eMedicine Specialties > Nephrology > Glomerular Diseases

Glomerulonephritis, Membranoproliferative: Treatment & Medication

Author: Pranay Kathuria, MD, MBBS, FACP, FASN, Chief, Section of Nephrology, Associate Professor of Medicine, Associate Director, Clinical Research Center, Schusterman Center, University of Oklahoma College of Medicine
Coauthor(s): Martin Senitko, MD, Fellow, Department of Internal Medicine, Division of Nephrology, University of Texas Southwestern Medical Center; Sandeep Singh, MD, Fellow, Department of Internal Medicine, Division of Nephrology, University of Texas Southwestern Medical Center
Contributor Information and Disclosures

Updated: Sep 4, 2008

Treatment

Medical Care

  • The optimal treatment of idiopathic membranoproliferative glomerulonephritis is not clearly defined.
  • Specific therapies should be reserved for patients with membranoproliferative glomerulonephritis who have proteinuria exceeding 3 g/d, interstitial disease on biopsy, or impaired renal function.
  • Treat the underlying cause of secondary forms of membranoproliferative glomerulonephritis.
  • Administer appropriate antimicrobial therapy for patients with infective endocarditis or infected atrioventricular shunts.
  • Various small reports discuss the benefit of antiviral therapy for patients with hepatitis C-induced renal disease and cryoglobulinemia.
    • One prospective controlled trial randomized 53 patients with HCV-associated type II cryoglobulinemia to interferon alfa-2a or conventional therapy. HCV RNA fell to undetectable levels in 60% of patients in the interferon alfa group. These patients showed improvement in cutaneous vasculitis, in cryoglobulin titers, and in plasma creatinine concentration. After treatment with interferon alfa-2a was discontinued, viremia and cryoglobulinemia recurred in all 15 HCV RNA-negative patients. On resumption of treatment, 3 of 4 patients had virologic, clinical, and biochemical responses. In comparison, no clinical or serologic improvement was noted in the patients receiving conventional therapy or in those given interferon alfa in whom there was no fall in HCV RNA in the plasma.
    • The appropriate dose and length of interferon alfa-2a therapy have not been established. A short course of a much higher dose of interferon alfa may be effective in patients in whom lower dose therapy fails. Relapses are common after stopping therapy. Furthermore, in some patients, interferon therapy may cause worsening renal function.
    • Combination therapies for interferon alfa-2a and ribavirin have also been studied in a small number of patients and have shown moderate success. The use of ribavirin in patients with creatinine clearances of less than 50 mL/min is contraindicated. Ribavirin can cause a dose-related hemolysis that can be severe and even life-threatening in patients with renal disease. There are anecdotal reports of patients with moderate renal insufficiency doing well with a proportionate reduction in the ribavirin dose and close monitoring, including measurement of plasma ribavirin levels. The use of ribavirin in patients with decreased GFR at the present time cannot be recommended.
    • Aggressive immunosuppression and plasmapheresis should be reserved for patients with severe acute disease and/or vasculitis. The immunosuppression protocols usually include pulse dose methylprednisone (0.5-1 g/d for 3-5 d) followed by 0.5-1.0 mg/kg/d of prednisone and cytotoxic agents (usually oral cyclophosphamide at 2 mg/kg/d) for 8-12 weeks. Plasmapheresis (exchanges of 3 L of plasma 3-4 times/wk for 2-3 wk) helps remove cryoglobulins and inflammatory mediators. Rituximab, a monoclonal antibody to B cells may be helpful in refractory cases. There is concern that such intensive therapy may increase virus replication and viremia, but, fortunately, there are no consistent reports of acute liver damage with short-term aggressive therapy. Antiviral therapy, though capable of suppressing viremia and cryoglobulinemia, is more often than not ineffective in controlling inflammation in such patients and can be associated with worsening renal disease.
    • Patients receiving liver transplants may go into remission; however, proteinuria reappears with a relapse of hepatitis C in the liver allograft.
  • Patients with hepatitis B virus–associated membranoproliferative glomerulonephritis often go into spontaneous remission but may benefit from antiviral agents. Little role exists for immunosuppression in these patients.
  • For patients with lupus and other rheumatologic conditions, offer treatment based on principles of care for those diseases.

Consultations

  • Nephrologist
  • Hepatologist, if hepatitis virus B or C–associated membranoproliferative glomerulonephritis
  • Nutrition specialist

Diet

  • Sodium: Restrict salt intake to 4-6 g/d to help control edema and hypertension.
  • Protein: Ensure that patients with normal renal function receive a protein intake of approximately 1 g/kg/d, plus the amount lost in urine. Confirm that the protein is of high biological value. Higher protein intake does not improve nutrition because protein catabolism increases proportionally; however, once renal insufficiency develops, recommend moderate protein restriction (eg, 0.65-0.80 g/kg/d, plus urinary losses).
  • Lipids: Recommend a low-cholesterol healthy-heart diet to patients because hyperlipidemia is common with nephrotic proteinuria.

Activity

  • No restriction of activity is recommended, unless the patient has uncontrolled severe hypertension.
  • Diuretics are most effective when the patient is supine. In patients with resistant edema, lying down after taking diuretics may increase their efficacy.

Medication

Membranoproliferative glomerulonephritis is a rare glomerulonephritis with a protracted natural history, which makes studies on treatment logistically difficult to conduct. No serological markers are available to assess disease activity. Most studies are confined to membranoproliferative glomerulonephritis type I and have a relatively short-term follow-up period; furthermore, hepatitis C virus is now known to be an important cause of many cases that were previously thought to be idiopathic membranoproliferative glomerulonephritis, making older treatment results difficult to interpret. Only a handful of randomized control trials have been published with sufficient power to determine the benefits of therapy for membranoproliferative glomerulonephritis. The use of variable end points (eg, reduction in proteinuria, renal function measured using variable techniques) further confounds the data.

Approaches to treatment have included immunosuppression, inhibiting platelet-induced injury with aspirin and dipyridamole, minimizing glomerular fibrin deposition with anticoagulants, and use of steroidal and nonsteroidal anti-inflammatory agents.

Anticoagulant, nonsteroidal, and immunosuppressive (cyclophosphamide) therapies have been found to have minimal beneficial effects and are associated with severe adverse effects.

Several other potential treatments of membranoproliferative glomerulonephritis type II are as follows:

  • Plasma infusion or plasmapheresis with plasma exchange in patients with defined pathologic mutation of factor H gene, to provide functionally intact factor H.
  • Strategies to reduce C3NeF include using mycophenolate or rituximab that specifically targets CD 20 surface antigen expressed on B lymphocytes. Mycophenolate mofetil (MMF) may provide some benefit, but it has not been sufficiently studied. Jones et al reported on 5 patients with idiopathic membranoproliferative glomerulonephritis who were treated with oral prednisolone and MMF and a control group of 6 patients who did not receive immunosuppression.1 A significant reduction in proteinuria was noted over an 18-month period in the treatment group compared with the control group. No significant change occurred in serum creatinine or creatinine clearance in the treatment group; however, in the control group, serum creatinine and creatinine clearance deteriorated significantly.   
  • New treatments on the horizon include eculizumab, an anti-C5 antibody, to decrease C5 mediated glomerular damage, and sulodexide, a combination of 2 glycosaminoglycans, which may prove to be useful by virtue of its inhibition of glomerular heparanase activity and its interference with inflammatory cells and complement interaction with the glomerular endothelium.
  • Anecdotal reports describe the benefit of cyclosporine and tacrolimus in steroid-resistant membranoproliferative glomerulonephritis type II.

The standard therapies are steroids for children and antiplatelet therapy for adults. The acceptable evidence-based modalities of treatment of membranoproliferative glomerulonephritis are summarized below.

Corticosteroids

Children with idiopathic membranoproliferative glomerulonephritis type I having nephrotic range proteinuria, interstitial disease, or renal insufficiency may benefit from corticosteroid therapy. No systemic evaluation of corticosteroid therapy has occurred in adults. Benefits in children include stabilization of the renal function, slowing of the decline in GFR, and a decrease in proteinuria. These therapies are associated with multiple complications, including hypertension and seizures in children. Because active inflammation is more likely to be present early in the disease, prompt initiation of therapy may provide better outcomes.

In the International Study of Kidney Disease in Children, alternate-day prednisone was administered for a mean of 130 months. Approximately 61% of the treatment group had stable renal function at the end of the study period as compared to 12% of the controls. The group at Cincinnati also has shown benefit of prolonged alternate-day steroid regimens. Renal survival rates improved, and findings on repeat kidney biopsy at 2 years demonstrated an increase in capillaries with open lumina and a decrease in mesangial matrix and cellularity; however, an increase in glomerular sclerosis and tubular atrophy occurred. The same group reported that patients with membranoproliferative glomerulonephritis type III respond poorly to steroids. Several other studies also documented the benefit of steroid therapy.


Prednisone (Deltasone, Sterapred, Orasone)

Immunosuppressant for treatment of autoimmune disorders. May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Adult

Not proven effective in adults

Pediatric

40 mg/m2 PO qod for 6-12 mo; lower doses may be continued for several y

Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; systemic infections; fungal or tubercular skin infections; GI disease

Pregnancy

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

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis of femoral and humoral heads, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use; other complications include seizures, growth retardation, pancreatitis, pseudotumor cerebri, alkalosis, weight gain, glaucoma, subcapsular cataracts, and impaired wound healing; may induce hypoadrenalism in infants of mothers who receive substantial doses of corticosteroids in pregnancy; breastfeeding is not recommended because corticosteroids are excreted in breast milk; can cause salt and water retention and worsen hypertension or precipitate CHF; do not administer live vaccines

Antiplatelet therapies

This therapy benefits adults. Inhibition of platelet inhibition, mesangial proliferation, and alteration of renal hemodynamics are the probable mechanisms that underlie the therapeutic benefits of aspirin. Dipyridamole may enhance effects of aspirin.

The use of antiplatelet agents administered over 1 year reduced the incidence of renal failure at 3-5 years, but the renal survival rate was no different at 10 years. Another study using these 2 agents showed significant reduction in proteinuria at 3 years in the treated group. One small uncontrolled study of membranoproliferative glomerulonephritis type I in children found improved outcome and attenuated inflammation on biopsy with the administration of a combination of prednisolone and dipyridamole.


Aspirin (Bayer Aspirin, Ascriptin, Anacin)

Inhibits prostaglandin synthesis, which prevents formation of platelet-aggregating thromboxane A2.

Adult

325-975 mg PO qd

Pediatric

<16 years: Not recommended
>16 years: Administer as in adults

Effects may decrease with antacids and urinary alkalinizers; corticosteroids decrease salicylate serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with coadministration of anticoagulants; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses > 2 g/d may potentiate glucose lowering effect of sulfonylurea drugs

Documented hypersensitivity; liver damage; hypoprothrombinemia; vitamin K deficiency; bleeding disorders; asthma; do not use in children (<16 y) because of association of aspirin with Reye syndrome

Pregnancy

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

Precautions

May cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia, active peptic ulcer disease, history of blood coagulation defects, or patients taking anticoagulants; avoid use in third trimester of pregnancy; excretion in breast milk may lead to platelet dysfunction and bleeding in infants


Dipyridamole (Persantine)

Platelet adhesion inhibitor that possibly inhibits RBC uptake of adenosine, itself an inhibitor of platelet reactivity. In addition, may inhibit phosphodiesterase activity, leading to increased cyclic-3', 5'-adenosine monophosphate within platelets and formation of the potent platelet activator thromboxane A2.

Adult

50-100 mg PO q8h

Pediatric

Not proven effective

Theophylline may increase hypotensive effects; antiplatelet activity may increase heparin toxicity

Pregnancy

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

Precautions

Caution in hypotension; has peripheral vasodilating effects; excreted in breast milk and should be avoided in women who are breastfeeding

More on Glomerulonephritis, Membranoproliferative

Overview: Glomerulonephritis, Membranoproliferative
Differential Diagnoses & Workup: Glomerulonephritis, Membranoproliferative
Treatment & Medication: Glomerulonephritis, Membranoproliferative
Follow-up: Glomerulonephritis, Membranoproliferative
Multimedia: Glomerulonephritis, Membranoproliferative
References
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References

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Further Reading

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Keywords

membranoproliferative glomerulonephritis, MPGN, mesangiocapillary glomerulonephritis, lobular glomerulonephritis, persistent hypocomplementemic glomerulonephritis, parietoproliferative glomerulonephritis, dense deposit disease, lobular nephritis

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Contributor Information and Disclosures

Author

Pranay Kathuria, MD, MBBS, FACP, FASN, Chief, Section of Nephrology, Associate Professor of Medicine, Associate Director, Clinical Research Center, Schusterman Center, University of Oklahoma College of Medicine
Pranay Kathuria, MD, MBBS, FACP, FASN is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Heart Association, American Society of Hypertension, American Society of Nephrology, and National Kidney Foundation
Disclosure: Nothing to disclose.

Coauthor(s)

Martin Senitko, MD, Fellow, Department of Internal Medicine, Division of Nephrology, University of Texas Southwestern Medical Center
Martin Senitko, MD is a member of the following medical societies: American College of Physicians and American Society of Nephrology
Disclosure: Nothing to disclose.

Sandeep Singh, MD, Fellow, Department of Internal Medicine, Division of Nephrology, University of Texas Southwestern Medical Center
Disclosure: Nothing to disclose.

Medical Editor

F John Gennari, MD, Director, Division of Nephrology, Associate Chair for Academic Affairs, Robert F and Genevieve B Patrick Professor, Department of Medicine, University of Vermont College of Medicine
F John Gennari, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, American Federation for Medical Research, American Heart Association, American Physiological Society, American Society for Clinical Investigation, American Society of Nephrology, and International Society of Nephrology
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

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

CME Editor

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 Osteopathic Internists, 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: Abbott Grant/research funds Speaking and teaching; Genzyme Honoraria Consulting; Roche Honoraria Consulting

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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