Pediatric IgA Nephropathy Medication

  • Author: Mohammad Ilyas, MD, FAAP; Chief Editor: Craig B Langman, MD   more...
 
Updated: Aug 3, 2010
 

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.

Next

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.

Previous
Next

Fish oil

Class Summary

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

View full drug information

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.

Previous
Next

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.

View full drug information

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.

Previous
Next

Angiotensin Receptor Antagonist

Class Summary

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

View full drug information

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.

Previous
Next

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.

View full drug information

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.

Previous
Proceed to Follow-up
 
 
Contributor Information and Disclosures
Author

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 and American Society of Nephrology

Disclosure: Nothing to disclose.

Coauthor(s)

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 & Dental Society, 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, and Southwest Pediatric Nephrology Study Group

Disclosure: The Osler Institute Honoraria Speaking and teaching

Specialty Editor Board

Deogracias Pena, MD  Medical Director of Dialysis, Department of Pediatrics, Cook Children's Medical Center; Clinical Associate Professor, Texas Tech University School of Medicine

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

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Pharmacy Editor, eMedicine

Disclosure: Nothing to disclose.

Adrian Spitzer, MD  Professor, Department of Pediatrics, Albert Einstein College of Medicine; Director of NIH Training Program, Children's Hospital at Montefiore Medical Center

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, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Howard Trachtman, MD  Program Director, Pediatrics Research, Schneider Children's Hospital, Department of Pediatrics, Division of Nephrology, Professor, Albert Einstein College of Medicine

Howard Trachtman, MD is a member of the following medical societies: American Society of Hypertension, American Society of Nephrology, American Society of Pediatric Nephrology, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

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

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

Disclosure: Merck Grant/research funds None; NIH Grant/research funds None; Raptor Pharmaceuticals, Inc Grant/research funds None; Alexion Pharmaceuticals, Inc. Grant/research funds None

References

  1. D'Amico G. Natural history of idiopathic IgA nephropathy and factors predictive of disease outcome. Semin Nephrol. May 2004;24(3):179-96. [Medline].

  2. [Best Evidence] Li LS; Liu ZH. Epidemiologic data of renal diseases from a single unit in China: analysis based on 13,519 renal biopsies. Kidney Int. Sep 2004;66(3):920-3. [Medline].

  3. Xie L, Wang L, Huang J, Fan J. IgA1 aberrant glycosylation in the pathogenesis of IgA nephropathy: an overivew. Sheng Wu Yi Xue Gong Cheng Xue Za Zhi. Feb 2010;27(1):227-30. [Medline].

  4. [Guideline] Cattran DC, Coppo R, Cook HT, et al. The Oxford classification of IgA nephropathy: rationale, clinicopathological correlations, and classification. Kidney Int. Sep 2009;76(5):534-45. [Medline].

  5. Lai FM, Szeto CC, Choi PC, et al. Characterization of early IgA nephropathy. Am J Kidney Dis. Oct 2000;36(4):703-8. [Medline].

  6. Dillon JJ. Treating IgA nephropathy. J Am Soc Nephrol. Apr 2001;12(4):846-7. [Medline].

  7. Donadio JV Jr, Grande JP. Immunoglobulin A nephropathy: a clinical perspective. J Am Soc Nephrol. Aug 1997;8(8):1324-32. [Medline].

  8. Yoshikawa N, Ito H, Sakai T, et al. A controlled trial of combined therapy for newly diagnosed severe childhood IgA nephropathy. The Japanese Pediatric IgA Nephropathy Treatment Study Group. J Am Soc Nephrol. Jan 1999;10(1):101-9. [Medline].

  9. Yoshikawa N, Tanaka R, Iijima K. Pathophysiology and treatment of IgA nephropathy in children. Pediatr Nephrol. May 2001;16(5):446-57. [Medline].

  10. Hotta O, Furuta T, Chiba S, et al. Regression of IgA nephropathy: a repeat biopsy study. Am J Kidney Dis. Mar 2002;39(3):493-502. [Medline].

  11. Frisch G, Lin J, Rosenstock J, Markowitz G, et al. Mycophenolate mofetil (MMF) vs placebo in patients with moderately advanced IgA nephropathy: a double-blind randomized controlled trial. Nephrol Dial Transplant. Oct 2005;20(10):2139-45. [Medline].

  12. Maes BD, Oyen R, Claes K, et al. Mycophenolate mofetil in IgA nephropathy: results of a 3-year prospective placebo-controlled randomized study. Kidney Int. May 2004;65(5):1842-9. [Medline].

  13. Tang S, Leung JC, Chan LY, et al. Mycophenolate mofetil alleviates persistent proteinuria in IgA nephropathy. Kidney Int. Aug 2005;68(2):802-12. [Medline].

  14. Chen X, Chen P, Cai G, et al. [A randomized control trial of mycophenolate mofeil treatment in severe IgA nephropathy]. Zhonghua Yi Xue Za Zhi. Jun 25 2002;82(12):796-801. [Medline].

  15. Odum J, Peh CA, Clarkson AR, et al. Recurrent mesangial IgA nephritis following renal transplantation. Nephrol Dial Transplant. 1994;9(3):309-12. [Medline].

  16. Park SB, Joo I, Suk J, et al. IgA nephropathy in renal transplant recipients: is it a significant cause of allograft failure?. Transplant Proc. Jun 1996;28(3):1540-2. [Medline].

  17. Wang AY, Lai FM, Yu AW, et al. Recurrent IgA nephropathy in renal transplant allografts. Am J Kidney Dis. Sep 2001;38(3):588-96. [Medline].

  18. MG Radford Jr, JV Donadio Jr, EJ Bergstralh and JP Grande. Predicting renal outcome in IgA nephropathy. J Am Soc Nephrol. Feb 1997;8(2):199-207. [Medline].

  19. D'Amico G. Natural history of idiopathic IgA nephropathy and factors predictive of disease outcome. Semin Nephrol. May 2004;24(3):179-96. [Medline].

  20. Donadio JV Jr, Larson TS, Bergstralh EJ, Grande JP. A randomized trial of high-dose compared with low-dose omega-3 fatty acids in severe IgA nephropathy. J Am Soc Nephrol. Apr 2001;12(4):791-9. [Medline]. [Full Text].

  21. Emancipator SN. IgA nephropathy: morphologic expression and pathogenesis. Am J Kidney Dis. Mar 1994;23(3):451-62. [Medline].

  22. Floege J, Feehally J. IgA nephropathy: recent developments. J Am Soc Nephrol. Dec 2000;11(12):2395-403. [Medline].

  23. Galla JH. IgA nephropathy. Kidney Int. Feb 1995;47(2):377-87. [Medline].

  24. Galla JH. IgA nephropathy. Kidney Int. Feb 1995;47(2):377-87. [Medline].

  25. Kobayashi Y, Sano T, Nakamura I, et al. Long-term effect of 2-year steroid therapy in progressive IgA nephropathy: A 30-year follow-up study compared with a non-steroid group. Nephrology (Carlton). Jan 2003;8 Suppl 4:A113-4. [Medline].

  26. Oortwijn BD, Rastaldi MP, Roos A, Mattinzoli D, Daha MR, van Kooten C. Demonstration of secretory IgA in kidneys of patients with IgA nephropathy. Nephrol Dial Transplant. Jun 2007;22(11):3191-5. [Medline]. [Full Text].

  27. [Best Evidence] Simon P; Ramee MP; Boulahrouz R; Stanescu C; Charasse C; Ang KS; Leonetti F; Cam G; Laruelle E; Autuly V; Rioux N. Epidemiologic data of primary glomerular diseases in western France. Kidney Int. Sep 2004;66(3):905-8. [Medline].

  28. IgA nephropathy. In: van Es LA, Massery SG, Glassock RJ, eds. Textbook of Nephrology. Vol 1. 2001:733-41.

  29. Wardle EN. Is IgA nephropathy induced by hyperproduction of interferon-alpha?. Med Hypotheses. 2004;62(4):625-8. [Medline].

  30. White RHR, Yoshikawa N, Freehally J. IgA nephropathy and Henoch-Schonlein nephritis. In: Barratt TM, Avner ED, Harmon WE, eds. Pediatric Nephrology. 4th ed. Baltimore, MD: Lippincott, Williams & Wilkins; 1999:691-706.

 
Previous
Next
 
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.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.