Antiglomerular Basement Membrane Disease Medication

Updated: May 23, 2018
  • Author: Ramesh Saxena, MD, PhD; Chief Editor: Vecihi Batuman, MD, FASN  more...
  • Print
Medication

Medication Summary

The standard treatment of antii–glomerular basement membrane (anti-GBM) nephritis consists of plasmapheresis in combination with intense immunosuppression. The latter involves high-dose corticosteroids in combination with cyclophosphamide. Rarely, azathioprine or cyclosporine may be used in patients who cannot tolerate cyclophosphamide.

Next:

Corticosteroids

Class Summary

Anti-GBM nephritis is a rapidly progressive disease associated with a high mortality rate if not treated. However, early diagnosis and prompt treatment can prevent progression, preserve renal function, and reduce mortality. High doses of corticosteroids constitute an important component of the intense immunosuppression for anti-GBM nephritis.

Methylprednisolone (Solu-Medrol)

Synthetic glucocorticoid for parenteral use. Extremely potent anti-inflammatory activity, ie, greater than that of prednisolone. Has less salt-retaining activity compared with prednisolone. Administered in high doses for the first 3 d in the treatment of anti-GBM nephritis.

Prednisolone (Delta-Cortef, Econopred, AK-Pred)

Synthetic glucocorticoid with potent anti-inflammatory properties. Readily absorbed from GI tract. Constitutes important component of immunosuppressive regimen in treatment of anti-GBM nephritis. Administration begins on day 4, after patient has received 3 doses of IV methylprednisolone.

Previous
Next:

Immunosuppressives

Class Summary

Cyclophosphamide (an alkylating agent) and corticosteroids constitute the standard immunosuppression regimen for anti-GBM nephritis.

Cyclophosphamide (Cytoxan, Neosar)

Synthetic alkylating agent chemically related to nitrogen mustards. Biotransformed in liver to active metabolites. Well absorbed after PO administration (>75% bioavailability). Approximately 5-25% is excreted unchanged in urine. One of its metabolites, acrolein, is thought to be responsible for urinary bladder toxicity.

Azathioprine (Imuran)

Antagonizes purine metabolism and inhibits synthesis of DNA, RNA, and proteins. May decrease proliferation of immune cells, which results in lower autoimmune activity.

Cyclosporine (Sandimmune, Neoral)

Cyclic polypeptide that suppresses some humoral immunity and, to a greater extent, cell-mediated immune reactions such as delayed hypersensitivity, allograft rejection, experimental allergic encephalomyelitis, and graft versus host disease for a variety of organs.

Previous