Lupus Nephritis Medication

  • Author: Lawrence H Brent, MD; Chief Editor: Vecihi Batuman, MD, FACP, FASN   more...
 
Updated: May 11, 2012
 

Medication Summary

Corticosteroids are used in all patients with clinically significant renal disease. Immunosuppressive agents, particularly cyclophosphamide, azathioprine, and mycophenolate mofetil, are used in patients with aggressive renal lesions because they improve the renal outcome. They may also be used in patients with inadequate response or excessive toxicity to corticosteroids. Cyclosporine has been used in some cases.

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Corticosteroids

Class Summary

Corticosteroids are very useful in controlling acute inflammatory manifestations of systemic lupus erythematosus (SLE). Alone, they may be adequate in treating milder forms of lupus nephritis with a lower risk of progressive renal dysfunction, such as minimal mesangial lupus nephritis, mesangial proliferative lupus nephritis, early focal lupus nephritis, or membranous lupus nephritis. Oral corticosteroids can be used in most patients. If adequate absorption is a concern (eg, bowel edema in a patient with nephrosis), intravenous (IV) methylprednisolone can be used.

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Prednisone

 

Prednisone is commonly used to treat inflammatory manifestations of SLE. Treatment of clinically significant lupus nephritis should include moderate-to-high doses initially.

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Methylprednisolone (Medrol, Solu-Medrol, A-Methapred)

 

Methylprednisolone is used in much the same manner as prednisone, but it has less mineralocorticoid effects and should be considered in patients with edema. The parenteral IV dosage form is used in the inpatient setting.

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Immunosuppressives

Class Summary

In particular, cyclophosphamide, mycophenolate, and azathioprine are used in patients with aggressive renal lesions (eg, focal or diffuse lupus nephritis) because they improve renal outcome. These agents can also be used in patients with inadequate response or excessive toxicity to corticosteroids. Mycophenolate mofetil has been shown to be effective for treatment of lupus nephritis. Mycophenolate mofetil was found to be superior to azathioprine in maintaining control and preventing relapses of lupus nephritis in patients who have responded to induction therapy.[48]

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Cyclophosphamide

 

Cyclophosphamide is indicated for treatment of most patients with focal lupus nephritis or diffuse lupus nephritis. Although it has significant toxicity, it has been shown to prevent the progression of nephritis and improve renal outcome.

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Azathioprine (Imuran, Azasan)

 

Azathioprine is useful in moderate-to-severe lupus nephritis. It improves renal outcome, but it does not appear to be as effective as cyclophosphamide, although it is less toxic.

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Mycophenolate mofetil (CellCept) or mycophenolic acid (Myfortic)

 

Mycophenolate mofetil is an option for induction therapy with class II/IV lupus nephritis. It has generally been well tolerated and, in several studies, has been as effective as (and possibly more effective than) more traditional therapies, including cyclophosphamide and azathioprine, with less toxicity. The American College of Rheumatology guidelines recommend mycophenolate mofetil as the preferred agent for African Americans and Hispanics.

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Hydroxychloroquine (Plaquenil)

 

The exact anti-inflammatory mechanism of action of hydroxychloroquine is not well understood. It is thought to elicit anti-inflammatory effects in vivo by antagonizing histamine and serotonin and inhibits prostaglandin synthesis. In vitro studies suggest hydroxychloroquine may inhibit chemotaxis of PMN leukocytes, macrophages, and eosinophils. The American College of Rheumatology guidelines recommend that all patients with SLE and nephritis be treated with a background of hydroxychloroquine, unless contraindicated.

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Contributor Information and Disclosures
Author

Lawrence H Brent, MD  Associate Professor of Medicine, Jefferson Medical College of Thomas Jefferson University; Chair, Program Director, Department of Medicine, Division of Rheumatology, Albert Einstein Medical Center

Lawrence H Brent, MD is a member of the following medical societies: American Association for the Advancement of Science, American Association of Immunologists, American College of Physicians, and American College of Rheumatology

Disclosure: Abbott Honoraria Speaking and teaching; Centocor Consulting fee Consulting; Genentech Grant/research funds Other; HGS/GSK Honoraria Speaking and teaching; Omnicare Consulting fee Consulting; Pfizer Honoraria Speaking and teaching; Roche Speaking and teaching; Savient Honoraria Speaking and teaching; UCB Honoraria Speaking and teaching

Coauthor(s)

Arati Karhadkar, MBBS  Fellow, Division of Rheumatology, Albert Einstein Medical Center

Disclosure: Nothing to disclose.

Eric Bloom, MD  Division Chief of Nephrology, Nephrology Fellowship Program Director, Attending Physician, Division of Nephrology, Department of Internal Medicine, Albert Einstein Medical Center

Eric Bloom, MD is a member of the following medical societies: American Society of Nephrology and National Kidney Foundation

Disclosure: Nothing to disclose.

Specialty Editor Board

Carlos J Lozada, MD  Director of Rheumatology Fellowship Program, Professor, Department of Medicine, Division of Rheumatology and Immunology, University of Miami, Leonard M Miller School of Medicine

Carlos J Lozada, MD is a member of the following medical societies: American College of Physicians and American College of Rheumatology

Disclosure: Pfizer Honoraria Speaking and teaching; Amgen Honoraria Speaking and teaching

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.

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 and editors of Medscape Reference gratefully acknowledge the contributions of previous author Irene Viola, MD, to the development and writing of the source article.

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Mesangial proliferative lupus nephritis with moderate mesangial hypercellularity. International Society of Nephrology/Renal Pathology Society 2003 class II (×200, hematoxylin-eosin).
Focal lupus nephritis. International Society of Nephrology/Renal Pathology Society 2003 class III (×100, hematoxylin-eosin).
Focal lupus nephritis. International Society of Nephrology/Renal Pathology Society 2003 class III (×200, immunofluorescence).
Diffuse lupus nephritis with hypertensive vascular changes. International Society of Nephrology/Renal Pathology Society 2003 class IV (×200, hematoxylin-eosin).
Diffuse lupus nephritis with early crescent formation. International Society of Nephrology/Renal Pathology Society 2003 class IV (×200, hematoxylin-eosin).
Diffuse lupus nephritis with extensive crescent formation (rapidly progressive glomerulonephritis). International Society of Nephrology/Renal Pathology Society 2003 class IV (×200, hematoxylin-eosin).
Membranous lupus nephritis. International Society of Nephrology/Renal Pathology Society 2003 class V (×200, hematoxylin-eosin).
Membranous lupus nephritis showing thickened glomerular basement membrane. International Society of Nephrology/Renal Pathology Society 2003 class V (×200, silver stain).
Advanced sclerosis lupus nephritis. International Society of Nephrology/Renal Pathology Society 2003 class VI (×100, hematoxylin-eosin).
Table 1. Genes Associated With Systemic Lupus Erythematosus
Gene LocusGene NameGene Product
1p13.2PTPN22Lymphoid-specific protein tyrosine phosphatase
1q21-q23CRPCRP
1q23FCGR2A, FCGR2BFcγRIIA (R131), FcγRIIB
1q23FCGR3A, FCGR3BFcγRIIIA (V176), FcγRIIIB
1q31-q32IL10IL-10
1q36.12C1QBC1q deficiency
2q32.2-q32.3STAT4Signal transducer and activator of transcription 4
2q33CTLA4Cytotoxic T-lymphocyte-associated protein 4 (CTLA-4)
6p21.3HLA-DRB1HLA-DRB1: DR2/*1501, DR3/*0301C1q deficiency
6p21.3C2, C4A, C4BC2, C4 deficiencies
6p21.3TNFTNF-a (promoter, -308)
10q11.2-q21MBL2Mannose-binding lectin
CRP = C-reactive protein; HLA = human leukocyte antigen; IL = interleukin; TNF = tumor necrosis factor.
Table 2. International Society of Nephrology/Renal Pathology Society 2003 Classification of Lupus Nephritis
Class I



Minimal mesangial lupus nephritis



Light microscopy findingsNormal
Immunofluorescence electron microscopy findingsMesangial immune deposits
Clinical manifestationsMild proteinuria
Class II



Mesangial proliferative lupus nephritis



Light microscopy findingsPurely mesangial hypercellularity or mesangial matrix expansion with mesangial immune deposits
Immunofluorescence electron microscopy findingsMesangial immune deposits; few immune deposits in subepithelial or subendothelial deposits possible
Clinical manifestationsMild renal disease such as asymptomatic hematuria or proteinuria that usually does not warrant specific therapy
Class III



Focal lupus nephritis



Class III (A)



Active lesions - Focal proliferative lupus nephritis



Class III (A/C)



Active and chronic lesions - Focal proliferative and sclerosing lupus nephritis



Class III (C)



Chronic inactive lesions - Focal sclerosing lupus nephritis



Light microscopy findingsActive or inactive focal, segmental, or global glomerulonephritis involving < 50% of all glomeruli
Immunofluorescence electron microscopy findingsSubendothelial and mesangial immune deposits
Clinical manifestationsActive generalized SLE and mild-to-moderate renal disease with hematuria and moderate proteinuria in many patients; worsening renal function in significant minority, potentially progressing to class IV lupus nephritis
Class IV



Diffuse lupus nephritis



Class IV-S (A)



Active lesions - Diffuse segmental proliferative lupus nephritis



Class IV-G (A)



Active lesions - Diffuse global proliferative lupus nephritis



Class IV-S (A/C)



Active and chronic lesions - Diffuse segmental proliferative and sclerosing lupus nephritis



Class IV-G (A/C)



Active and chronic lesions - Diffuse global proliferative and sclerosing lupus nephritis



Class IV-S (C)



Chronic inactive lesions with scars - Diffuse segmental sclerosing lupus nephritis



Class IV-G (C)



Chronic inactive lesions with scars - Diffuse global sclerosing lupus nephritis



Light microscopy findingsActive or inactive diffuse, segmental or global glomerulonephritis involving = 50% of all glomeruli; subdivided into diffuse segmental (class IV-S) when = 50% of involved glomeruli have segmental lesions (involving less than half of glomerular tuft) and diffuse global (class IV-G) when = 50% of involved glomeruli have global lesions
Immunofluorescence electron microscopy findingsSubendothelial immune deposits
Clinical manifestationsClinical evidence of renal disease including hypertension, edema, active urinary sediment, worsening renal function, and nephrotic range proteinuria in most cases; active extrarenal SLE in many patients
Class V



Membranous lupus nephritis



Light microscopy findingsDiffuse thickening of glomerular basement membrane without inflammatory infiltrate; possibly, subepithelial deposits and surrounding basement membrane spikes on special stains, including silver and trichrome; may occur in combination with class II or IV; may show advanced sclerosis
Immunofluorescence electron microscopy findingsSubepithelial and intramembranous immune deposits; subendothelial deposits present only when associated proliferative component is present
Clinical manifestationsClinical and laboratory features of nephrotic syndrome, usually without manifestations of active SLE
Class VI



Advanced sclerosis lupus nephritis



Light microscopy findingsAdvanced glomerular sclerosis involving = 90% of glomeruli, interstitial fibrosis, and tubular atrophy, all morphological manifestations of irreversible renal injury
Clinical manifestationsSignificant renal insufficiency or end-stage renal disease in most cases; unlikely to respond to medical therapy
SLE = systemic lupus erythematosus.
Table 3. Active and Chronic Glomerular Lesions
Activity IndexChronicity Index
• Endocapillary hypercellularity with or without leukocyte infiltration; luminal reduction



• Karyorrhexis



• Fibrinoid necrosis



• Rupture of glomerular basement membrane



• Cellular or fibrocellular crescents



• Subendothelial deposits on light microscopy



• Intraluminal immune aggregates



• Glomerular sclerosis; segmental, global



• Fibrous adhesion



• Fibrous crescents



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