eMedicine Specialties > Rheumatology > Systemic Rheumatic Disease

Nephritis, Lupus: Treatment & Medication

Author: Lawrence H Brent, MD, Associate Professor of Medicine, Thomas Jefferson University; Chair, Program Director, Department of Medicine, Division of Rheumatology, Albert Einstein Medical Center
Coauthor(s): Arati Karhadkar, MBBS, Fellow, Division of Rheumatology, Albert Einstein Medical Center, Philadelphia, PA; Eric Bloom, MD, Attending Physician, Division of Nephrology, Department of Internal Medicine; Division Chief, Nephrology; Nephrology Fellowship Program Director, Albert Einstein Medical Center
Contributor Information and Disclosures

Updated: Jun 23, 2009

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Treatment

Medical Care

  • General4,29
    • The principal goal of therapy in lupus nephritis is to normalize renal function or, at least, to prevent the progressive loss of renal function. Therapy differs depending on the pathologic lesion.
    • Strongly consider renal biopsy in patients who present with lupus nephritis.
    • Assess activity and chronicity indices.
    • Treat extrarenal manifestations and other variables that may affect the kidneys.
  • Medications30,29
    • Corticosteroid therapy should be instituted if the patient has clinically significant renal disease. Use immunosuppressive agents, particularly cyclophosphamide, azathioprine, or mycophenolate mofetil, if the patient has aggressive proliferative renal lesions, as they improve the renal outcome. They can also be used if the patient has an inadequate response or excessive sensitivity to corticosteroids.31
    • Treat hypertension aggressively. Consider angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) if the patient has significant proteinuria without significant renal insufficiency.
    • Restrict fat intake or use lipid-lowering therapy such as statins for hyperlipidemia secondary to nephrotic syndrome.
    • Restrict protein intake if renal function is significantly impaired.
    • Administer calcium supplementation to prevent osteoporosis if the patient is on long-term corticosteroid therapy and consider adding a bisphosphonate.
    • Avoid drugs that affect renal function, including nonsteroidal anti-inflammatory drugs (NSAIDs), especially in patients with elevated creatinine levels. Nonacetylated salicylates can be used to safely treat inflammatory symptoms in patients with renal disease.
    • Patients with active lupus nephritis should avoid pregnancy, as it may worsen their renal disease.
    • Patients with end-stage renal disease, sclerosis, and a high chronicity index based on renal biopsy findings are unlikely to respond to aggressive therapy. In these cases, focus therapy on extrarenal manifestations of systemic lupus erythematosus (SLE) and on possible kidney transplantation.
  • Therapies for specific types of lupus nephritis based on renal pathology4
    • Class I: Minimal mesangial lupus nephritis require no specific therapy.
    • Class II: Mesangial proliferative lupus nephritis may require treatment if proteinuria is greater than 1000 mg/d. Consider prednisone in low-to-moderate doses (ie, 20-40 mg/d) for 1-3 months, with subsequent taper.
    • Classes III and IV: Patients with either focal or diffuse lupus nephritis are at high risk of progressing to end-stage renal disease and require aggressive therapy.
      • Administer prednisone 1 mg/kg/d for at least 4 weeks, depending on clinical response. Then, taper it gradually to a daily maintenance dose of 5-10 mg/d for approximately 2 years. In acutely ill patients, intravenous methylprednisolone of up to 1000 mg/d for 3 days may be used to initiate corticosteroid therapy.
      • Use immunosuppressive drugs in addition to corticosteroids in patients who do not respond to corticosteroids alone, who have unacceptable toxicity to corticosteroids, who have worsening renal function, who have severe proliferative lesions, or who have evidence of sclerosis on renal biopsy specimens. Both cyclophosphamide and azathioprine are effective in proliferative lupus nephritis, although cyclophosphamide is apparently more effective in preventing progression to end-stage renal disease. Mycophenolate mofetil has been shown to be effective in treating these patients and may be used alone32,33 or sequentially after a 6-month course of intravenous cyclophosphamide.34
      • Recently, Appel et al (2009) studied 370 patients with lupus nephritis in a randomized open-label study comparing mycophenolate mofetil and intravenous cyclophosphamide. The study included induction and maintenance therapy, and both groups received prednisone. No significant difference in clinical improvement was observed with mycophenolate mofetil compared with intravenous cyclophosphamide.35
      • Administer intravenous cyclophosphamide monthly for 6 months and every 2-3 months thereafter, depending on clinical response. The usual duration of therapy is 2-2.5 years. Reduce the dose if the creatinine clearance is less than 30 mL/min. Adjust the dose depending on the hematologic response.36,37 Gonadotropin-releasing hormone analog, leuprolide acetate, protects against ovarian failure.38
      • Azathioprine can also be used as a second-line agent, with dose adjustments depending on hematologic response.
      • Mycophenolate mofetil is useful in patients with focal or diffuse lupus nephritis and has been shown to be at least as effective as intravenous cyclophosphamide with less toxicity in patients with stable renal function.32,33
    • Class V: Patients with membranous lupus nephritis are generally treated with prednisone for 1-3 months, followed by tapering for 1-2 years if a response occurs. If no response occurs, the drug is discontinued. Immunosuppressive drugs are generally not used unless renal function worsens or a proliferative component is present on renal biopsy samples. Some clinical evidence indicates that azathioprine, cyclophosphamide, cyclosporine, and chlorambucil are effective in reducing proteinuria. Mycophenolate mofetil may also be effective.
  • Investigational therapies for lupus nephritis and SLE
    • Rituximab, a B-lymphocyte–depleting therapy, appears to be effective in SLE and is being investigated as a treatment for SLE and lupus nephritis. Several small case series of rituximab have shown benefit in SLE and lupus nephritis.39,40,41,42 Initial results of a large placebo-controlled, double-blind study of rituximab in SLE without nephritis failed to meet any clinical endpoints. A similar study in lupus nephritis is in progress.
    • Other therapies under investigation for SLE and lupus nephritis include the following:31,43,44,45
      • B-cell–depleting agents - Other anti-CD20 monoclonal antibodies such as ocrelizumab (humanized) and ofatumumab (human), epratuzumab (anti-CD22 monoclonal antibody), and TRU-015 (anti-CD20 small modular immunopharmaceutical [SMIP])43
      • B-cell cytokine inhibitors, which inhibit B cell activation and proliferation - Belimumab (anti–B-lymphocyte stimulator [BLyS] monoclonal antibody), atacicept (TACI-Ig fusion protein that inhibits BLyS and a proliferation-inducing ligand [APRIL])45
      • Abetimus - B-lymphocyte tolerogen that was found to be ineffective in preventing flares of lupus nephritis in a large controlled trial, although it did reduce levels of anti-DNA antibodies44
      • Other potential therapies - Anti-cytokine therapies, including monoclonal antibodies directed against interferon-alpha, IL-1, IL-6, IL-10, and TNF-alpha, among others45
  • End-stage renal disease
    • Patients with end-stage renal disease require dialysis and are good candidates for kidney transplantation.
    • Patients with end-stage renal disease secondary to SLE represent 1.5% of all patients on dialysis in the United States. The survival rate among patients on dialysis is fair (ie, 5-y survival rate of 60-70%) and is comparable with patients on dialysis who do not have SLE.
    • Hemodialysis is preferred over peritoneal dialysis; several studies have documented higher anti-dsDNA levels, more thrombocytopenia, and higher steroid requirements in patients with SLE and end-stage renal disease who are on peritoneal dialysis. Hemodialysis also has anti-inflammatory effects with decreased T-helper lymphocyte levels. SLE is generally quiescent in patients on hemodialysis, although flares, including rash, arthritis, serositis, fever, and leukopenia may occur, requiring specific treatment.

Surgical Care

  • Patients with SLE account for 3% of all renal transplantations in the United States.
  • Ensure that the patient does not have active SLE disease at the time of transplantation.
  • A 3-month period of dialysis is usually prudent to prevent spontaneous renal recovery.
  • Substantial evidence shows that patients with SLE fare worse than patients without SLE in terms of graft survival. Living-related allografts show better outcomes than cadaveric allografts.
  • In patients with SLE, reasons for a more severe outcome after transplantation include recurrent lupus nephritis and concomitant antiphospholipid antibody syndrome resulting in allograft loss.

Consultations

  • Nephrologist (for renal biopsy or, if desired, for help in management of renal disease)
  • Pathologist (for renal biopsy): The experience of pathologists in reading lupus nephritis biopsy specimens varies considerably. The most consistent readers are usually found in larger academic centers with substantial populations of patients with SLE.

Diet

Alter the diet according to the presence of hypertension, hyperlipidemia, and renal insufficiency.

Medication

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.

Corticosteroids

These agents are very useful in controlling acute inflammatory manifestations of systemic lupus erythematosus (SLE). Corticosteroids alone 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 methylprednisolone can be used.


Prednisone (Deltasone, Orasone, Sterapred)

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

Adult

40-60 mg/d PO; taper as clinical condition improves

Pediatric

0.5-1 mg/kg/d PO qd; taper as clinical condition improves

May cause water and salt retention, exacerbating hypertension and increasing requirement for antihypertensive drugs in hypertensive patients; may aggravate hyperglycemia, increasing requirement for hypoglycemic agents in patients with diabetes; metabolism may be increased by drugs that induce hepatic microsomal enzymes, including phenytoin, phenobarbital, carbamazepine, and rifampin, thus increasing corticosteroid requirements

No absolute contraindications; severe bacterial, viral, or fungal infection; active peptic ulcer disease; diabetes mellitus

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Toxicities include weight gain, dyspepsia, mood changes, infection, peptic ulcer disease, hypertension, diabetes mellitus, osteoporosis, avascular necrosis, cataracts, glaucoma, myopathy, and skin changes; growth retardation in children; abrupt discontinuation may result in adrenal crisis


Methylprednisolone (Medrol, Solu-Medrol)

Used in a similar manner to prednisone but has less mineralocorticoid effects and should be considered in patients with edema. Parenteral IV dosage form is used in the inpatient setting.

Adult

40-60 mg/d PO qd, taper as clinical condition improves
Alternatively, 30 mg/kg/d IV for 3 d

Pediatric

0.5-1 mg/kg/d PO qd, taper as clinical condition improves
Alternatively, administer IV as in adults

May cause water and salt retention, exacerbating hypertension and increasing requirement for antihypertensive drugs in hypertensive patients (less likely to do this than prednisone); may aggravate hyperglycemia, increasing requirement for hypoglycemic agents in patients with diabetes; metabolism may be increased by drugs that induce hepatic microsomal enzymes, including phenytoin, phenobarbital, carbamazepine, and rifampin, thus increasing corticosteroid requirements

No absolute contraindications; severe bacterial, viral, or fungal infection; active peptic ulcer disease; diabetes mellitus

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Toxicities include weight gain, dyspepsia, mood changes, infection, peptic ulcer disease, hypertension, diabetes mellitus, osteoporosis, avascular necrosis, cataracts, glaucoma, myopathy, and skin changes; growth retardation in children; abrupt discontinuation may result in adrenal crisis

Immunosuppressives

In particular, cyclophosphamide and azathioprine are used in patients with aggressive renal lesions (eg, focal lupus nephritis, 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.


Cyclophosphamide (Cytoxan)

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

Adult

500-1000 mg/m2 IV qmo; adjust dose depending on clinical response, hematologic response, and toxicity; reduce dose to 500 mg/m2 if CrCl is <30 ml/min; after 6 mo, administer q2-3mo for 2-2.5 y; usually administered with antiemetic agents and may be administered with mesna

Pediatric

Administer as in adults

Long-term high-dose phenobarbital therapy may increase metabolism to its active metabolite, increasing toxicity; inhibits cholinesterase activity for up to 10 d after an intravenous dose, which can potentiate effects of succinylcholine chloride

Documented hypersensitivity; infection; severely depressed bone marrow function; severe cytopenias

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Toxicities include nausea and vomiting, leukopenia, thrombocytopenia, anemia, infection, alopecia, hemorrhagic cystitis, infertility, teratogenicity, and risk of malignancy


Azathioprine (Imuran)

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

Adult

2-3 mg/kg/d PO single or divided dose
Initial: 1 mg/kg/d; increase depending on clinical and hematologic response and toxicity

Pediatric

Administer as in adults

When administered with allopurinol, decrease dose by 65-75% because azathioprine is metabolized by xanthine oxidase; may cause anemia or severe leukopenia in combination with ACE inhibitors; may reduce anticoagulant effect of warfarin

Documented hypersensitivity; active infection (relative); severe cytopenias (relative)

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Nausea and vomiting, leukopenia, thrombocytopenia, anemia, infection, and abnormal liver function test results may occur


Mycophenolate mofetil (CellCept) or mycophenolic acid (Myfortic)

Has been shown useful in mild-to-moderate lupus nephritis in several recent studies. Has generally been well tolerated and, in these studies, has been as effective (possibly more effective) as more traditional therapies including cyclophosphamide and azathioprine, with less toxicity.

Adult

Mycophenolate mofetil: 1000 mg PO bid; starting dose is 500 mg/d PO and titrated up to 1000 mg PO bid over 2 mo as tolerated; may increase to 3000 mg/d in occasional patients; doses >2000 mg/d should be avoided in patients with significant renal impairment
Mycophenolic acid: 720 mg PO bid; starting dose is 720 mg/d PO and titrated up to 720 mg PO bid

Pediatric

Mycophenolate mofetil: 600 mg/m2 PO bid; titrate to maximum of 1000 mg PO bid over 2 mo
Mycophenolic acid: 400 mg/m2 PO bid; titrate to a maximum of 720 mg PO bid over 2 mo

Antacids that contain magnesium and aluminum may reduce absorption when administered simultaneously; live attenuated vaccines should be avoided during therapy

Documented hypersensitivity; active infection (relative); severe cytopenias (relative)

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Nausea, vomiting, and other GI symptoms may occur; anemia and leukopenia are not uncommon; patients may be at risk for opportunistic infections, most likely viral; occasionally, abnormal LFT results may occur

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References
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Further Reading

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Keywords

lupus nephritis, systemic lupus erythematosus, SLE, end-stage renal disease, ESRD, end-stage kidney disease, chronic kidney disease, chronic renal disease, chronic renal failure, glomerulonephritis, hematuria, renal failure, kidney failure, mesangial nephritis, hypertension, proteinuria, active lupus nephritis, focal proliferative lupus nephritis, diffuse proliferative lupus nephritis, mesangial lupus nephritis, membranous lupus nephritis, active nephritis, sclerosing lupus nephritis, mesangial proliferative lupus nephritis, focal lupus nephritis, diffuse lupus nephritis, focal sclerosing lupus nephritis, diffuse segmental proliferative lupus nephritis, diffuse global proliferative lupus nephritis, diffuse segmental sclerosing lupus nephritis, diffuse global sclerosing lupus nephritis, advanced sclerosis lupus nephritis

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Contributor Information and Disclosures

Author

Lawrence H Brent, MD, Associate Professor of Medicine, 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: Genentech Honoraria Speaking and teaching; Genentech Grant/research funds Other; Amgen Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching; Abbott Immunology Honoraria Speaking and teaching; Takeda Honoraria Speaking and teaching; UCB  Speaking and teaching; Omnicare Consulting fee Consulting; Centocor Consulting fee Consulting

Coauthor(s)

Arati Karhadkar, MBBS, Fellow, Division of Rheumatology, Albert Einstein Medical Center, Philadelphia, PA
Disclosure: Nothing to disclose.

Eric Bloom, MD, Attending Physician, Division of Nephrology, Department of Internal Medicine; Division Chief, Nephrology; Nephrology Fellowship Program Director, 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.

Medical Editor

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

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Ajay K Singh, MB, MRCP, MBA, Associate Professor of Medicine, Harvard Medical School; Clinical Chief, Renal Division, Director of Dialysis, Brigham and Women's Hospital; Consulting Staff, Faulkner Hospital
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Senior Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
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.

 
 
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