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