IgA Nephropathy Medication

  • Author: Mona Brake, MD; Chief Editor: Vecihi Batuman, MD, FACP, FASN   more...
 
Updated: Jan 5, 2012
 

Medication Summary

Currently, no cure exists for IgA nephropathy. However, therapies that can delay the onset of need for dialysis and transplantation are available. Hypertension should be treated early and aggressively. ACE inhibitors are the antihypertensives of choice.

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Angiotensin-converting enzyme inhibitors

Class Summary

Comparative studies show ACE inhibitors are more effective than other antihypertensives (ie, beta blockers, calcium channel blockers) in reducing blood pressure and proteinuria, protecting renal function, and delaying onset of ESRD.

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Benazepril (Lotensin)

 

Prevents conversion of angiotensin I to angiotensin II, which is a potent vasoconstrictor. Also causes lower aldosterone secretion, thus reducing systemic and glomerular capillary pressure.

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Angiotensin II receptor antagonists

Class Summary

Reduce blood pressure and proteinuria, protect renal function, and delay onset of ESRD.

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Losartan (Cozaar)

 

Nonpeptide angiotensin II receptor antagonist that blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II. May induce a more complete inhibition of the renin-angiotensin system than ACE inhibitors, do not affect the response to bradykinin, and are less likely to be associated with cough and angioedema. For patients unable to tolerate ACE inhibitors.

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Corticosteroids

Class Summary

Prednisone should be used in patients with nephrotic syndrome and minimal histologic findings. When treated with corticosteroids, patients with proteinuria and preserved renal function (ie, CrCl >70 mL/min) have shown significant delay of disease progression compared to patients not receiving corticosteroids.

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Prednisone (Sterapred)

 

Immunosuppressant for treating autoimmune disorders. Decreases inflammation by reducing capillary permeability and suppressing PMN activity. Stabilizes lysosomal membranes and suppresses lymphocyte and antibody production.

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Omega-3 polyunsaturated fatty acids

Class Summary

Orphan drug indicated for treatment of IgA nephropathy. Used in patients with proteinuria and decreased renal function.

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Omega-3 polyunsaturated fatty acid (Fish oil)

 

May be of benefit by decreasing mediators of glomerular injury and decreasing platelet aggregation.

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Immunosuppressive agents

Class Summary

Cyclophosphamide is used in nonmalignant renal diseases for its immunosuppressive effects.

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Cyclophosphamide (Neosar, Cytoxan)

 

Cyclic polypeptide that suppresses some humoral activity. Chemically related to nitrogen mustards. Activated in the liver to its active metabolite, 4-hydroxycyclophosphamide, which alkylates the target sites in susceptible cells in an all-or-none type reaction. As an alkylating agent, the mechanism of action of the active metabolites may involve cross-linking of DNA, which may interfere with growth of normal and neoplastic cells.

Biotransformed by cytochrome P-450 system to hydroxylated intermediates that break down to active phosphoramide mustard and acrolein. Interaction of phosphoramide mustard with DNA considered cytotoxic.

When used in autoimmune diseases, mechanism of action is thought to involve immunosuppression due to destruction of immune cells via DNA cross-linking.

In high doses, affects B cells by inhibiting clonal expansion and suppression of production of immunoglobulins. With long-term low-dose therapy, affects T cell functions.

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Contributor Information and Disclosures
Author

Mona Brake, MD  Assistant Professor, Department of Internal Medicine, Kansas University School of Medicine

Mona Brake, MD is a member of the following medical societies: American College of Physicians and American Society of Nephrology

Disclosure: Nothing to disclose.

Coauthor(s)

Douglas Somers, MD  Assistant Professor, Department of Internal Medicine, Division of Nephrology, University of Iowa Medical Center

Douglas Somers, MD is a member of the following medical societies: American Society of Nephrology

Disclosure: Nothing to disclose.

Specialty Editor Board

James H Sondheimer, MD, FACP  Associate Professor of Medicine, Wayne State University School of Medicine; Medical Director of Hemodialysis, Harper University Hospital at Detroit Medical Center; Medical Director, DaVita Greenview Dialysis (Southfield)

James H Sondheimer, MD, FACP is a member of the following medical societies: American College of Physicians and American Society of Nephrology

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Salary Employment

Christie P Thomas, MBBS, FRCP, FASN, FAHA  Professor, Department of Internal Medicine, Division of Nephrology, Medical Director, Kidney and Kidney/Pancreas Transplant Program, University of Iowa Hospitals and Clinics

Christie P Thomas, MBBS, FRCP, FASN, FAHA is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, and Royal College of Physicians

Disclosure: Nothing to disclose.

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 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: Renal Ventures Ownership interest Other

Chief Editor

Vecihi Batuman, MD, FACP, FASN  Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology

Disclosure: Nothing to disclose.

Additional Contributors

The authors thank Dr. Tim Timmerman, pathologist, for his invaluable help with the pathology slides.

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Light microscopy of a glomerulus from a patient with immunoglobulin A nephropathy showing increased mesangial matrix and cellularity.
Electron microscopy showing large dark mesangial deposits.
Immunofluorescence microscopy demonstrating large mesangial immunoglobulin A (IgA) deposits diagnostic of IgA nephropathy.
 
 
 
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