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Pediatric IgA Nephropathy Medication

  • Author: Mohammad Ilyas, MD, FAAP; Chief Editor: Craig B Langman, MD  more...
Updated: Feb 27, 2014

Medication Summary

The risks and benefits of immunoglobulin A (IgA) nephropathy (IgAN) treatment with steroids, fish oil, ACE inhibitors, or ARB and immunosuppressant (eg, mycophenolate mofetil) should be discussed with patients and parents. These agents theoretically may protect the kidney and prolong the interval between onset and renal failure.


Anti-inflammatory and immunosuppressive agents

Class Summary

These agents elicit anti-inflammatory and immunosuppressive properties and cause profound and varied metabolic effects. They modify the body's immune response to diverse stimuli and reduce immune-mediated renal injury resulting from IgA deposition in the kidney.

Prednisone (Deltasone) or methylprednisolone (Solu-Medrol)


Potent anti-inflammatory and immunosuppressive therapy with corticosteroids has been reported to reduce the rate of progression of IgAN.


Fish oil

Class Summary

Several investigators have suggested that fish oil delays the progression of renal disease. The precise mechanism is not fully understood.

Omega-3 polyunsaturated fatty acid (Promega, Lovaza)


May be beneficial by decreasing mediators of glomerular injury and decreasing platelet aggregation. Omega-3 fatty acids may be used as nondrug dietary supplements in early high-risk coronary disease and IgAN.


Angiotensin-converting enzyme (ACE) inhibitors

Class Summary

In 1980, captopril became the first ACE inhibitor approved by the US Food and Drug Administration. Subsequently, at least 40 compounds have been identified. ACE inhibitors reduce the production of angiotensin II, thereby, lowering intraglomerular filtration pressure, reducing proteinuria, and slowing the decline of glomerular function in several chronic renal diseases. All ACE inhibitors probably have similar renal protective effects.

Enalapril (Vasotec)


Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.


Angiotensin Receptor Antagonist

Class Summary

Angiotensin II receptor antagonists may be considered if ACE inhibitors are not tolerated.

Losartan (Cozaar)


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, does not affect the response to bradykinin, and is less likely to be associated with cough and angioedema. For patients unable to tolerate ACE inhibitors.

Angiotensin II receptor blockers reduce blood pressure and proteinuria, protecting renal function, and delaying onset of end-stage renal disease.


Immunosuppressant Agent

Class Summary

Limited data exist for use of mycophenolate mofetil (MMF). A short course (< 6 months) of MMF in patients with persistent proteinuria (>1.5 g/d) and well-maintained renal function (serum creatinine < 1.5 mg/dL) despite maximum ACE inhibitor/ARB therapy may be considered in patients with mild renal histopathology on biopsy.

Mycophenolate (CellCept)


Inhibits inosine monophosphate dehydrogenase (IMPDH) and suppresses de novo purine synthesis by lymphocytes, thereby inhibiting their proliferation. Inhibits antibody production.

Two formulations are available and are not interchangeable. The original formulation, mycophenolate mofetil (MMF, Cellcept) is a prodrug that once hydrolyzed in vivo, releases the active moiety mycophenolic acid. A newer formulation, mycophenolic acid (MPA, Myfortic) is an enteric-coated product that delivers the active moiety.

Contributor Information and Disclosures

Mohammad Ilyas, MD, FAAP Assistant Professor of Pediatrics, University of Florida College of Medicine; Consulting Staff, Department of Pediatrics, Section of Nephrology, Wolfson Children Hospital and Shands Hospital Jacksonville

Mohammad Ilyas, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American Society of Nephrology

Disclosure: Nothing to disclose.


Richard Neiberger, MD, PhD Director of Pediatric Renal Stone Disease Clinic, Associate Professor, Department of Pediatrics, Division of Nephrology, University of Florida College of Medicine and Shands Hospital

Richard Neiberger, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Federation for Medical Research, American Medical Association, American Society of Nephrology, American Society of Pediatric Nephrology, Christian Medical and Dental Associations, Florida Medical Association, International Society for Peritoneal Dialysis, International Society of Nephrology, National Kidney Foundation, New York Academy of Sciences, Shock Society, Sigma Xi, Southern Medical Association, Southern Society for Pediatric Research, Southwest Pediatric Nephrology Study Group

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Adrian Spitzer, MD Clinical Professor Emeritus, Department of Pediatrics, Albert Einstein College of Medicine

Adrian Spitzer, MD is a member of the following medical societies: American Academy of Pediatrics, American Federation for Medical Research, American Pediatric Society, American Society of Nephrology, American Society of Pediatric Nephrology, International Society of Nephrology, Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Craig B Langman, MD The Isaac A Abt, MD, Professor of Kidney Diseases, Northwestern University, The Feinberg School of Medicine; Division Head of Kidney Diseases, The Ann and Robert H Lurie Children's Hospital of Chicago

Craig B Langman, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Nephrology, International Society of Nephrology

Disclosure: Received income in an amount equal to or greater than $250 from: Alexion Pharmaceuticals; Raptor Pharmaceuticals; Eli Lilly and Company; Dicerna<br/>Received grant/research funds from NIH for none; Received grant/research funds from Raptor Pharmaceuticals, Inc for none; Received grant/research funds from Alexion Pharmaceuticals, Inc. for none; Received consulting fee from DiCerna Pharmaceutical Inc. for none.

Additional Contributors

Deogracias Pena, MD Medical Director of Dialysis, Medical Director of Pediatric Nephrology and Transplantation, Cook Children's Medical Center; Clinical Associate Professor, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Medical Director of Pediatric Nephrology, Florida Hospital for Children

Deogracias Pena, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society of Pediatric Nephrology

Disclosure: Nothing to disclose.

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Glomerulus with mesangial hypercellularity and intact capillary loops. Trichrome Stain, original magnification 400x. Image courtesy of Patrick D Walker, MD.
Mesangial deposits of immunoglobulin A (IgA). Fluoresceinated Anti-IgA Antibody, Immunofluorescence microscopy, original magnification 400x. Image courtesy of Patrick D Walker, MD.
Electron photomicrograph showing mesangial electron dense deposits (arrow). Uranyl acetate and lead citrate stain, original magnification 12,000x. Image courtesy of Patrick D Walker, MD.
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