Diffuse Proliferative Glomerulonephritis Medication

  • Author: Moro O Salifu, MD, MPH, FACP; Chief Editor: Vecihi Batuman, MD, FACP, FASN   more...
 
Updated: Jan 12, 2012
 

Medication Summary

Corticosteroids and cytotoxic therapy can induce remission. Corticosteroids are potent anti-inflammatory agents and immunosuppressants. These drugs suppress cellular and humoral response to tissue injury, thereby reducing inflammation. Oral prednisone generally is required for maintenance therapy. Cytotoxic drugs induce alkylation of DNA.

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Corticosteroids

Class Summary

Have anti-inflammatory (glucocorticoid) and salt-retaining (mineralocorticoid) properties. Glucocorticoids have profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli.

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Prednisone (Deltasone, Orasone, Meticorten, Sterapred)

 

Most patients require long-term oral prednisone after inducing remission. Immunosuppressants for treatment of autoimmune disorders may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

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Methylprednisolone (Solu-Medrol)

 

For pulse therapy. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.

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Cytotoxins

Class Summary

Inhibit cell growth and proliferation.

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Cyclophosphamide (Cytoxan)

 

DOC in DPGN. Chemically related to nitrogen mustards. 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.

Low dose is used when creatinine clearance is < 33 mL/min.

Maintain white blood cell count >2000/mL.

A dose of 50-100 mg/m2 PO qd is associated with a higher incidence of hemorrhagic cystitis.

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Mycophenolate (CellCept, Myfortic)

 

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.

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Contributor Information and Disclosures
Author

Moro O Salifu, MD, MPH, FACP  Associate Professor, Department of Internal Medicine, Chief, Division of Nephrology, Director of Nephrology Fellowship Program and Transplant Nephrology, State University of New York Downstate Medical Center

Moro O Salifu, MD, MPH, FACP is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Artificial Internal Organs, American Society of Diagnostic and Interventional Nephrology, American Society of Nephrology, American Society of Transplantation, and National Kidney Foundation

Disclosure: Nothing to disclose.

Coauthor(s)

Barbara G Delano, MD, MPH  Director of Home Hemodialysis and Peritoneal Dialysis, Professor, Department of Internal Medicine, Division of Nephrology, State University of New York at Brooklyn

Barbara G Delano, MD, MPH is a member of the following medical societies: American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, and Sigma Xi

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

Ajay K Singh, MB, MRCP, MBA  Associate Professor of Medicine, Harvard Medical School; Director of Dialysis, Renal Division, Brigham and Women's Hospital; Director, Brigham/Falkner Dialysis Unit, Faulkner Hospital

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.

References

  1. Xie Q, Liu Y, Liu G, Yang N, Yin G. Diffuse proliferative glomerulonephritis associated with dermatomyositis with nephrotic syndrome. Rheumatol Int. Apr 2010;30(6):821-5. [Medline].

  2. Vachvanichsanong P, Dissaneewate P, McNeil E. Diffuse proliferative glomerulonephritis does not determine the worst outcome in childhood onset lupus nephritis: a 23-year experience in a single centre. Nephrol Dial Transplant. Apr 25 2009;[Medline].

  3. Demircin G, Oner A, Erdogan O, et al. Long-term efficacy and safety of quadruple therapy in childhood diffuse proliferative lupus nephritis. Ren Fail. 2008;30(6):603-9. [Medline].

  4. Haas M, Rahman MH, Cohn RA, et al. IgA nephropathy in children and adults: comparison of histologic features and clinical outcomes. Nephrol Dial Transplant. Aug 2008;23(8):2537-45. [Medline].

  5. Sahin GM, Sahin S, Kantarci G, Ergin H. Mycophenolate mofetil treatment for therapy-resistant glomerulopathies. Nephrology (Carlton). 2007;Jun;12(3):285-8. [Medline].

  6. Opastirakul S, Chartapisak W. Pulse cyclophosphamide induction treatment in Thai children with diffuse proliferative lupus nephritis. Nephrology (Carlton). Dec 19 2011;[Medline].

  7. Tani C, Mosca M, d'Ascanio A, Neri R, Tavoni A, Carli L, et al. [Long term outcome of treatment of diffuse proliferative glomerulonephritis with pulse steroids and short course pulse cyclophosphamide]. Reumatismo. Jul-Sep 2010;62(3):215-20. [Medline].

  8. Ong LM, Hooi LS, Lim TO, et al. Randomized controlled trial of pulse intravenous cyclophosphamide versus mycophenolate mofetil in the induction therapy of proliferative lupus nephritis. Nephrology (Carlton). Oct 2005;10(5):504-10. [Medline].

  9. Jayne D. Current management of lupus nephritis: popular misconceptions. Lupus. 2007;16(3):217-20. [Medline].

  10. Chan TM, Li FK, Tang CS. Efficacy of mycophenolate mofetil in patients with diffuse proliferative lupus nephritis. Hong Kong-Guangzhou Nephrology Study Group. N Engl J Med. Oct 19 2000;343(16):1156-62. [Medline].

  11. Ginzler EM, Dooley MA, Aranow C, et al. Mycophenolate mofetil or intravenous cyclophosphamide for lupus nephritis. N Engl J Med. Nov 24 2005;353(21):2219-28. [Medline]. [Full Text].

  12. Kamijo Y, Hashimoto K, Takahashi K, Ehara T, Shigematsu H, Higuchi M. Treatment with cyclosporine A improves SLE disease activity of Japanese patients with diffuse proliferative lupus nephritis. Clin Nephrol. Aug 2011;76(2):136-43. [Medline].

  13. [Best Evidence] Bao H, Liu ZH, Xie HL, et al. Successful treatment of class V+IV lupus nephritis with multitarget therapy. J Am Soc Nephrol. Oct 2008;19(10):2001-10. [Medline].

  14. Glassock RJ. IgA nephropathy: challenges and opportunities. Cleve Clin J Med. 2008;Aug;75(8):569-76. [Medline]. [Full Text].

  15. Hiramatsu N, Kuroiwa T, Ikeuchi H, et al. Revised classification of lupus nephritis is valuable in predicting renal outcome with an indication of the proportion of glomeruli affected by chronic lesions. Rheumatology (Oxford). May 2008;47(5):702-7. [Medline].

  16. Aasarod K, Iversen BM, Hammerstrom J. Wegener's granulomatosis: clinical course in 108 patients with renal involvement. Nephrol Dial Transplant. May 2000;15(5):611-8. [Medline].

  17. Andrews M, Edmunds M, Campbell A. Systemic vasculitis in the 1980s--is there an increasing incidence of Wegener's granulomatosis and microscopic polyarteritis?. J R Coll Physicians Lond. Oct 1990;24(4):284-8. [Medline].

  18. Austin HA, Balow JE. Natural history and treatment of lupus nephritis. Semin Nephrol. Jan 1999;19(1):2-11. [Medline].

  19. Bosch X, Mirapeix E, Font J. [Neutrophil anticytoplasmic antibodies: their diagnostic utility in vasculitis and glomerulonephritis]. Med Clin (Barc). Mar 26 1994;102(11):412-7. [Medline].

  20. Chan TM, Tse KC, Tang CS, et al. Long-term study of mycophenolate mofetil as continuous induction and maintenance treatment for diffuse proliferative lupus nephritis. J Am Soc Nephrol. Apr 2005;16(4):1076-84. [Medline].

  21. Clark WF, Moist LM. Management of chronic renal insufficiency in lupus nephritis: role of proteinuria, hypertension and dyslipidemia in the progression of renal disease. Lupus. 1998;7(9):649-53. [Medline].

  22. Coppo R, Gianoglio B, Porcellini MG. Frequency of renal diseases and clinical indications for renal biopsy in children (report of the Italian National Registry of Renal Biopsies in Children). Group of Renal Immunopathology of the Italian Society of Pediatric Nephrology and Group of Renal. Nephrol Dial Transplant. Feb 1998;13(2):293-7. [Medline].

  23. D'Amico G. Natural history of idiopathic IgA nephropathy: role of clinical and histological prognostic factors. Am J Kidney Dis. Aug 2000;36(2):227-37. [Medline].

  24. Flanc RS, Roberts MA, Strippoli GF. Treatment of diffuse proliferative lupus nephritis: a meta-analysis of randomized controlled trials. Am J Kidney Dis. Feb 2004;43(2):197-208. [Medline].

  25. Frisch G, Lin J, Rosenstock J. 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.

  26. Garrett PJ, Dewhurst AG, Morgan LS. Renal disease associated with circulating antineutrophil cytoplasm activity. Q J Med. Oct 1992;85(306):731-49. [Medline].

  27. Golbus J, McCune WJ. Lupus nephritis. Classification, prognosis, immunopathogenesis, and treatment. Rheum Dis Clin North Am. Feb 1994;20(1):213-42. [Medline].

  28. Grotz W, Wanner C, Keller E. Crescentic glomerulonephritis in Wegener's granulomatosis: morphology, therapy, outcome. Clin Nephrol. Jun 1991;35(6):243-51. [Medline].

  29. Haas M. Histologic subclassification of IgA nephropathy: a clinicopathologic study of 244 cases. Am J Kidney Dis. Jun 1997;29(6):829-42. [Medline].

  30. Huong DL, Papo T, Beaufils H. Renal involvement in systemic lupus erythematosus. A study of 180 patients from a single center. Medicine (Baltimore). May 1999;78(3):148-66. [Medline].

  31. Ioannidis JP, Boki KA, Katsorida ME. Remission, relapse, and re-remission of proliferative lupus nephritis treated with cyclophosphamide. Kidney Int. Jan 2000;57(1):258-64. [Medline].

  32. Jindal KK. Management of idiopathic crescentic and diffuse proliferative glomerulonephritis: evidence-based recommendations. Kidney Int Suppl. Jun 1999;70:S33-40. [Medline].

  33. Kasinath BS, Neilson EG, Hebert L. Short-term prognosis of severe proliferative lupus nephritis. Am J Kidney Dis. Oct 1986;8(4):239-43. [Medline].

  34. Lim CS, Chin HJ, Jung YC. Prognostic factors of diffuse proliferative lupus nephritis. Clin Nephrol. Sep 1999;52(3):139-47. [Medline].

  35. Little MA, Pusey CD. Rapidly progressive glomerulonephritis: current and evolving treatment strategies. J Nephrol. Nov-Dec 2004;17 Suppl 8:S10-9.

  36. McCarty DJ, Manzi S, Medsger TA Jr. Incidence of systemic lupus erythematosus. Race and gender differences. Arthritis Rheum. Sep 1995;38(9):1260-70. [Medline].

  37. Mekhail TM, Hoffman GS. Longterm outcome of Wegener's granulomatosis in patients with renal disease requiring dialysis. J Rheumatol. May 2000;27(5):1237-40. [Medline].

  38. Nolin L, Courteau M. Management of IgA nephropathy: evidence-based recommendations. Kidney Int Suppl. Jun 1999;70:S56-62. [Medline].

  39. Polenakovic M, Grcevska L. Survival rate of patients with glomerulonephritis. Acta Med Croatica. 1992;46(1):15-20. [Medline].

  40. Research Group on Progressive Chronic Renal Disease. Nationwide and long-term survey of primary glomerulonephritis in Japan as observed in 1,850 biopsied cases. Research Group on Progressive Chronic Renal Disease. Nephron. 1999;82(3):205-13. [Medline].

  41. Shoji T, Nakanishi I, Suzuki A. Early treatment with corticosteroids ameliorates proteinuria, proliferative lesions, and mesangial phenotypic modulation in adult diffuse proliferative IgA nephropathy. Am J Kidney Dis. Feb 2000;35(2):194-201. [Medline].

  42. Tomino Y. IgA nephropathy. From molecules to men. Contrib Nephrol. 1999;126:III-IX, 1-115. [Medline].

  43. Wyatt RJ, Julian BA, Baehler RW. Epidemiology of IgA nephropathy in central and eastern Kentucky for the period 1975 through 1994. Central Kentucky Region of the Southeastern United States IgA Nephropathy DATABANK Project. J Am Soc Nephrol. May 1998;9(5):853-8. [Medline].

  44. Yahya TM, Pingle A, Boobes Y. Analysis of 490 kidney biopsies: data from the United Arab Emirates Renal Diseases Registry. J Nephrol. May-Jun 1998;11(3):148-50. [Medline].

 
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Light microscopy (trichrome stain) shows globally increased cellularity, numerous polymorphonuclear cells, cellular crescent (at left of photomicrograph) and fibrinoid necrosis (brick red staining at right of photomicrograph). These findings are characteristic of diffuse proliferative glomerulonephritis.
Diffuse proliferative glomerulonephritis (DPGN). Immunofluorescent microscopy shows (except for anti–glomerular basement membrane [GBM] disease) a granular deposition of immunoglobulins, complement, and fibrin along the GBM, tubular basement membranes, and peritubular capillaries (image 2a). Linear deposition occurs in the GBM in anti-GBM disease (image 2b).
Diffuse proliferative glomerulonephritis (DPGN). Using electron microscopy, electron-dense deposits are visible in the mesangial, subendothelial, intramembranous, and subepithelial locations.
 
 
 
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