrishnan J, Appel GB. Hyperlipidemia and thrombotic complications in patients with membranous nephropathy. Semin Nephrol. Jul 2003;23(4):406-11. [Medline].

  16. Orth SR, Ritz E. The nephrotic syndrome. N Engl J Med. Apr 23 1998;338(17):1202-11. [Medline].

  17. Zini L, Haulon S, Leroy X, et al. Endoluminal occlusion of the inferior vena cava in renal cell carcinoma with retro- or suprahepatic caval thrombus. BJU Int. Jun 2006;97(6):1216-20.

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Further Reading

Clinical guidelines

Venous thromboembolism.
Institute for Clinical Systems Improvement - Private Nonprofit Organization.  1998 Jun (revised 2007 Jun).  91 pages.  [NGC Update Pending] NGC:005885

Antithrombotic therapy supplement.
Institute for Clinical Systems Improvement - Private Nonprofit Organization.  2001 Sep (revised 2007 Aug).  64 pages.  NGC:005971

Prevention of venous thromboembolism. American College of Chest Physicians evidence-based clinical practice guidelines (8th edition).
American College of Chest Physicians - Medical Specialty Society.  2001 Jan (revised 2008 Jun).  73 pages.  NGC:006665

Clinical trials

Use of Low Molecular Weight Heparin (Tinzaparin) to Treat Blood Clots in Patients With Kidney Failure

Impact of Providing High Protein Bar to Dialysis Patients With Low Serum Albumin

CNI-Free de Novo Protocol in Patients Undergoing Liver Transplantation With Renal Impairment

Related eMedicine topics

 Renal Vein Thrombosis  (Radiology)

Chronic Renal Failure

Pulmonary Embolism

Renal Cell Carcinoma

Inferior Vena Caval Thrombosis

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Keywords

renal vein thrombosis, thrombosis, renal vein, RVT, nephrotic syndrome, hypercoagulable state, renal vein, clotting, clot, hypoalbuminemia, hypercholesterolemia, arterial thrombosis, renal dysfunction, renal failure, thromboembolism

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Contributor Information and Disclosures

Author

Igor A Laskowski, MD, Assistant Professor of Surgery, Section of Vascular Surgery, New York Medical College, Westchester Medical Center
Igor A Laskowski, MD is a member of the following medical societies: American College of Surgeons, American Hepato-Pancreato-Biliary Association, Peripheral Vascular Surgery Society, Society for Vascular Surgery, and Transplantation Society
Disclosure: Nothing to disclose.

Coauthor(s)

Louis Schwing, MD, Consulting Staff, Department of Internal Medicine, Carle Clinic Associates
Louis Schwing, MD is a member of the following medical societies: American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Richard A Santucci, MD, FACS, Chief of Urology, Detroit Receiving Hospital; Specialist-in-Chief of Urology, Detroit Medical Center; Chief of Urologic Trauma Surgery, Sinai Grace Hospital; Director, The Center for Urologic Reconstruction; Clinical Professor of Urology, Michigan State College of Medicine
Richard A Santucci, MD, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association, and Société Internationale d'Urologie (International Society of Urology)
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Travis J Phifer, MD, Chief, Division of Vascular Surgery, Professor, Department of Surgery and Radiology, Louisiana State University Health Sciences Center in Shreveport
Travis J Phifer, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Surgeons, American Medical Association, Association for Academic Surgery, Society for Academic Emergency Medicine, Society for Vascular Surgery, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

CME Editor

Rebecca J Schmidt, DO, FACP, FASN, Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine
Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Osteopathic Internists, American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association
Disclosure: Abbott Grant/research funds Speaking and teaching; Genzyme Honoraria Consulting; Amgen Honoraria Speaking and teaching; Ortho Biotech Honoraria Speaking and teaching

Chief Editor

William H Pearce, MD, Chief, Division of Vascular Surgery, Violet and Charles Baldwin Professor of Vascular Surgery, Department of Surgery, Northwestern University School of Medicine
William H Pearce, MD is a member of the following medical societies: American College of Surgeons, American Heart Association, American Surgical Association, Association for Academic Surgery, Association of VA Surgeons, Central Surgical Association, New York Academy of Sciences, Society for Vascular Surgery, Society of Critical Care Medicine, Society of University Surgeons, and Western Surgical Association
Disclosure: Nothing to disclose.

 
 
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