eMedicine Specialties > Pediatrics: General Medicine > Nephrology

Anti-GBM Antibody Disease: Treatment & Medication

Author: Agnieszka Swiatecka-Urban, MD, FASN, Assistant Professor, Department of Pediatrics, Cell Biology and Physiology, University of Pittsburgh School of Medicine; Assistant Professor, Department of Nephrology, Children's Hospital of Pittsburgh
Coauthor(s): Prasad Devarajan, MD, Louise M Williams Endowed Chair in Pediatrics, Professor of Pediatrics and Developmental Biology, Director of Nephrology and Hypertension, Director of Clinical Nephrology Laboratories, Chief Executive Officer of Dialysis Unit, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine
Contributor Information and Disclosures

Updated: Mar 31, 2009

Treatment

Medical Care

Hospitalization is required for prompt diagnosis and treatment, close monitoring, and supportive care in patients with anti-glomerular basement membrane (GBM) antibody disease. Patients may initially require intensive care.

  • The therapeutic regimen depends on the patient's potential to respond.
    • Patients with moderate glomerulonephritis (serum creatinine level <5 mg/dL and crescents in <50-75% of glomeruli) and patients with acute disease (brief illness, lack of chronicity on histology) are likely to respond to therapy. The treatment of choice consists of repeated plasmapheresis combined with glucocorticosteroids and cyclophosphamide.
    • Patients with advanced disease (serum creatinine level >5 mg/dL and crescents in >75% of glomeruli) and histologic signs of chronicity are unlikely to improve with any therapy and should be spared the clinically significant risks of aggressive treatment. Supportive care and eventual renal transplantation are recommended.
    • Patients who are antineutrophilic cytoplasmic antibody (ANCA) positive with clinical presentations consistent with vasculitis are likely to benefit from aggressive therapy independent of the severity of disease.
    • Most patients with pulmonary hemorrhage respond rapidly to methylprednisolone pulses, plasma exchange, or plasmapheresis.
    • Patients with mild renal disease who do not have pulmonary hemorrhage may be successfully treated with prednisone alone.
  • In patients with renal insufficiency, treatment should be commensurate with the severity of disease and includes therapy for hypertension, fluid overload, and electrolyte and acid-base imbalances.
  • Early plasmapheresis removes circulating anti-GBM antibodies and other mediators of inflammation and has been advocated as the treatment of choice.
    • Plasmapheresis with immunosuppression is effective in the treatment of pulmonary hemorrhage and substantially improves renal function in patients with serum creatinine levels of less than 7 mg/dL or with crescents in less than 50% of the glomeruli.
    • Therapy usually consists of 14 treatments during 2-3 weeks.
    • Concomitant administration of cyclophosphamide and steroids is essential to prevent rebound antibody formation.
    • Additional plasmapheresis may be required if anti-GBM antibody titers remain elevated after the treatments.
    • Patients undergoing plasmapheresis who develop serious infections benefit from intravenous administration of immunoglobulins.
  • Experimental and future treatment
    • Preliminary data suggest that removal of anti-GBM antibody by means of immunoadsorption may be beneficial in patients with Goodpasture disease. These results must be verified before immunoadsorption can be recommended.
    • The effect of blocking CD28-B7, the costimulatory pathway for T-cell activation, was evaluated in a rat model of anti-GBM disease. The rationale for this attempt was the observation that T-cell–mediated mechanisms may play a direct role in the glomerular and alveolar injury that occurs in anti-GBM disease.

Surgical Care

  • In patients with irreversible renal failure, renal transplantation is usually deferred for at least 1 year to decrease the risk of recurrence.

Consultations

  • A nephrologist may be needed to manage glomerulonephritis and renal insufficiency.
  • A pulmonologist may be needed to manage pulmonary hemorrhage.
  • An intense care specialist may need to be consulted to treat critically ill patients.
  • A surgeon may need to be consulted to establish dialysis access and perform renal transplantation.

Diet

Dietary modifications for patients with renal insufficiency include the following:

  • Adjustments in fluid intake based on urine output
  • Eating foods with low levels of sodium and phosphate

Activity

  • Patients should avoid strenuous activity.

Medication

The treatment of choice is a combination of plasmapheresis to remove circulating anti-glomerular basement membrane (GBM) antibodies and immunosuppression with glucocorticoids and cytotoxic agents to inhibit further autoantibody formation.

Glucocorticoids

These agents are used as adjuncts to plasmapheresis to minimize antibody formation. Glucocorticoids have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the body's immune response to diverse stimuli.


Methylprednisolone (Medrol, Solu-Medrol)

DOC. Should be started concomitantly with plasmapheresis.

Adult

30 mg/kg IV qd for 3 d; not to exceed 3 g/dose

Pediatric

Administer as in adults

Phenobarbital, phenytoin, and rifampin may increase glucocorticoid metabolism (consider increasing maintenance dose); monitor for hypokalemia when taken with diuretics; may interfere with immune response to live virus vaccine (MMR vaccine) and reduce efficacy or allow for infection

Documented hypersensitivity; administration of live virus vaccines and systemic fungal infections; infection; immunosuppression; upper GI bleeding

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hypertension, congestive heart failure, ulcerative colitis, or thromboembolic disease; may precipitate hypertension, GI irritation, and avascular bone necrosis


Prednisone (Deltasone, Orasone, Liquid Pred)

Administer after methylprednisolone pulses and continue for 6-12 mo, depending on response and adverse effects.

Adult

2 mg/kg PO qod for 1 mo, then slowly taper over 11 mo

Pediatric

Administer as in adults

Barbiturates, phenytoin, or rifampin may decrease effectiveness

Documented hypersensitivity; serious bacterial infections (excluding meningitis and septic shock) and fungal infections

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Varicella particularly dangerous in immunosuppressed patients (if exposed, the patient should receive specific immunoglobulin [VZIG] within 24-48 h); caution in hypertension, congestive heart failure, ulcerative colitis, or thromboembolic disease; may precipitate hypertension, GI irritation, avascular bone necrosis, and growth retardation; administer with meals to decrease GI upset; taper when used longer than burst treatment; early adverse effects include glucose intolerance, hypertension, agitation, and indigestion; late adverse effects include immunosuppression and increased susceptibility to sepsis, adrenal suppression, hypertension, urinary calcium loss and osteopenia, gastric irritation, and bleeding

Immunosuppressive agents

Immunosuppressants are used as adjuncts to plasmapheresis and glucocorticoids to minimize new antibody formation. Therapy is continued for 6-12 months, the time usually required to stop the formation of anti-GBM antibodies.


Cyclophosphamide (Cytoxan, Neosar)

DOC because of long-standing use in adults and children.

Adult

2 mg/kg/d PO starting dose; taper for 6-12 mo, depending on anti-GBM antibody titers

Pediatric

Administer as in adults

Allopurinol, phenobarbital, phenytoin, and chloral hydrate may increase conversion of cyclophosphamide to active metabolite; allopurinol, chlorambucil, phenothiazines, and imipramine may inhibit metabolism and increase bone marrow suppression

Documented hypersensitivity; severe hemorrhagic cystitis; GFR <25%

Pregnancy

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

Precautions

Adjust dose in decreased GFR (ie, decrease dose by 50% if GFR is 25-50% of normal); maintain dose with WBC count (<3.5 X 109 [<3.5 X 103/µL or 3500/mm3]), platelet count (<100 X 109 [<100 X 103/µL or <100,000/mm3]), or serious concurrent infection; cumulative dose of 300 mg/kg poses significant risk of gonadal toxicity; may precipitate bone marrow suppression, hemorrhagic cystitis, and hair loss; moderate-to-high emetogenic potential (based on dose); causes anorexia, diarrhea, stomatitis, and mucositis

More on Anti-GBM Antibody Disease

Overview: Anti-GBM Antibody Disease
Differential Diagnoses & Workup: Anti-GBM Antibody Disease
Treatment & Medication: Anti-GBM Antibody Disease
Follow-up: Anti-GBM Antibody Disease
Multimedia: Anti-GBM Antibody Disease
References
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Further Reading

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Keywords

anti-glomerular basement membrane antibody disease, anti-GBM antibody disease, Goodpasture disease, Goodpasture's disease, Goodpasture syndrome, Goodpasture's syndrome, glomerulonephritis, pulmonary hemorrhage, renal failure, end-stage renal disease, nephritis, hematuria, oliguria, edema, treatment, diagnosis, tachycardia, tachypnea, hypertension, pulmonary rales, rash, skin rash, influenza, Alport syndrome

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Contributor Information and Disclosures

Author

Agnieszka Swiatecka-Urban, MD, FASN, Assistant Professor, Department of Pediatrics, Cell Biology and Physiology, University of Pittsburgh School of Medicine; Assistant Professor, Department of Nephrology, Children's Hospital of Pittsburgh
Agnieszka Swiatecka-Urban, MD, FASN is a member of the following medical societies: American Society of Nephrology, American Society of Pediatric Nephrology, International Society of Nephrology, and Women in Nephrology
Disclosure: Nothing to disclose.

Coauthor(s)

Prasad Devarajan, MD, Louise M Williams Endowed Chair in Pediatrics, Professor of Pediatrics and Developmental Biology, Director of Nephrology and Hypertension, Director of Clinical Nephrology Laboratories, Chief Executive Officer of Dialysis Unit, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine
Prasad Devarajan, MD is a member of the following medical societies: American Heart Association, American Society of Nephrology, American Society of Pediatric Nephrology, National Kidney Foundation, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Medical Editor

Uri S Alon, MD, Director of Research and Education, Department of Pediatrics, Division of Pediatric Nephrology, Children's Mercy Hospital of Kansas City; Professor, University of Missouri at Kansas City
Uri S Alon, MD is a member of the following medical societies: American Federation for Medical Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

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.

CME Editor

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: Amgen Grant/research funds None; Altus Pharmaceuticals Grant/research funds None; Genzyme Grant/research funds None; Merck Grant/research funds None; NIH Grant/research funds None

 
 
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