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Renal Vein Thrombosis Medication

  • Author: Igor A Laskowski, MD; Chief Editor: Vincent Lopez Rowe, MD  more...
 
Updated: Dec 08, 2014
 

Medication Summary

Reduction in proteinuria is essential in the treatment of renal vein thrombosis (RVT) in patients who are nephrotic. The current standard is to use angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin-receptor blockers (ARBs). Pulmonary emboli from RVT should be diagnosed and treated exactly as they are when resulting from other sources (ie, heparin, warfarin). If 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 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. Pregnant patients with RVT are best treated with heparin alone.

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Angiotensin-converting enzyme inhibitors

Class Summary

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.

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.

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.

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.

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.

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.

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.

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Angiotensin receptor blockers

Class Summary

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.

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.

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.

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.

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.

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.

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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, Society for Vascular Surgery, Americas Hepato-Pancreato-Biliary Association, Vascular and Endovascular Surgery Society, Transplantation Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Travis J Phifer, MD 

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, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Chief Editor

Vincent Lopez Rowe, MD Professor of Surgery, Program Director, Vascular Surgery Residency, Department of Surgery, Division of Vascular Surgery, Keck School of Medicine of the University of Southern California

Vincent Lopez Rowe, MD is a member of the following medical societies: American College of Surgeons, American Heart Association, Society for Vascular Surgery, Vascular and Endovascular Surgery Society, Society for Clinical Vascular Surgery, Pacific Coast Surgical Association, Western Vascular Society

Disclosure: Nothing to disclose.

Additional Contributors

Richard A Santucci, MD, FACS Specialist-in-Chief, Department of Urology, Detroit Medical Center; Chief of Urology, Detroit Receiving Hospital; Director, The Center for Urologic Reconstruction; Clinical Professor of Urology, Michigan State University College of Medicine

Richard A Santucci, MD, FACS is a member of the following medical societies: American College of Surgeons, Societe Internationale d'Urologie (International Society of Urology), American Urological Association

Disclosure: Nothing to disclose.

Acknowledgements

Sateesh C Babu, MD Professor of Clinical Surgery, New York Medical College; Chief, Vascular and Endovascular Surgery, Westchester Medical Center

Disclosure: Nothing to disclose.

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.

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This renal biopsy shows membranous nephropathy. Light (hematoxylin and eosin) stain shows thickened capillary loops via electron microscopy, with subepithelial deposits.
This CT scan shows renal vein thrombosis secondary to renal cell cancer. The arrow is pointed at the thrombosed renal vein.
This MRI is from a patient with renal cell cancer and renal vein thrombosis. The arrow is on the thrombosed vein.
 
 
 
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