eMedicine Specialties > Nephrology > Glomerular Diseases

Glomerulonephritis, Membranoproliferative: Follow-up

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

Follow-up

Further Outpatient Care

  • Hypertension: Aggressively control blood pressure. The target blood pressure for adults with proteinuria exceeding 1 g/d is less than 125/75 mm Hg.
  • Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers: Administer these drugs to decrease proteinuria and to retard the progression of glomerular disease. No direct evidence suggests that these agents are beneficial in membranoproliferative glomerulonephritis, although their efficacy is demonstrated in other renal diseases.
  • Nondihydropyridine calcium channel blockers: Verapamil and diltiazem may also have antiproteinuric effects. Combination therapy with angiotensin-converting enzyme inhibitors and/or angiotensin receptor blockers may provide additional benefit.
  • Edema: Prescribe salt restriction and administer diuretics to treat patients with edema.
  • Hyperlipidemia: Control lipids according to the National Cholesterol Education Program guidelines, although several nephrologists recommend low-density lipoprotein (LDL) cholesterol levels to be maintained below 70 mg/dL.
  • Laboratory studies: At regular intervals, evaluate kidney function, proteinuria and clearances, lipid profiles, and serum albumin. The urine protein–to–creatinine ratio may be used as a rough guide to 24-hour urinary protein excretion.
  • Immunizations: Offer the pneumococcal vaccine and yearly influenza vaccine to all patients.
  • Monitor patients for medication adverse effects.
  • Monitor patient nutritional status by using the subjective global assessment scale.

Complications

  • Progressive decline in kidney function and end-stage renal disease (ESRD) (see Prognosis)
  • Recurrent disease after transplantation: Recurrent disease is a risk among those patients who receive a renal transplant. Of patients with membranoproliferative glomerulonephritis type I, 30-70% develop recurrent membranoproliferative glomerulonephritis, and 30-40% of the recurrences lead to graft failure. The rate of recurrence of membranoproliferative glomerulonephritis type II ranges from 50-100%; while recurrences may be mild, eventually 50% of the grafts fail. Recurrence rates of membranoproliferative glomerulonephritis type III are not known. Recurrent membranoproliferative glomerulonephritis needs to be differentiated from transplant glomerulopathy, which has a similar histology but lacks immune deposits.
  • Secondary hypertension: Hypertension is present in 80% of patients at presentation. Patients generally develop worsening of hypertension with the progression of renal insufficiency.
  • Edema
    • Dietary sodium restriction and the judicious use of diuretics are helpful in managing edema.
    • Thiazide diuretics suffice for many patients.
    • Loop diuretics may be indicated for more refractory edema with renal insufficiency.
    • Combination of diuretics acting at different sites in the tubule may be needed in some patients.
    • Potassium-sparing diuretics may be used concomitantly to prevent hypokalemia.
    • Patients with severe and refractory edema and those with hypovolemia and orthostatic hypotension may respond to salt-free albumin infusions.
  • Infections: The propensity for infections with encapsulated bacteria, including Streptococcus, Haemophilus, and Klebsiella species, is increased. Prophylactic antibiotics and hyperimmune globulins may be useful in some patients. Administer the pneumococcal vaccine and yearly influenza vaccination to all patients.
  • Thromboembolism tendency: Loss of anticoagulant antithrombin III, protein C and S, increased procoagulants, defective fibrinolysis, increased platelet aggregability, hyperlipidemia, endothelial cell injury, and steroids may lead to thrombosis. The renal vein is a common site of thrombosis because of hemoconcentration and loss of the anticoagulants through glomerular filtration.
  • Hyperlipidemia
    • This condition is a significant adverse event in patients with nephrotic syndrome. Very low-density lipoprotein (VLDL), LDL, and intermediate density lipoprotein (IDL) levels are increased early in the disease. High-density lipoprotein (HDL) levels may be variable, but levels of the cardioprotective fraction HDL2 usually are decreased. Lipoprotein-a levels are increased.
    • Hyperlipidemia in patients with nephrotic syndrome may cause accelerated atherosclerosis and increased coronary events. Also, hyperlipidemia may accelerate the progression of renal disease.
  • Miscellaneous
    • Protein calorie malnutrition
    • Growth retardation
    • Anemia - Often multifactorial; urinary losses of transferrin, causing iron deficiency, decreased production of erythropoietin, and complement mediated red cell lysis
    • Hypocalcemia and secondary hyperparathyroidism - May result from vitamin D deficiency due to urinary losses of cholecalciferol-binding globulin and failure to form activated vitamin D
    • Depressed total thyroxine levels - May be caused by loss of the thyroxine-binding globulin; TSH and free thyroxine levels usually normal

Prognosis

  • The main predictors of an adverse outcome are nephrotic syndrome and hypertension at presentation, low GFR at 1 year, and older age.
  • Histologic characteristics of crescent formation, interstitial fibrosis, tubular atrophy, and multiple sclerotic glomeruli indicate a poor prognosis.
  • Hypocomplementemia is not a predictor of disease severity or prognosis.
  • Membranoproliferative glomerulonephritis type I with nephrotic syndrome is a progressive disease, with 50% of patients developing ESRD after 10 years and 90% of patients developing ESRD after 20 years. Membranoproliferative glomerulonephritis type I without nephrotic proteinuria has a 10-year renal survival rate of 85%.
  • Membranoproliferative glomerulonephritis type II generally is more aggressive than membranoproliferative glomerulonephritis type I and has a median renal survival rate of 5-12 years. ESRD develops in 50% of the patients within 10 years of diagnosis.
  • There is very limited data on outcomes with membranoproliferative glomerulonephritis type III. Iitaka et al found that 7 patients who were followed for 9-17 years maintained their renal function over this period.2 On the other hand, Anders et al reported 4 of 8 patients in his series developed ESRD.3 Braun et al compared therapy with alternate day corticosteroids in 21 patients with type I and 25 patients with type III, followed for a minimum of 5 years, found that patients with type III had a greater decline in GFR, but there was no difference in the number of patients reaching ESRD in the 2 groups.4

Patient Education

  • Renal education: Ensure that patients with progressive azotemia receive timely education regarding renal replacement options.
  • Dietary education: Recommend that patients have frequent follow-up visits with a dietitian, which are essential to ensuring patient diet compliance.
  • For excellent patient education resources, visit eMedicine's Kidneys and Urinary System Center. Also, see eMedicine's patient education article Blood in the Urine.
  • For further information, see Mayo Clinic - Kidney Transplant Information.

Miscellaneous

Medicolegal Pitfalls

  • Failure to identify secondary causes of membranoproliferative glomerulonephritis
  • Failure to control hypertension
  • Failure to monitor for complications of nephrotic syndrome

Special Concerns

  • Pregnancy
    • Underlying renal diseases, including membranoproliferative glomerulonephritis, increase the risk of fetal loss, intrauterine growth retardation, and prematurity. Patients with hypertension, renal insufficiency, and nephrotic syndrome have increased risks for a more unfavorable fetal outcome. Better fetal outcome is reported in patients with dense deposit disease who have normal renal function, as compared to patients with membranoproliferative glomerulonephritis type I.
    • Preeclampsia develops in 20-40% of patients with underlying renal disease. The development of preeclampsia increases the risks of fetal wastage.
    • Patients with membranoproliferative glomerulonephritis are more likely than those with most other glomerular diseases to develop deterioration of renal function, increasing proteinuria, or worsening of hypertension during pregnancy. The risk for adverse outcomes depends on the patient's severity of hypertension, 24-hour proteinuria, and the level of renal function prior to pregnancy.
    • Close monitoring of the patient by a high-risk obstetrician and a nephrologist is essential during pregnancy.
 


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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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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