Membranoproliferative Glomerulonephritis

Membranoproliferative glomerulonephritis (MPGN) is also known as mesangiocapillary glomerulonephritis. Membranoproliferative glomerulonephritis is a pattern of glomerular injury characterized by mesangial hypercellularity, endocapillary proliferation, and thickening of the glomerular basement membrane (double contour formation). The changes are due to the deposition of Igs, complement factors, or both, in the glomerular mesangium and along the glomerular capillary walls. The pathogenic variants include immune complex/monoclonal Ig-mediated (e.g., from infections, autoimmune diseases) and complement-mediated MPGN. In rare cases, MPGN is not associated with Igs and the complement system, such as in the case of endothelial injury. With multiple etiologies, the presentation and clinical course vary. Presenting features can be asymptomatic proteinuria and hematuria, nephrotic syndrome Nephrotic syndrome Nephrotic syndrome is characterized by severe proteinuria, hypoalbuminemia, and peripheral edema. In contrast, the nephritic syndromes present with hematuria, variable loss of renal function, and hypertension, although there is sometimes overlap of > 1 glomerular disease in the same individual. Nephrotic Syndrome, nephritic syndrome Nephritic syndrome Nephritic syndrome is a broad category of glomerular diseases characterized by glomerular hematuria, variable loss of renal function, and hypertension. These features are in contrast to those of nephrotic syndrome, which includes glomerular diseases characterized by severe proteinuria, although there is sometimes overlap of > 1 glomerular disease in the same individual. Nephritic Syndrome, or chronic renal failure. Definitive diagnosis requires renal biopsy, although additional laboratory and imaging tests may point to the associated disease. Treatment is based on the underlying cause. Steroids, immunosuppressants Immunosuppressants Immunosuppressants are a class of drugs widely used in the management of autoimmune conditions and organ transplant rejection. The general effect is dampening of the immune response. Immunosuppressants, and kidney transplantation are among the commonly used treatment modalities.

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Editorial responsibility: Stanley Oiseth, Lindsay Jones, Evelin Maza

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Overview

Definition

Membranoproliferative glomerulonephritis (MPGN) is a glomerular injury characterized by glomerular basement membrane (GBM) thickening (“membrano-”) and increased endocapillary and mesangial cellularity (“proliferative”).

  • The GBM thickens from deposits of immune complexes, complement factors, and/or interposed cells (between the GBM and endothelial cells).
  • Proliferation of mesangial cells and monocytes contributes to increased cellularity, creating a lobulated glomerular tuft.
  • MPGN is a histologic finding and not a specific disease; thus, it is associated with multiple etiologies.
  • Also called mesangiocapillary glomerulonephritis

Epidemiology

  • Accounts for 7%–10% of cases of biopsy-confirmed glomerulonephritis
  • The idiopathic or primary form affects the younger population (8–30 years of age).
  • The secondary form is seen predominantly in individuals > 30 years of age.

Pathophysiology and Etiology

Glomerular injury

  • Pathogenetic mechanisms:
    • Immune complex/monoclonal Ig-mediated mechanism:
      • Deposition of immune complexes or monoclonal Ig
      • Leads to complement activation
    • Complement-mediated mechanism:
      • Alternative complement pathway (where C3 is at a constant low level in circulation) becomes dysregulated, causing persistent activation.
      • Deposition of complement products in the glomeruli (capillary walls and mesangium)
    • Unrelated to complement or Ig deposition (seen in the case of endothelial injury)
  • Insults to the glomeruli and mesangium result in:
    • Acute mesangial and capillary injury from the deposition of immune complexes, monoclonal Igs, or complement factors
    • Influx of inflammatory cells
    • Histologic changes:
      • New mesangial matrix is produced → mesangium expands → glomerular tuft becomes lobular
      • New GBM is formed that looks like a basement membrane with a double contour → “tram track”

Classification (electron microscopy)

Traditionally, MPGN was classified based on electron microscopy findings (old classification):

  • Based on electron microscopy:
    • MPGN type I:
      • Characterized by immune deposits in the subendothelial space (subendothelial deposits) and mesangium (mesangial deposits)
      • Seen in lupus nephritis, infections
    • MPGN type II:
      • Dense deposit disease (DDD)
      • Additional intramembranous deposits
      • Along the GBMs, tubules, and Bowman’s capsule, continuous dense ribbon-like deposits are seen.
      • Associated with C3 nephritic factor (C3NeF)
    • MPGN type III: similar to MPGN type I, but with subendothelial, mesangial, and subepithelial deposits
  • Overlapping features of the different types are noted (e.g., type I can be found to have features of complement-mediated or immune complex-mediated MPGN).

Classification (immunofluorescence microscopy) and etiology

A different classification based on the pathogenetic process helps point to the underlying etiology or disease, thus directing treatment.

  • Pathogenesis is identified based on immunofluorescence findings.
  • Classification based on the pathogenesis (immune complex/monoclonal Ig versus complement): 
    • Immune complex/monoclonal Ig-mediated MPGN:
      • Chronic viral infections (e.g., hepatitis B Hepatitis B Hepatitis B virus (HBV) is a partially double-stranded DNA virus, which belongs to the Orthohepadnavirus genus and the Hepadnaviridae family. Most individuals with acute HBV infection are asymptomatic or have mild, self-limiting symptoms. Chronic infection can be asymptomatic or create hepatic inflammation, leading to liver cirrhosis and hepatocellular carcinoma (HCC). Hepatitis B Virus or C)
      • Chronic bacterial infections (e.g., endocarditis Endocarditis Endocarditis is an inflammatory disease involving the inner lining (endometrium) of the heart, most commonly affecting the cardiac valves. Both infectious and noninfectious etiologies lead to vegetations on the valve leaflets. Patients may present with nonspecific symptoms such as fever and fatigue. Endocarditis, shunt nephritis, and abscesses)
      • Fungal and parasitic infections
      • Autoimmune diseases (e.g., systemic lupus erythematosus Systemic lupus erythematosus Systemic lupus erythematosus (SLE) is a chronic autoimmune, inflammatory condition that causes immune-complex deposition in organs, resulting in systemic manifestations. Women, particularly those of African American descent, are more commonly affected. Systemic Lupus Erythematosus, Sjögren syndrome, rheumatoid arthritis Rheumatoid arthritis Rheumatoid arthritis (RA) is a symmetric, inflammatory polyarthritis and chronic, progressive, autoimmune disorder. Presentation occurs most commonly in middle-aged women with joint swelling, pain, and morning stiffness (often in the hands). Rheumatoid Arthritis)
      • Paraproteinemias (e.g., MGUS, Waldenstrom macroglobulinemia)
      • Malignancies (e.g., non- Hodgkin lymphoma Hodgkin lymphoma Hodgkin lymphoma (HL) is a malignancy of B lymphocytes originating in the lymph nodes. The pathognomonic histologic finding of HL is a Hodgkin/Reed-Sternberg (HRS) cell (giant multinucleated B cells with eosinophilic inclusions). The disease presents most commonly with lymphadenopathy, night sweats, weight loss, fever, splenomegaly and hepatomegaly. Hodgkin Lymphoma)
      • Splenorenal shunt for portal hypertension Portal hypertension Portal hypertension is increased pressure in the portal venous system. This increased pressure can lead to splanchnic vasodilation, collateral blood flow through portosystemic anastomoses, and increased hydrostatic pressure. There are a number of etiologies, including cirrhosis, right-sided congestive heart failure, schistosomiasis, portal vein thrombosis, hepatitis, and Budd-Chiari syndrome. Portal Hypertension
      • Idiopathic/primary
    • Complement-mediated MPGN (less common):
      • C3 glomerulonephritis (C3GN)
      • C3 DDD: most cases have C3NeF → binds to alternative pathway C3 convertase → sustained C3 activation
      • C4 glomerulopathies (C4GN, C4 DDD)
      • Genetic causes
    • MPGN without Ig or complement deposition (commonly from endothelial injury, followed by repair):
      • Thrombotic microangiopathies
      • Antiphospholipid antibody syndrome
      • After bone marrow Bone marrow Bone marrow, the primary site of hematopoiesis, is found in the cavities of cancellous bones and the medullary canals of long bones. There are 2 types: red marrow (hematopoietic with abundant blood cells) and yellow marrow (predominantly filled with adipocytes). Composition of Bone Marrow transplantation
      • Chronic kidney allograft nephropathy
      • Radiation nephritis
      • Malignant hypertension Hypertension Hypertension, or high blood pressure, is a common disease that manifests as elevated systemic arterial pressures. Hypertension is most often asymptomatic and is found incidentally as part of a routine physical examination or during triage for an unrelated medical encounter. Hypertension

Clinical Presentation and Diagnosis

Manifestations

  • Variable (can present as acute/ rapidly progressive glomerulonephritis Rapidly Progressive Glomerulonephritis Rapidly progressive glomerulonephritis (RPGN) is a syndrome of severe glomerular disease with progressive loss of kidney function within weeks to months. Histologically, crescents (the proliferation of epithelial cells and the infiltration of monocytes/macrophages in the Bowman space) are found in the glomeruli and arise from immunologic injury. Rapidly Progressive Glomerulonephritis ( RPGN RPGN Rapidly progressive glomerulonephritis (RPGN) is a syndrome of severe glomerular disease with progressive loss of kidney function within weeks to months. Histologically, crescents (the proliferation of epithelial cells and the infiltration of monocytes/macrophages in the Bowman space) are found in the glomeruli and arise from immunologic injury. Rapidly Progressive Glomerulonephritis) or as CKD CKD Chronic kidney disease (CKD) is kidney impairment that lasts for ≥ 3 months, implying that it is irreversible. Hypertension and diabetes are the most common causes; however, there are a multitude of other etiologies. In the early to moderate stages, CKD is usually asymptomatic and is primarily diagnosed by laboratory abnormalities. Chronic Kidney Disease)
  • Typical findings:
    • Hematuria: typically with dysmorphic red cells or red cell casts
    • Serum creatinine may be elevated or normal.
    • Proteinuria: sometimes similar to the levels seen in nephrotic syndrome Nephrotic syndrome Nephrotic syndrome is characterized by severe proteinuria, hypoalbuminemia, and peripheral edema. In contrast, the nephritic syndromes present with hematuria, variable loss of renal function, and hypertension, although there is sometimes overlap of > 1 glomerular disease in the same individual. Nephrotic Syndrome
    • Edema
    • Hypertension
  • Low complement levels or hypocomplementemia (↓C3 and ↓CH50 levels) are common (although complement levels may be normal):
    • Immune complex-mediated MPGN:
      • Classic complement pathway is activated.
      • ↓ C3 and C4
    • Complement-mediated MPGN:
      • Alternative pathway is activated.
      • ↓ C3, but normal C4
  • Extrarenal manifestations: macular retinal deposits (drusen) and upper body lipodystrophy in DDD

Diagnosis

  • Although the clinical presentation may be suggestive, a biopsy is required for diagnosis:
    • Biopsy establishes a histologic lesion but not a clinical diagnosis.
    • Further workup is needed to determine the underlying entity causing MPGN.
  • Biopsy findings: based on histologic changes determined using light microscopy, immunofluorescence, and electron microscopy
Table: Microscopy findings in MPGN (based on pathogenetic process)
Immune complex/monoclonal Ig-mediated MPGN Complement-mediated MPGN MPGN with no Ig or complement
LM “Tram tracking” (double contouring) of basement membrane
IM
  • Positive staining for polyclonal Ig and complement (C3)
  • Monoclonal Ig: clonal B cell or plasma cell disorder likely
Complement positive and no (or minimal) staining for Ig No Ig or complement staining
EM Subendothelial and mesangial deposits (in some autoimmune diseases, + subepithelial deposits)
  • Mesangial, subendothelial deposits (sometimes, + subepithelial and intramembranous deposits)
  • Dense intramembranous deposits (DDD only)
No electron-dense deposits along the capillary walls
Differential diagnosis
  • Autoimmune diseases
  • Infections
  • Monoclonal gammopathies
  • Idiopathic
  • C3 glomerulopathies (C3GN, C3 DDD)
  • C4 glomerulopathies (C4GN, C3 DDD)
Endothelial injury, which can be from:
  • TTP, HUS, APLS
  • BMT
  • Renal allograft nephropathy
  • Malignant hypertension Hypertension Hypertension, or high blood pressure, is a common disease that manifests as elevated systemic arterial pressures. Hypertension is most often asymptomatic and is found incidentally as part of a routine physical examination or during triage for an unrelated medical encounter. Hypertension
  • Radiation nephritis
APLS: antiphospholipid syndrome Antiphospholipid syndrome Antiphospholipid syndrome (APLS) is an acquired autoimmune disorder characterized by the persistent presence of antiphospholipid antibodies, which create a hypercoagulable state. These antibodies are most commonly discovered during a workup for a thrombotic event or recurrent pregnancy loss, which are the 2 most common clinical manifestations. Antiphospholipid Syndrome
BMT: bone marrow Bone marrow Bone marrow, the primary site of hematopoiesis, is found in the cavities of cancellous bones and the medullary canals of long bones. There are 2 types: red marrow (hematopoietic with abundant blood cells) and yellow marrow (predominantly filled with adipocytes). Composition of Bone Marrow transplantation
DDD: dense deposit disease
EM: electron microscopy
GN: glomerulonephritis
HUS: hemolytic-uremic syndrome
IM: immunofluorescence microscopy
LM: light microscopy
MPGN: membranoproliferative glomerulonephritis
TTP: thrombotic thrombocytopenic purpura Thrombotic thrombocytopenic purpura Thrombotic thrombocytopenic purpura (TTP) is a life-threatening condition due to either a congenital or an acquired deficiency of ADAMTS-13, a metalloproteinase that cleaves multimers of von Willebrand factor (VWF). The large multimers then aggregate excessive platelets resulting in microvascular thrombosis and an increase in consumption of platelets. Thrombotic Thrombocytopenic Purpura
Table: Immunofluorescence microscopy of specific diseases causing MPGN
Etiology Microscopic findings
Immune complex/monoclonal Ig-mediated MPGN Hepatitis B or C (or other viral infections)
  • Granular deposition of IgM, C3
  • Kappa and lambda light chains
Monoclonal gammopathy Kappa OR lambda light chains
Autoimmune diseases “Full-house pattern”:
  • IgG, IgM, IgA
  • C1q, C3, C4
  • Kappa and lambda light chains
Complement-mediated MPGN C3 glomerulopathy
  • Brightly stained C3 along the capillary walls and mesangium
  • No (or minimal) Ig staining
C4 glomerulopathy
  • Brightly stained C4d (degradation product of C4)
  • No (or minimal) Ig staining
MPGN not associated with complement or Ig deposition Microangiopathies (commonly associated with endothelial injury) No significant Ig or complement deposition seen
MPGN: membranoproliferative glomerulonephritis
Membranoproliferative glomerulonephritis (mpgn) vs normal glomeruli

Membranoproliferative glomerulonephritis (MPGN) vs normal glomeruli:
A: normal glomerulus (with open capillary loops, ≤ 3 nuclei in each mesangial area, intact foot processes, and no deposits or proliferation)
B: MPGN: Glomeruli become lobulated with endocapillary proliferation and the glomerular basement membrane has a split appearance (from subendothelial deposits and mesangial interposition).
C: MPGN with mesangial deposits and intramembranous deposits (as seen in dense deposit disease)

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Additional workup

Additional workup is indicated when biopsy shows changes consistent with:

  • Immune complex/monoclonal Ig-mediated MPGN; further tests may include:
    • Workup for infections:
      • Blood cultures
      • Serology to determine hepatitis B Hepatitis B Hepatitis B virus (HBV) is a partially double-stranded DNA virus, which belongs to the Orthohepadnavirus genus and the Hepadnaviridae family. Most individuals with acute HBV infection are asymptomatic or have mild, self-limiting symptoms. Chronic infection can be asymptomatic or create hepatic inflammation, leading to liver cirrhosis and hepatocellular carcinoma (HCC). Hepatitis B Virus and hepatitis C Hepatitis C Hepatitis C is an infection of the liver caused by the hepatitis C virus (HCV). The infection can be transmitted through infectious blood or body fluids and may be transmitted during childbirth or through IV drug use or sexual intercourse. Hepatitis C virus can cause both acute and chronic hepatitis, ranging from a mild to a serious, lifelong illness including liver cirrhosis and hepatocellular carcinoma (HCC). Hepatitis C Virus infections
      • PCR and serologic tests to determine viral, bacterial, and fungal infections in the relevant clinical context
    • Workup for autoimmune diseases: screening for autoimmune diseases, followed by specific tests as indicated
    • Workup for monoclonal gammopathies:
      • Serum protein electrophoresis and immunofixation
      • Serum free light chains
      • Urine protein electrophoresis and immunofixation
      • Bone Bone Bone is a compact type of hardened connective tissue composed of bone cells, membranes, an extracellular mineralized matrix, and central bone marrow. The 2 primary types of bone are compact and spongy. Structure of Bones marrow studies may also be indicated.
  • Complement-mediated MPGN; check for:
    • Activation of the classic complement pathways: C3, C4, CH50
    • Activation of the alternative complement pathway: AH50
    • Genetic analysis for mutations and allele variants of complement factors
    • Autoantibodies to complement regulating proteins (e.g., factors H and I)
    • Testing for C3NeF
    • Serum levels of the membrane attack complex

Management

Treatment

  • Treat the underlying disease (e.g., antiviral therapy for hepatitis B Hepatitis B Hepatitis B virus (HBV) is a partially double-stranded DNA virus, which belongs to the Orthohepadnavirus genus and the Hepadnaviridae family. Most individuals with acute HBV infection are asymptomatic or have mild, self-limiting symptoms. Chronic infection can be asymptomatic or create hepatic inflammation, leading to liver cirrhosis and hepatocellular carcinoma (HCC). Hepatitis B Virus or C, immunosuppression for autoimmune disorders).
  • While most cases can be classified, the underlying disease is not found (idiopathic) in a small number of cases.
    • Management depends on:
      • Proteinuria
      • Degree of kidney failure
    • In mild disease (normal kidney function, non-nephrotic–range proteinuria (< 3.5 g/day), and no significant hematuria):
      • ACE inhibitors (ACEis) or ARBs
      • Regular follow up of renal function (creatinine, urinalysis, urine protein)
    • Upon deterioration (e.g., > 1.5 g/day proteinuria or abnormal creatinine), the therapeutic options considered are:
      • Immunosuppression (corticosteroids, mycophenolate, cyclophosphamide, cyclosporine, tacrolimus)
      • Plasma exchange if C3NeF is present
      • Eculizumab (monoclonal antibody to C5)
    • Renal transplantation (recurrence possible in the graft)

Prognosis

  • Poor prognostic factors:
    • Nephrotic syndrome
    • Hypertension
    • Elevated creatinine
    • Crescents on biopsy
    • Tubulointerstitial disease
  • Good prognostic factors:
    • Non-nephrotic range proteinuria
    • Normal blood pressure
    • Normal creatinine

Differential Diagnosis

  • IgA nephropathy IgA nephropathy IgA nephropathy (Berger's disease) is a renal disease characterized by IgA deposition in the mesangium. It is the most common cause of primary glomerulonephritis in most developed countries. Patients frequently present in the second and third decades of life and, historically, with a preceding upper respiratory or GI infection. IgA Nephropathy: a renal disease characterized by IgA deposition in the mesangium. Immunoglobulin A nephropathy frequently presents in the 2nd and 3rd decades of life and, historically, with a preceding upper respiratory or GI infection. Presenting features are gross hematuria or asymptomatic, microscopic hematuria. The course is often benign, with renal biopsy performed only in cases of severe, progressive renal disease. Treatment depends on the severity of proteinuria, renal function, and pathologic changes. To reduce disease progression, ACEis or ARBs are often used. Immunosuppressants are administered to address persistent proteinuria and increasing creatinine levels.
  • Lupus nephritis (glomerulonephritis caused by systemic lupus erythematosus Systemic lupus erythematosus Systemic lupus erythematosus (SLE) is a chronic autoimmune, inflammatory condition that causes immune-complex deposition in organs, resulting in systemic manifestations. Women, particularly those of African American descent, are more commonly affected. Systemic Lupus Erythematosus): Clinical presentations include hematuria, nephrotic range proteinuria, and, in advanced disease, azotemia. Diagnosis is based on renal biopsy. Treatment usually involves corticosteroids and cytotoxic agents, or other immunosuppressant drugs.
  • Poststreptococcal glomerulonephritis Poststreptococcal Glomerulonephritis Post-streptococcal glomerulonephritis (PSGN) is a type of nephritis that is caused by a prior infection with group A beta-hemolytic Streptococcus (GAS). The clinical presentation of PSGN can range from asymptomatic, microscopic hematuria to full-blown acute nephritic syndrome, which is characterized by red-to-brown urine, proteinuria, edema, and acute kidney injury. Poststreptococcal Glomerulonephritis: a type of nephritis caused by a prior infection with group A beta-hemolytic Streptococcus Streptococcus Streptococcus is one of the two medically important genera of gram-positive cocci, the other being Staphylococcus. Streptococci are identified as different species on blood agar on the basis of their hemolytic pattern and sensitivity to optochin and bacitracin. There are many pathogenic species of streptococci, including S. pyogenes, S. agalactiae, S. pneumoniae, and the viridans streptococci. Streptococcus (GAS). The clinical presentation can range from asymptomatic, microscopic hematuria to full-blown acute nephritic syndrome Nephritic syndrome Nephritic syndrome is a broad category of glomerular diseases characterized by glomerular hematuria, variable loss of renal function, and hypertension. These features are in contrast to those of nephrotic syndrome, which includes glomerular diseases characterized by severe proteinuria, although there is sometimes overlap of > 1 glomerular disease in the same individual. Nephritic Syndrome, which is characterized by red-to-brown urine, proteinuria, edema Edema Edema is a condition in which excess serous fluid accumulates in the body cavity or interstitial space of connective tissues. Edema is a symptom observed in several medical conditions. It can be categorized into 2 types, namely, peripheral (in the extremities) and internal (in an organ or body cavity). Edema, and AKI AKI Acute kidney injury refers to sudden and often reversible loss of renal function, which develops over days or weeks. Azotemia refers to elevated levels of nitrogen-containing substances in the blood that accompany AKI, which include BUN and creatinine. Acute Kidney Injury. The diagnosis is made based on clinical findings in the setting of a recent GAS infection. The management is supportive and involves treating the clinical manifestations. The prognosis is generally favorable, especially in children.
  •   RPGN RPGN Rapidly progressive glomerulonephritis (RPGN) is a syndrome of severe glomerular disease with progressive loss of kidney function within weeks to months. Histologically, crescents (the proliferation of epithelial cells and the infiltration of monocytes/macrophages in the Bowman space) are found in the glomeruli and arise from immunologic injury. Rapidly Progressive Glomerulonephritis: a syndrome of severe glomerular disease with progressive loss of kidney function within weeks to months. Rapidly progressive glomerulonephritis is a manifestation of different diseases. Histologically, crescents are found in the glomeruli. Crescents arise from immunologic injury, major mechanisms of which are classified into anti-GBM disease, pauci-immune crescentic disease, and immune complex-mediated injury. Hematuria, proteinuria, edema Edema Edema is a condition in which excess serous fluid accumulates in the body cavity or interstitial space of connective tissues. Edema is a symptom observed in several medical conditions. It can be categorized into 2 types, namely, peripheral (in the extremities) and internal (in an organ or body cavity). Edema, and hypertension Hypertension Hypertension, or high blood pressure, is a common disease that manifests as elevated systemic arterial pressures. Hypertension is most often asymptomatic and is found incidentally as part of a routine physical examination or during triage for an unrelated medical encounter. Hypertension are the manifestations of RPGN RPGN Rapidly progressive glomerulonephritis (RPGN) is a syndrome of severe glomerular disease with progressive loss of kidney function within weeks to months. Histologically, crescents (the proliferation of epithelial cells and the infiltration of monocytes/macrophages in the Bowman space) are found in the glomeruli and arise from immunologic injury. Rapidly Progressive Glomerulonephritis. Diagnosis is by presentation, laboratory tests, imaging, and renal biopsy. Prompt treatment is essential and includes corticosteroids, immunosuppressants Immunosuppressants Immunosuppressants are a class of drugs widely used in the management of autoimmune conditions and organ transplant rejection. The general effect is dampening of the immune response. Immunosuppressants, and plasmapheresis, depending on the underlying disease.

References

  1. Alchi, B., Jayne, D. (2010). Membranoproliferative glomerulonephritis. Pediatric nephrology (Berlin, Germany). 25, 1409–1418. https://doi.org/10.1007/s00467-009-1322-7
  2. Fervenza, F.C., et al. (2021). Membranoproliferative glomerulonephritis: Classification, clinical features, and diagnosis. In Glassock, R.J., et al. (Ed.), UpToDate. Retrieved Sept 30, 2021, from https://www.uptodate.com/contents/membranoproliferative-glomerulonephritis-classification-clinical-features-and-diagnosis
  3. Fervenza, F.C., et al. (2020). Membranoproliferative glomerulonephritis: Treatment and prognosis. In Glassock, R.J., et al. (Ed.), UpToDate. Retrieved Sept 30, 2021, from https://www.uptodate.com/contents/membranoproliferative-glomerulonephritis-treatment-and-prognosis
  4. Kathuria, P., Patel, A. (2019). Membranoproliferative glomerulonephritis. Medscape. Retrieved August 11, 2021, from https://emedicine.medscape.com/article/240056
  5. O’Brien, F. (2021). Membranoproliferative glomerulonephritis. MSD Manual Professional Version. Retrieved August 10, 2021, from https://www.msdmanuals.com/professional/genitourinary-disorders/glomerular-disorders/membranoproliferative-glomerulonephritis
  6. Sethi, S., Fervenza, F.C. (2012). Membranoproliferative Glomerulonephritis — A New Look at an Old Entity. N Engl J Med. 366, 1119–1931. https://pubmed.ncbi.nlm.nih.gov/22435371/
  7. Salvadori, M., Rosso, G. (2016). Reclassification of membranoproliferative glomerulonephritis: Identification of a new GN: C3GN. World Journal of Nephrology. 5, 308–320. https://doi.org/10.5527/wjn.v5.i4.308
  8. Trachtman, H. (2017). Membranoproliferative glomerulonephritis. In Lerma, E.V., et al. (Eds.), CURRENT Diagnosis & Treatment: Nephrology & Hypertension, 2e. McGraw Hill. https://accessmedicine.mhmedical.com/content.aspx?bookid=2287&sectionid=177428874

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