eMedicine Specialties > Nephrology > Glomerular Diseases

Minimal-Change Disease: Treatment & Medication

Author: Abeera Mansur, MD, Consultant Nephrologist, Doctors Hospital and Medical Center, Pakistan
Coauthor(s): Florin Georgescu, MD, Consulting Staff, Kidney Specialists of Savannah; Susie Lew, MD, Professor, Department of Medicine, Division of Renal Diseases and Hypertension and Nephrology, George Washington University Medical Center
Contributor Information and Disclosures

Updated: Oct 15, 2009

Treatment

Medical Care

Corticosteroids are the treatment of choice, leading to complete remission of proteinuria in most cases. Approximately 90% of children respond within 2 weeks to prednisone at a dose of 60 mg/msq/d. The treatment is continued for another 6 weeks, at lower doses of prednisone, after the remission of proteinuria. In some children, proteinuria fails to clear by 6-8 weeks, and performing a renal biopsy may be useful to determine if another process may be present.

Adults respond more slowly than children. A response in up to 80-90% has been recorded in adolescents and adults. However, the time to remission is up to 16 weeks. If patients are steroid-resistant or they relapse frequently, a trial of immunosuppressants is given.

The choice of immunosuppressants includes cyclophosphamide and chlorambucil. These drugs expose the patient to a wide range of serious adverse effects that include life-threatening infections, gonadal dysfunction, bone marrow dysfunction, and, in the case of chlorambucil, increased risk of leukemia. Pulse cyclophosphamide failed to adequately suppress recurrence of minimal-change nephrotic syndrome in a small group of children who were steroid-dependent. Cyclosporine is considered to be an acceptable drug for maintenance therapy in patients with frequent relapses and steroid dependency. However, it is less efficacious than cyclophosphamide at maintaining sustained remission.

Mycophenolate mofetil (MMF) has been shown in limited studies to be beneficial to patients who are steroid-dependent or with frequent remissions. Unfortunately, the evidence for the benefit of this drug is scant at this time, and it should be considered only when patients develop serious adverse effects to steroid treatment and refuse treatment with cyclophosphamide. One case report describes long-term remission with rituximab (an anti-CD20 antibody) in a patient who had failed conventional immunosuppressive therapy.4

MCD secondary to Hodgkin lymphoma is frequently resistant to steroids and will remit with cure of the primary disease.

Angiotensin converting enzyme inhibitors and angiotensin II receptor blockers, alone or in combination should be used with a goal of reducing the proteinuria. Blood pressure and renal function should be monitored closely in patients on angiotensin converting enzyme inhibitors and angiotensin II receptor blockers.

  • Hypovolemia
    • This necessitates immediate volume expansion with purified plasma protein fraction and isotonic sodium chloride solution.
    • The administration of parenteral albumin infusion is not appropriate long-term management for patients with hypoalbuminemia because it has only a transient effect. Such crises should be avoided with recognition of the earlier signs of hypovolemia, including abdominal pain, increase in hematocrit, and response to contributing factors (eg, diarrhea, septicemia, diuretic therapy).
  • Edema
    • This condition should be controlled by dietary sodium restriction.
    • Small amounts of edema are not of much clinical significance.
    • The use of diuretics should be reserved for patients with severe cases of edema, particularly in the presence of respiratory or gastrointestinal symptoms, and when the condition restricts activity.
  • Thrombotic episodes should be prevented by mobilization and meticulous attention to venipuncture and intravenous infusion sites. Established episodes should be managed with heparinization.
  • Infections
    • These must be treated aggressively.
    • Cellulitis, peritonitis, otitis, and pneumonia are common infections.
    • Susceptibility to pneumococcal infections warrants the administration of penicillin prophylaxis to patients in relapse; corticosteroids increase the problem of infection.

Consultations

  • Consultation with a nephrologist generally is needed. The nephrologist has the expertise to perform and interpret the renal biopsy.
  • A renal pathologist has the expertise to interpret biopsy findings under light microscopy, immunofluorescence, and electron microscopy.

Diet

  • An adequate dietary protein intake, in accordance with the recommended daily allowance (RDA) is necessary. No evidence suggests that hepatic albumin synthesis is elevated with protein intake that is higher than the RDA.
  • Dietary sodium restriction helps forestall the progression of edema and also is prudent in the management of hypertension.

Activity

  • Mobilization, rather than bed rest, is indicated to avoid thromboembolic complications.

Medication

Diuretics are used to decrease severe edema. NSAIDs also can be used to decrease proteinuria. Patients usually respond to steroids. The response of patients to steroids is used to divide patients into various groups. The following terms are used to categorize the response of patients:

Complete remission: This is defined as complete resolution of proteinuria for at least 3-5 consecutive days.

Partial remission: This is defined as a reduction in the degree of proteinuria without complete clearing.

Relapse: This is defined as a reoccurrence of proteinuria for at least 3-5 consecutive days.

Because MCNS accounts for 90% of all cases of idiopathic nephrotic syndrome in children, steroids are started empirically. A biopsy is performed only in those cases where no remission occurs. In comparison, a biopsy is performed in all adults before the initiation of treatment. Adults tend to respond more slowly, with more than 25% taking as long as 12-16 weeks to undergo complete remission. A typical initial regimen in adults consists of oral prednisone in a daily dosage of 1 mg/kg of body weight for 8-16 weeks (or for 1 wk after remission has been induced). The patient is then placed on an alternate-day single-dose (1 mg/kg) regimen to minimize the incidence of adverse effects. If proteinuria disappears or is reduced to a very low level, high-dose alternate-day therapy is continued for several weeks to 1 month and then slowly tapered over several months in an attempt to reduce the likelihood of relapse.

To prevent relapse, steroids are continued for several weeks after remission. Patients are grouped into the following:

Steroid-sensitive patients: These patients have complete remission within 8-12 weeks with infrequent relapses. Children usually respond within 4-6 weeks, whereas adults respond in up to 15 weeks. Treatment usually is continued for another 6 weeks after complete remission of proteinuria occurs.

Steroid-dependent patients or frequent relapsers: If remission is followed by recurrence, a second course of steroids is given. Those patients who need steroids repeatedly are categorized as frequent relapsers or steroid-dependent patients. Relapse in these patients can occur either during tapering of steroids or after cessation of therapy. In these patients, cytotoxic drugs, such as Cytoxan, chlorambucil, or cyclosporine, can be considered to either induce a remission or decrease the adverse effects of continuous steroid use. Cytotoxic drugs, such as 2 mg/kg/d of cyclophosphamide for 8-12 weeks, can be used in such patients. Cyclosporine (4-6 mg/kg/d) also can be used in patients who continue to relapse or who are steroid-dependent. Because cyclophosphamide is cheaper and has a better response rate, it is preferable over cyclosporine in most patients with steroid-dependent or frequently relapsing MCD.

MMF may also be beneficial to patients with frequent relapses. This was suggested by a small study where 7 patients with MCD and FSGS with multiple relapses were treated with MMF (1 g bid). After 1 year, 5 of the 7 patients were still in remission, and the steroid dose was significantly decreased. In addition, the immunomodulator levamisole also has been used in children.

Steroid-resistant patients: If no reduction in proteinuria occurs by 12-16 weeks, adults are considered steroid-resistant. The most common cause of this is misdiagnosis. Studies in adults and children have shown that both cyclophosphamide and cyclosporine added to steroid treatment may induce remission.5 Moreover, if these patients relapse at a later time, they tend to become steroid-sensitive.

Secondary steroid-resistant: Some patients develop secondary steroid resistance after an initial response to steroids.

In children, repeat biopsy can alter the treatment plan in a significant number of patients. In patients who do not respond to treatment, follow-up biopsies have been found to show either IgM nephropathy or FSGS.

A study by Swartz et al of 55 children with steroid-resistant or steroid-dependent MCD determined that 23 of these patients also had mesangial IgM that was visible through immunofluorescence (one of the characteristics of IgM nephropathy).6 The investigators also found that the children with MCD and immunofluorescently-visible IgM responded better to treatment with cyclosporine than to therapy with cyclophosphamide.

Adults are particularly prone to the adverse effects of corticosteroids, but they do well on cyclophosphamide.

Cyclosporine may be used as an alternative to cyclophosphamide in order to avoid toxicities associated with the latter.7 Keeping the dosage of cyclosporine at a minimum and carefully monitoring the drug’s levels have been shown to be helpful in avoiding cyclosporine-associated nephrotoxicity.

Rituximab has been shown to be effective against minimal-change disease.4 Relapse has been linked to the reappearance of B19 cells, which rituximab depletes. Rituximab may therefore have a role in the treatment of steroid-dependent and multirelapsing patients

The treatment of MCD with tacrolimus has produced varying results.8,9,10

Diuretics

These agents control volume overload.


Furosemide (Lasix)

Has potent diuretic effects by blocking the sodium reabsorption in the thick ascending limb of the loop of Henle.

Adult

20-80 mg PO/IV qd; not to exceed 600 mg qd

Pediatric

1-2 mg/kg/dose PO/IV q6h; not to exceed 6 mg/kg/dose

Alcohol and CNS depressants may exacerbate orthostatic hypotension; antagonized by indomethacin; may alter salicylate and lithium levels; hearing loss may occur with aminoglycosides; potentiates therapeutic effect of other antihypertensives; ethacrynic acid should be used for those allergic to sulfa (ototoxicity may be slightly more with ethacrynic acid than furosemide); antagonizes effects of d-tubocurarine, potentiates action of succinylcholine

Documented hypersensitivity; hepatic coma, anuria, and state of severe electrolyte depletion

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 renal or hepatic dysfunction; perform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter; adverse effects may include GI upset, dizziness, vertigo, paresthesias, orthostatic hypotension, hyperglycemia, jaundice, hyperuricemia, rash, photosensitivity, tinnitus, hearing loss, interstitial nephritis, and blood dyscrasias

Corticosteroids

For remission of proteinuria.


Prednisone (Deltasone, Orasone, Sterapred)

Exerts anti-inflammatory effect via the inhibition of inflammatory mediator gene transcription.

Adult

1 mg/kg/d PO qod

Pediatric

2 mg/kg/d PO

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, and fungal or tubercular infections

Pregnancy

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

Precautions

Tuberculosis, ocular herpes simplex, peptic ulcer, hypertension, osteoporosis, and diabetes; supplement with additional steroids in physiologic stress; avoid abrupt cessation; alternate-day, intermittent, or single-day doses at 8:00 AM minimize adrenal suppression; monitor weight, growth, fluid, and electrolyte balance; adverse effects include HPA axis suppression, masks infection, glaucoma, cataracts, secondary infections, hypokalemia, hypocalcemia, hypernatremia, hypertension, psychic disorders, myopathy, osteonecrosis, osteoporosis, peptic ulcer, dermal atrophy, increased intracranial pressure, and carbohydrate intolerance

Antineoplastic agents

For remission of nephrotic syndrome.


Cyclophosphamide (Cytoxan, Neosar)

Interferes with normal function of DNA by alkylation and cross-linking strands of DNA and by possible protein modification.

Adult

2 mg/kg/d PO for 8-12 wk after inducing remission with prednisone

Pediatric

2.5-3 mg/kg/d PO; not to exceed 90 d

Allopurinol may increase risk of bleeding or infection and enhance myelosuppressive effects of cyclophosphamide; may potentiate doxorubicin-induced cardiotoxicity; may reduce digoxin serum levels and antimicrobial effects of quinolones; chloramphenicol may increase half-life of cyclophosphamide while decreasing metabolite concentrations; may increase effect of anticoagulants; coadministration with high doses of phenobarbital may increase rate of metabolism and leukopenic activity of cyclophosphamide; thiazide diuretics may prolong cyclophosphamide-induced leukopenia and neuromuscular blockade by inhibiting cholinesterase activity

Documented hypersensitivity; severely depressed bone marrow function; breastfeeding

Pregnancy

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

Precautions

Infection, previous radiation or cytotoxic chemotherapy, and tumor infiltration of bone marrow; caution in hepatic or renal impairment, leukopenia, and thrombocytopenia; adverse effects include CHF, secondary malignancies, leukopenia, renal tubular necrosis, poor wound healing, anorexia, nausea, vomiting, alopecia, thrombocytopenia, anemia, hemorrhagic and nonhemorrhagic cystitis, gonadal suppression (which may be of special concern when prescribing to the pediatric population), interstitial pulmonary fibrosis, pigmentation changes, dermatitis, and jaundice

Immunosuppressant agents

For remission of nephrotic syndrome.


Cyclosporine A (Sandimmune, Neoral)

Inhibits production and release of IL-2, leading to inhibition of IL-2–mediated activation of T lymphocytes.

Adult

4-6 mg/kg/d PO in 2 divided doses to keep trough level at 120-200 ng/mL

Pediatric

4-6 mg/kg PO; some children may require 10-14 mg/kg to induce remission

Carbamazepine, phenytoin, isoniazid, rifampin, and phenobarbital may decrease concentrations; azithromycin, itraconazole, nicardipine, ketoconazole, fluconazole, erythromycin, verapamil, grapefruit juice, diltiazem, aminoglycosides, acyclovir, amphotericin B, and clarithromycin may increase toxicity; acute renal failure, rhabdomyolysis, myositis, and myalgias increase when taken concurrently with lovastatin; nifedipine may increase incidence of gingival hyperplasia

Documented hypersensitivity; uncontrolled hypertension or malignancies; do not administer concomitantly with PUVA or UVB radiation in psoriasis because it may increase risk of cancer

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

Glaucoma, Tourette syndrome, infections, and lymphoma may occur; use drug levels to monitor dose; airway and other supportive measures should be available for treatment of anaphylaxis when giving an IV dose; nephrotoxic; can raise blood pressure; adverse effects include hypertension, hirsutism, gingival hypertrophy, hypomagnesemia, hypokalemia, tremor, seizure, headache, nephrotoxicity, nausea, vomiting, leg cramps, hepatotoxicity, hyperlipidemia, glucose intolerance, increased immunologic and infectious complications, hyperuricemia, and increased incidence of thromboembolic events


Chlorambucil (Leukeran)

To induce remission of proteinuria. Interferes with DNA replication and RNA transcription.

Adult

0.1-0.2 mg/kg/d PO

Pediatric

0.1-0.2 mg/kg/d PO for 2 mo

Myelosuppressives and radiotherapy potentiate antineoplastic effect; antigout agents are antagonized; should not be given with live vaccine

Documented hypersensitivity; previous resistance

Pregnancy

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

Precautions

Myelosuppression, adverse dermatologic effects, nausea, vomiting, hyperuricemia, gonadal toxicities, oral ulcerations, and CNS effects may occur

Immunomodulators

To induce remission of nephrotic syndrome.


Levamisole (Ergamisol)

Stimulates formation of antibodies and enhances T-cell responses. Acts as a biochemical modulator of fluorouracil.

Adult

Not established

Pediatric

2.5 mg/kg PO; not to exceed 150 mg

Increases toxicity/serum levels of phenytoin; causes disulfiram reactions when taken with alcohol

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

GI toxicities, rash, pruritus, and flulike symptoms may occur; CNS symptoms, such as dizziness, ataxia, depression, confusion, and reversible neutropenia, have been reported


Mycophenolate mofetil (CellCept)

Inhibitor of de novo purine pathway with preferential inhibitory effects on T and B lymphocyte proliferation, has been used to treat steroid-dependent nephrotic syndrome.

Adult

1000 mg PO bid; starting dose is 250 mg PO bid and titrate up to maximum 2 g/d

Pediatric

20-25 mg/kg/d PO in 2 divided doses or 600 mg/m2 PO bid; titrate to maximum 1000 mg PO bid over 2 mo

Antacids containing 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; abnormal LFT results may occur

More on Minimal-Change Disease

Overview: Minimal-Change Disease
Differential Diagnoses & Workup: Minimal-Change Disease
Treatment & Medication: Minimal-Change Disease
Follow-up: Minimal-Change Disease
References
Further Reading
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Keywords

minimal-change disease, nephrotic syndrome, focal segmental glomerulosclerosis, idiopathic nephrotic syndrome of childhood, lipoid nephrosis, minimal-change nephropathy, minimal-change nephrotic syndrome, nil disease, steroid-sensitive nephrotic syndrome

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Contributor Information and Disclosures

Author

Abeera Mansur, MD, Consultant Nephrologist, Doctors Hospital and Medical Center, Pakistan
Abeera Mansur, MD is a member of the following medical societies: American College of Physicians and American Society of Nephrology
Disclosure: Nothing to disclose.

Coauthor(s)

Florin Georgescu, MD, Consulting Staff, Kidney Specialists of Savannah
Florin Georgescu, MD is a member of the following medical societies: American College of Physicians, American Medical Association, and American Society of Nephrology
Disclosure: Nothing to disclose.

Susie Lew, MD, Professor, Department of Medicine, Division of Renal Diseases and Hypertension and Nephrology, George Washington University Medical Center
Susie Lew, MD is a member of the following medical societies: American College of Physicians, American Society of Nephrology, International Society of Nephrology, and National Kidney Foundation
Disclosure: Amgen Consulting fee Consulting; Amgen Grant/research funds investigator; Amgen Honoraria Speaking and teaching; OrthoBio Honoraria Speaking and teaching; Fresineus Honoraria Speaking and teaching; Affymax Grant/research funds Other

Medical Editor

Anil Kumar Mandal, MD, Clinical Professor, Department of Internal Medicine, Division of Nephrology, University of Florida School of Medicine
Anil Kumar Mandal, MD is a member of the following medical societies: American College of Clinical Pharmacology, American College of Physicians, American Society of Nephrology, and Central Society for Clinical Research
Disclosure: Nothing to disclose.

Pharmacy Editor

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

Managing Editor

Eleanor Lederer, MD, Consulting Staff, Louisville VA Hospital; Professor of Medicine; Interim Chief of Nephrology; Director of Nephrology Training Program; Director, Metabolic Stone Clinic; Director of Outpatient Clinics, Kidney Disease Program, University of Louisville School of Medicine
Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa
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; Amgen Honoraria Speaking and teaching; Ortho Biotech Honoraria Speaking and teaching

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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