MyEClinic
MyEClinic
Health Dictionary Find a Doctor

Membranous glomerulonephritis

For patient information page, click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Syed Ahsan Hussain, M.D.[2] Cafer Zorkun, M.D., Ph.D. [3] Syed Hassan A. Kazmi BSc, MD [4] Jogeet Singh Sekhon, M.D. [5]

Synonyms and keywords: Extramembranous glomerulopathy; Heymann nephritis; idiopathic membranous glomerulonephritis; idiopathic membranous nephropathy; membranous glomerulonephropathy; membranous glomerulopathy; membranous nephropathy; nephropathy, membranous

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Ahsan Hussain, M.D.[2]

Overview

Historical Perspective

Membranous glomerulonephritis was first discovered by David Jones, renal pathologist from Syracuse University in New York, in 1957.

Classification

There is no established system for the classification of MGN. however it can be divided in two groups based on etiology of MGN.

Pathophysiology

Membranous glomerulonephritis is caused by immune complex formation in the glomerulus. The immune complexes are formed by binding of antibodies to antigens in the glomerular basement membrane. The antigens damage the basement membrane and activates the immune response. The immune complex serves as an activator that triggers a response from the complement system. PLA2R antigen detected within immune deposits by immunofluorescence of the biopsy specimen. Formation of the immune complex. Immune complex formation results in release of cytokines which release membrane attack complex C5-C9. Release of C5-C9 lead to injury of podocyte which causes loss of glomerular permeablity. The damage to podocyte reults in proteinuria.

Causes

The main causes of Membranous Glomerulonephritis are Infectious causes like Hepatitis B, drugs like captopril and autoimmune diseases like systemic lupus erythematosus.

Differentiating Hereditary pancreatitis from Other Diseases

MGN must be differentiated from other diseases that cause proteinuria, weight loss, and renal failure, such as MPGN, MCD, and FSGC.

Epidemiology and Demographics

The incidence rate of membranous glomerulonephritis is 27 per 100.000. The prevalence rate of membranous glomerulonephritis is 690 per 100,000. The prevalence of membranous glomerulonephritis is approximately 690 per 100,000 individuals worldwide. In 2001, the mortality rate of membranous glomerulonephritis is approximately 380 per 100,000. The incidence of membranous glomerulonephritis increases with age; the median age at diagnosis is 40 years. Membranous glomerulopathy usually affects individuals of the caucasian race and chinese population. Membranous glomerulonephritis affects men and women equally. Membranous glomerulonephritis tends to affect Caucasian population and Chinese population.

Risk Factors

The most common risk factors of membranous glomerulonephritis include SLE and drugs like captopril, penicilliamine.

Screening

There is insufficient evidence to recommend routine screening for membranous glomerulonephritis.

Natural History, Complications, and Prognosis

The symptoms of membranous glomerulonephritis usually develop in the fourth decade of life in males. Approximately 5-30% patients with MN have spontanous remission. Common complications of membranous glomerulonephritis include renal failure, hypertension, proteinuria, dyslipidemia, hypercoagulable state leading to thromboembolism, Increased risk of infection. Prognosis is generally good, and 1 year mortality rate of patients with membranous glomerulonephritis is approximately 0.38%. The presence of proteinuria and baseline renal insuffiency are associated with a particularly poor prognosis among patients with membranous glomerulonephritis. Membranous glomerulonephritis caused by NSAIDS is associated with the most favorable prognosis.

Diagnosis

Diagnostic Criteria

The most efficient and sensitive test is ANA, ds-DNA antibodies specific test that is utilized for diagnosis of membranous glomerulonephritis. The gold standard test for the diagnosis of biopsy.

History and Symptoms

The hallmark of membranous glomerulonephritis is nephrotic syndrome. A positive history of forthy urine and headache are suggestive of membranous glomerulonephritis.

Physical Examination

Common physical examination findings of membranous glomerulonephritis include edematous feets and headache.

Laboratory Findings

The major laboratory workup includes blood workup, auto-immune workup and urine workup.

Electrocardiogram

There are no ECG findings associated with membranous glomerulonephritis.

X-ray

There are no x-ray findings associated with membranous glomerulonephritis.

Ultrasound

There are no echocardiography and ultrasound findings associated with membranous glomerulonephritis.

CT scan

There are no CT scan findings associated with membranous glomerulonephritis.

MRI

There are no MRI findings associated with membranous glomerulonephritis.

Other Imaging Findings

There are no other imaging findings associated with membranous glomerulonephritis

Other Diagnostic Studies

The patients with compromised renal functions are indicated for biopsy

Treatment

Medical Therapy

Pharmacologic medical therapy is recommended among patients who has infectious, autoimmune causes of membranous glomerulonephritis. The drugs like prednisone and cyclophospamide are recomended for the treatment of autoimmune cause of membranous glomerulonephritis. Drug like Angiotensin receptor inhibitior (ACEi) is recomended for managment of hypertension.

Surgery

Surgery is not the first-line treatment option for patients with MGN. Surgery is usually reserved for patients requiring renal transplant.

Primary Prevention

Vaccine against heptatis B and treatment of hepatitis C can be preventive for membranous glomerulopathy.

Secondary Prevention

Early detection and treatment of hepatitis C can be preventive for developing membranous glomerulopathy. Safe sexual practice can prevent the risk of HIV which can eventually decreases the risk of MN. Safe sexual practice can prevent the risk of syphilis which can be preventive the risk of MN.

References


Template:WikiDoc Sources

Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Ahsan Hussain, M.D.[2]

Overview

Membranous glomerulonephritis was first discovered by David Jones, renal pathologist from Syracuse University in New York, in 1957

Historical Perspective

Discovery

Following is the course of events that lead to important discoveries in spectrum of membranous glomerulonephritis:[1][2]

  • Membranous glomerulonephritis (MGN) was first discovered by David Jones, renal pathologist from Syracuse University in New York, in 1957
  • in 1929 Bell introduced the term membranous glomerulonephritis to differentiate the membranous glomerulonephritis with nephrotic syndrome.

References

  1. ↑ JONES DB (1957). “Nephrotic glomerulonephritis”. Am J Pathol. 33 (2): 313–29. PMC 1934622. PMID 13402889.
  2. ↑ Rosen, Seymour (1971). “Membranous glomerulonephritis: Current status”. Human Pathology. 2 (2): 209–231. doi:10.1016/S0046-8177(71)80035-7. ISSN 0046-8177.

Template:WH Template:WS

Classification

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Ahsan Hussain, M.D.[2]

Overview

There is no established system for the classification of membranous glomerulonephritis (MGN).

Classification

There is no established system for the classification of membranous glomerulonephritis (MGN).

References

Template:WH Template:WS

Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Ahsan Hussain, M.D.[2] Pervaiz Laghari, MD[3]

Overview

Membranous glomerulonephritis is caused by immune complex formation in the glomerulus. The immune complexes are formed by binding of antibodies to antigens in the glomerular basement membrane. The antigens damage the basement membrane and activates the immune response. The immune complex serves as an activator that triggers a response from the complement system. .PLA2R antigen detected within immune deposits by immunofluorescence of the biopsy specimen. Formation of the immune complex. Immune complex formation results in release of cytokines which release membrane attack complex C5-C9. Release of C5-C9 lead to injury of podocyte which causes loss of glomerular permeablity. The damage to podocyte reults in proteinuria.

Pathophysiology

  • The membranous glomerulonephritis is a result of multiple changes, which are:[1][2][3][4][5][6][7]
    • Membranous glomerulonephritis is caused by immune complex formation in the glomerulus.
    • The immune complexes are formed by binding of antibodies to antigens in the glomerular basement membrane.
    • The antigens damage the basement membrane and activates the immune response.
    • The immune complex serves as an activator that triggers a response from the complement system.

Phospholipase A2 receptor

  • The M-type PLA2R is the major antigen in human idiopathic membranous glomerulonephritis. It is expressed in glomerular podocytes.T
  • here was no colocalization of PLA2R in secondary membranous glomerulonephritis biopsies
  • .PLA2R antigen detected within immune deposits by immunofluorescence of the biopsy specimen. Formation of the immune complex.
  • Immune complex formation results in release of cytokines which release membrane attack complex C5-C9.
  • Release of C5-C9 lead to injury of podocyte which causes loss of glomerular permeablity.
  • The damage to podocyte reults in proteinuria.
 
 
 
HLA susceptibility 1
 
 
 
Environmental factors
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Variant of PLA2R1 on podocyte surface
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Innate immunity activation and inflammation
dendritic cell sense epitope of PLA2R1
and present them for adaptive immunity
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Production of auto-immune antibody IgG4/IgG1 which attach them self to epitope on podocyte surface
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
In Situ formation and shedding of subepithelial immune complex
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Which lead to
cytokine release
oxygen derivative release
membrane attack complex C5-C9
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Podocyte injury by apoptosis
altered lectin cytoskeleton
loss of silt pore integrity
loss of glomerular permeability
proteinuria
 
 
 
 
 

Genetics

  • Single-nucleotide polymorphisms (SNPs) at two loci that are highly associated with idiopathic membranous glomerulonephritis.[5][6]
  • The two loci are within the genes for the PLA2R on chromosome 2q24.
  • The human leukocyte antigen (HLA) complex class II alpha chain 1A (”HLA-DQA1”) on chromosome 6p21.
  • The PLA2R has been identified as a major antigen in idiopathic membranous glomerulonephritis.

Associated Conditions

Consitions associated with membranous glomerulonephritis include:[8]

Gross Pathology

  • On gross pathology examination there is no characteristic findings present

Microscopic Pathology

Microscopic pathologic findings characteristic of membranous glomerulonephritis include:[1][2]

  • Early biopsies may be normal.
  • Later: uniform diffuse capillary wall thickening without hypercellularity, no mesangial sclerosis and inflammatory cells.
  • Proximal convoluted tubules: hyaline droplets, reflecting protein reabsorption.
  • Membrane thickening and narrow capillary lumina.
  • Mesangial sclerosis and glomerulosclerosis.

Immunofluorescence

  • Granular diffuse peripheral deposits, usually IgG and C3, also C5b–C9 and occasionally IgM or IgA.
  • C4d immunostaining may be diagnostic.


The microscopic,immunofluorscence and electron microscopic features are listed in the following table:[1][2]

Stage Glomerular Basement Membrane Immunofluorescence Electron Microscopy
Stage 1 Normal or slightly thickned BM Fine granular IgG, C3 Scattered small subepithelial electron dense deposits no foot effacement
Stage 2 Moderately thickened BM with spikes and vacuolization Granular IgG, C3 Diffuse spikes due to subepithelial deposits, diffuse foot process effacement
Stage 3 Moderately thickened BM residual spikes and vacuoles Chain like appearance IF, coarsely granular IgG, C3 Intramembraneous deposits, spikes, neomembrane formation and diffuse foot process effacement
Stage 4 Markedly thick GBM, few spikes, vacoules and glomerulosclerosis Focal IgG, C3 Sclerotic GBM, few deposits and lacunae
  • Membranous Glomerulonephritis: Electron micrography. An excellent example to show thickened basement membrane and immune complexes.
    Membranous Glomerulonephritis: Electron micrography. An excellent example to show thickened basement membrane and immune complexes.
  • Membranous Glomerulonephritis: Micro trichrome high mag excellent to show thickened capillary basement membranes
    Membranous Glomerulonephritis: Micro trichrome high mag excellent to show thickened capillary basement membranes
  • Membranous Glomerulonephritis: Micro PAS high mag excellent example of this lesion
    Membranous Glomerulonephritis: Micro PAS high mag excellent example of this lesion
  • Membranous Glomerulonephritis: Micro PAS med mag
    Membranous Glomerulonephritis: Micro PAS med mag

References

  1. ↑ 1.0 1.1 1.2 Cybulsky AV, Quigg RJ, Salant DJ (October 2005). “Experimental membranous nephropathy redux”. Am. J. Physiol. Renal Physiol. 289 (4): F660–71. doi:10.1152/ajprenal.00437.2004. PMC 1325222. PMID 16159900.
  2. ↑ 2.0 2.1 2.2 Nangaku M, Shankland SJ, Couser WG (May 2005). “Cellular response to injury in membranous nephropathy”. J. Am. Soc. Nephrol. 16 (5): 1195–204. doi:10.1681/ASN.2004121098. PMID 15800119.
  3. ↑ Cunningham PN, Quigg RJ (May 2005). “Contrasting roles of complement activation and its regulation in membranous nephropathy”. J. Am. Soc. Nephrol. 16 (5): 1214–22. doi:10.1681/ASN.2005010096. PMID 15800113.
  4. ↑ Kanigicherla D, Gummadova J, McKenzie EA, Roberts SA, Harris S, Nikam M, Poulton K, McWilliam L, Short CD, Venning M, Brenchley PE (May 2013). “Anti-PLA2R antibodies measured by ELISA predict long-term outcome in a prevalent population of patients with idiopathic membranous nephropathy”. Kidney Int. 83 (5): 940–8. doi:10.1038/ki.2012.486. PMID 23364522.
  5. ↑ 5.0 5.1 Debiec H, Ronco P (February 2011). “PLA2R autoantibodies and PLA2R glomerular deposits in membranous nephropathy”. N. Engl. J. Med. 364 (7): 689–90. doi:10.1056/NEJMc1011678. PMID 21323563.
  6. ↑ 6.0 6.1 Hoxha E, Kneißler U, Stege G, Zahner G, Thiele I, Panzer U, Harendza S, Helmchen UM, Stahl RA (October 2012). “Enhanced expression of the M-type phospholipase A2 receptor in glomeruli correlates with serum receptor antibodies in primary membranous nephropathy”. Kidney Int. 82 (7): 797–804. doi:10.1038/ki.2012.209. PMID 22673885.
  7. ↑ Svobodova B, Honsova E, Ronco P, Tesar V, Debiec H (July 2013). “Kidney biopsy is a sensitive tool for retrospective diagnosis of PLA2R-related membranous nephropathy”. Nephrol. Dial. Transplant. 28 (7): 1839–44. doi:10.1093/ndt/gfs439. PMID 23223223.
  8. ↑ Wasserstein AG (April 1997). “Membranous glomerulonephritis”. J. Am. Soc. Nephrol. 8 (4): 664–74. PMID 10495797.

Template:WH Template:WS

References

Template:WH Template:WS

Causes

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Ahsan Hussain, M.D.[2]

Overview

The main causes of membranous glomerulonephritis are infections like hepatitis B, hepatitis C, HIV, syphilis, leprosy, drugs like captopril, penicilliamine, autoimmune diseases like systemic lupus erythematosus, Guillian-Barre nephropathy and neoplastic diseases like non-hodgkin`s lymphoma, chronic lymphocytic leukemia, occasionally hodgkin`s lymphoma.

Causes:

Life-threatening Causes

Common Causes

Infectious Causes

Drugs and toxicity

Neoplastic causes:

Less common causes:

Infectious causes:

Drug and toxicity:

Neoplastic disease

Miscellaneous

Causes by Organ System

  • The causes of membranous glomerulonephritis are given below:[1][2][3]
Cardiovascular No underlying causes
Chemical/Poisoning Volatile hydrocarbons
Dental No underlying causes
Dermatologic Bullous pemphigoid
Drug Side Effect Captopril, Penicilliamine
Ear Nose Throat No underlying causes
Endocrine Diabetes mellitus, Hashimoto`s thyroiditis
Environmental No underlying causes
Gastroenterologic No underlying causes
Genetic Weber-christian disease
Hematologic Sickle cell anemia
Iatrogenic No underlying causes
Infectious Disease Hepatitis B, Hepatitis C, secondary and congenital syphilis, HIV nephropathy, Schistosomiasis, Leprosy, Hydatid disease, Loaiasis (filaria), Quartan malaria
Musculoskeletal/Orthopedic Rheumatoid arthritis
Neurologic Guillain-Barre nephropathy, Myasthenia gravis
Nutritional/Metabolic No underlying causes
Obstetric/Gynecologic No underlying causes
Oncologic Non-Hodgkin`s Lymphoma, Chronic Lymphocytic Leukemia, Hodgkin`s Lymphoma
Ophthalmologic No underlying causes
Overdose/Toxicity Captopril, Gold, Penicilliamine
Psychiatric No underlying causes
Pulmonary Sarcoidosis
Renal/Electrolyte No underlying causes
Rheumatology/Immunology/Allergy Rheumatoid arthritis, Mysthenia gravis, Primary biliary cirrhosis, Guillain-Barre nephropathy, Systemic lupus erythematosis
Sexual No underlying causes
Trauma No underlying causes
Urologic No underlying causes
Miscellaneous No underlying causes

Causes in Alphabetical Order

List the causes of the disease in alphabetical order:[1][2][3]

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Wasserstein AG (April 1997). “Membranous glomerulonephritis”. J. Am. Soc. Nephrol. 8 (4): 664–74. PMID 10495797.
  2. ↑ 2.0 2.1 2.2 2.3 Reichert, LJ; Koene, RA; Wetzels, JF (1998). “Prognostic factors in idiopathic membranous nephropathy”. American Journal of Kidney Diseases. 31 (1): 1–11. doi:10.1053/ajkd.1998.v31.pm9428445. ISSN 0272-6386.
  3. ↑ 3.0 3.1 3.2 Troyanov, S.; Roasio, L.; Pandes, M.; Herzenberg, A.M.; Cattran, D.C. (2006). “Renal pathology in idiopathic membranous nephropathy: A new perspective”. Kidney International. 69 (9): 1641–1648. doi:10.1038/sj.ki.5000289. ISSN 0085-2538.

Template:WH Template:WS

Differentiating Membranous glomerulonephritis from other Diseases

Differentiating Membranous glomerulonephritis from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mehrian Jafarizade, M.D [2], Syed Hassan A. Kazmi BSc, MD [3]

Overview

MGN must be differentiated from other diseases that cause proteinuria, weight loss, and renal failure, such as MPGN, MCD, and FSGC.

Differentiating Membranous Glomerulonephritis From Other Diseases

The various types of glomerular diseases should be differentiated from each other based on associations, presence of pitting edema, hematuria, hypertension, hemoptysis, oliguria, peri-orbital edema, hyperlipidemia, type of antibodies, light and electron microscopic features. The following table differentiates between various types of glumerular diseases:

Glomerular diseases Disease History and Symtoms Laboratory Findings Pathology
History Systemic symptoms Hemeturia Proteinuria Hypertension Pitting edema Oliguria Nephrotic features Nephritic features Hyperlipidemia and hypercholesterolemia Auto-antibodies,

Complements

Light microscope Electron microscope Immunoflourescence pattern
Acute Nephritic Syndromes Poststreptococcal Glomerulonephritis[1][2][3] +/- + +/- +/- +/- +/- +/- +/-
  • Immune complex GN
  • Granular deposit
Renal disease due to Subacute Bacterial Endocarditis, or cardiac shunt (Atrioventricular)[4][5] +/- + +/- +/- +/- +/- +/- +/-
  • Crescentic GN is the most common pathological features
  • Mesangial deposits,
  • Subendothelial deposits
  • Subepithelial “humps,” in minority of cases
  • Pauci-immune GN
Lupus Nephritis[6]
  • History of SLE features
 +/- + +/- +/- +/- +/- +/- +/-
  • Differs based on the disease classification
  • Differs based on the disease classification
  • Differs based on the disease classification, mostly immune complex GN
  • Granular deposit
Antiglomerular Basement Membrane Disease (Goodpasture’s syndrome)[7][8]
  • Young adults
 + + + + + + – – Diffuse thickening of the glomerular basement membrane with absence of sub-epithelial and sub-endothelial deposits 
  • Immune complex GN
  • Linear deposit
IgA Nephropathy[9][10] + +/- + +/- + – + –
  • Immune complex deposition
  • Crescent formation
  • Immune complex GN, granular deposite
Disease History Systemic symptoms Hemeturia Proteinuria Hypertension Pitting edema Oliguria Nephrotic features Nephritic features Hyperlipidemia and hypercholesterolemia Auto-antibodies,

Complements

Light microscope Electron microscope Immunoflourescence pattern
ANCA Small-Vessel Vasculitis[11][12] Granulomatosis with Polyangiitis (Wegener’s)[13][14][15]
  • Middle age male
 + + + +/- + – + –
  •  Pauci-immune GN
Microscopic Polyangiitis[16] +/- + + + + + + –
  •  Pauci-immune GN
Churg-Strauss Syndrome[17] +/- + + + + + + –
  •  Pauci-immune GN
Membranoproliferative Glomerulonephritis[18][19] + + + +/- + + – – –
  • Immune complex GN
  • Granular deposite
Henoch-Schönlein purpura [20] + + + +/- + + – – –
  • Diffuse mesangial IgA deposits often associated with mesangial hypercellularity
  • Diffuse mesangial IgA deposits often associated with mesangial hypercellularity
  • Immune complex GN, granular deposite
Disease History Systemic symptoms Hemeturia Proteinuria Hypertension Pitting edema Oliguria Nephrotic features Nephritic features Hyperlipidemia and hypercholesterolemia Auto-antibodies,

Complements

Light microscope Electron microscope Immunoflourescence pattern
Cryoglobulinemia[21] Patients having cryoglobulinemia may have positive history of: Pulmonary symptoms:
  • Cough

Cutaneous symptoms:

Gastrointestinal symptoms:

  • Abdominal pain

General symptoms:

+/- + +/- + +/- +/- +/- +/- +/-
  • Prominent IgM and C3
Nephrotic Syndrome Minimal Change Disease[22][23] – + – + +/- + – +
  • Normal
 –
Focal Segmental Glomerulosclerosis[24][25][26] – + – + +/- + – + –
Membranous Glomerulonephritis[27][28] – + – + +/- + – + Immune complex deposition Immune complex GN, granular deposite
Diabetic Nephropathy[29][30][31][32][33][34][35][36][37][38] For more information on diabetes click here. – + – + +/- + – +
  • Diffuse mesangial matrix expansion (nodular glomerulosclerosis)
  • Increased mesangial hypercellularity
  • Prominent glomerular basement membranes
  • Thick basement membrane without any deposit
  • Nodular glomerulosclerosis
 –
Disease History Systemic symptoms Hemeturia Proteinuria Hypertension Pitting edema Oliguria Nephrotic features Nephritic features Hyperlipidemia and hypercholesterolemia Auto-antibodies,

Complements

Light microscope Electron microscope Immunoflourescence pattern
 Glomerular Deposition Diseases  Light Chain Deposition Disease[39]
  • Occurs in the setting of high tumor burden
 – – + – + +/- + – + –
  • Light-chain deposits
  • Granular deposits on electron microscopy
  • Detection of light chain deposits using anti–light chain antibody
Renal Amyloidosis[40][41][42][43] – + – + +/- + – + –
  • Diffuse glomerular deposition of amorphous hyaline material (nodular pattern), in mesangium (weakly staining with periodic acid-Schiff (PAS)
  • Nodular deposit
  • AA amyloidosis type: negative for immunoglobulins and complement
  • AL amyloidosis type: Positive for lambda or kappa light chains
Fibrillary-Immunotactoid Glomerulopathy[44] – +/- + +/- +/- +/- + +/- +/- –
  • Diffuse sclerosing glomerulonephritis
  • Diffuse proliferative glomerulonephritis
  • Membranoproliferative glomerulonephritis
  • Mesangioproliferative/sclerosing disease
  • Membranous glomerulonephritis
  • Large fibrillar deposits in the mesangium randomly
  • Glomerular capillary walls different from amloidosis
  • No staining with Congo red or thioflavine-T or with antibodies to a specific type
  • Positive for immunoglobulin G (IgG), C3
  • Kappa and lambda (ie, polyclonal) light chains
Fabry’s Disease[45][46][47] – + – + +/- + – + –
  • Vacuolization of visceral glomerular epithelial cells (podocytes) and distal tubular epithelial cells
  • Glycolipid accumulation
  • Myeloid or zebra bodies: Gb3 deposition within enlarged secondary lysosomes as lamellated membrane structures
  • Inclusions, composed of concentric layers (onion skin appearance)
 –
Basement Membrane Syndrome Alport’s Syndrome[48][49][50][51][52][53]
  • Positive family history
 Auditary:

Occular problems:

  • Refractory Error
 – + – + +/- + – + –
  • Early stage: unremarkable
Disease History Systemic symptoms Hemeturia Proteinuria Hypertension Pitting edema Oliguria Nephrotic features Nephritic features Hyperlipidemia and hypercholesterolemia Auto-antibodies,

Complements

Light microscope Electron microscope Immunoflourescence pattern
Thin Basement Membrane Disease[54][55] – – + -/+ – -/+ – -/+ – – – Diffuse thinning of the glomerular basement membranes (GBM) –
Nail-Patella Syndrome[56][57]
  • Positive family history
  • Poorly developed fingernails, toe nails, and patellae (kneecaps).
  • Elbow deformities
  • Abnormally shaped pelvis bone (hip bone)
  • Knee may be small, deformed or absent
 + + – – – – – – –
  • Mostly unremarkable changes
  • Secondary FSGS
  • Late stages:
    • Global glomerulosclerosis,
    • Tubulointerstitial fibrosis
  • Glomerular basement membranes (GBMs): Focal or diffuse irregular thickening with electron-lucent areas (moth-eaten appearance) containing type III collagen bundles.
  • Similar collagen fibrils can be seen in mesangial matrix.
  • Podocytes: Segmental effacement of foot processes.
  • Nonspecific IgM and C3 deposition may be seen in sclerotic glomeruli.
 Glomerular-Vascular Syndromes  Hypertensive Nephrosclerosis[58] Chronic hypertension +/- +/- + +/- +/- +/- – +/- –
  • Interstitial fibrosis and atrophy
  • Medial thickening and intimal fibrosis of medium-sized and larger vessels
  • Arteriolar thickening, and hyalinosis
  • Chronic stages:
Cholesterol Emboli[59]
  • Depends on the organ involved
 +/- +/- + +/- +/- +/- – +/- –
  • Atheroemboli are seen in interlobular and arcuate arteries, as lance-shaped clefts, due to dissolution of cholesterol crystals
  • Acute lesions:
    • Atheroemboli are surrounded by red blood cells, fibrin, and leukocytes, with multinucleated giant cell reactions
  • Chronic lesions:
    • Cholesterol clefts are surrounded by intimal fibrosis
    • Vessel recanalization of chronic lesions can occur.
  • Global and segmental sclerosis of glomeruli may be present.
  • Extensive foot process effacement can be seen
  • Not specific changes
Disease History Systemic symptoms Hemeturia Proteinuria Hypertension Pitting edema Oliguria Nephrotic features Nephritic features Hyperlipidemia and hypercholesterolemia Auto-antibodies,

Complements

Light microscope Electron microscope Immunoflourescence pattern
Sickle Cell Disease[60]
  • Positive family history
 +/- +/- +/- – – – – – –
  • Glomerular hypertrophy
  • Hemosiderin deposits
  • Focal areas of hemorrhage or necrosis
  • Chronic stage: interstitial inflammation, edema, fibrosis, tubular atrophy, and papillary infarcts
  • Glomerular enlargement and focal segmental glomerulosclerosis (FSGS)
Thrombotic Microangiopathies[61] Click for more information on Thrombotic Microangiopathies. + +/- + +/- +/- +/- – – –
  • Acute stage:
    • Inravasculr fibrin thrombi
  • Chronic stage:
    • Endocapillary hypercellularity.
    • Intimal proliferation of arterioles
  • Swollen glomerular endothelial cells with loss of fenestrations
  • Chronic stage: interposed cells with new GBM matrix material deposition.
Antiphospholipid Antibody Syndrome [62][63][64] + +/- + +/- +/- +/- – – –
  • Swollen glomerular endothelial cells with loss of fenestrations
  • Chronic stage: interposed cells with new GBM matrix material deposition.


Some infectious diseases such as HIV, HBV, HCV, syphilis, leprosy, malaria, and schistosomiasis may cause glomerular diseases.

References

  1. ↑ GERMUTH FG (1953). “A comparative histologic and immunologic study in rabbits of induced hypersensitivity of the serum sickness type”. J Exp Med. 97 (2): 257–82. PMC 2136196. PMID 13022878.
  2. ↑ Germuth FG, Senterfit LB, Dreesman GR (1972). “Immune complex disease. V. The nature of the circulating complexes associated with glomerular alterations in the chronic BSA-rabbit system”. Johns Hopkins Med J. 130 (6): 344–57. PMID 5031005.
  3. ↑ Radhakrishnan J, Cattran DC (2012). “The KDIGO practice guideline on glomerulonephritis: reading between the (guide)lines–application to the individual patient”. Kidney Int. 82 (8): 840–56. doi:10.1038/ki.2012.280. PMID 22895519.
  4. ↑ Neugarten J, Baldwin DS (August 1984). “Glomerulonephritis in bacterial endocarditis”. Am. J. Med. 77 (2): 297–304. PMID 6380288.
  5. ↑ Arze RS, Rashid H, Morley R, Ward MK, Kerr DN (January 1983). “Shunt nephritis: report of two cases and review of the literature”. Clin. Nephrol. 19 (1): 48–53. PMID 6831779.
  6. ↑ Weening JJ, D’Agati VD, Schwartz MM, Seshan SV, Alpers CE, Appel GB, Balow JE, Bruijn JA, Cook T, Ferrario F, Fogo AB, Ginzler EM, Hebert L, Hill G, Hill P, Jennette JC, Kong NC, Lesavre P, Lockshin M, Looi LM, Makino H, Moura LA, Nagata M (February 2004). “The classification of glomerulonephritis in systemic lupus erythematosus revisited”. Kidney Int. 65 (2): 521–30. doi:10.1111/j.1523-1755.2004.00443.x. PMID 14717922.
  7. ↑ Bolton WK (November 1996). “Goodpasture’s syndrome”. Kidney Int. 50 (5): 1753–66. PMID 8914046.
  8. ↑ Mathew TH, Hobbs JB, Kalowski S, Sutherland PW, Kincaid-Smith P (February 1975). “Goodpasture’s syndrome: normal renal diagnostic findings”. Ann. Intern. Med. 82 (2): 215–8. PMID 1090223.
  9. ↑ Suzuki H, Kiryluk K, Novak J, Moldoveanu Z, Herr AB, Renfrow MB, Wyatt RJ, Scolari F, Mestecky J, Gharavi AG, Julian BA (October 2011). “The pathophysiology of IgA nephropathy”. J. Am. Soc. Nephrol. 22 (10): 1795–803. doi:10.1681/ASN.2011050464. PMC 3892742. PMID 21949093.
  10. ↑ Wyatt RJ, Julian BA (June 2013). “IgA nephropathy”. N. Engl. J. Med. 368 (25): 2402–14. doi:10.1056/NEJMra1206793. PMID 23782179.
  11. ↑ Higgins RM, Goldsmith DJ, Connolly J, Scoble JE, Hendry BM, Ackrill P, Venning MC (January 1996). “Vasculitis and rapidly progressive glomerulonephritis in the elderly”. Postgrad Med J. 72 (843): 41–4. PMC 2398323. PMID 8746284.
  12. ↑ Jennette JC (March 2003). “Rapidly progressive crescentic glomerulonephritis”. Kidney Int. 63 (3): 1164–77. doi:10.1046/j.1523-1755.2003.00843.x. PMID 12631105.
  13. ↑ Renaudineau Y, Le Meur Y (October 2008). “Renal involvement in Wegener’s granulomatosis”. Clin Rev Allergy Immunol. 35 (1–2): 22–9. doi:10.1007/s12016-007-8066-6. PMID 18172777.
  14. ↑ Weiss MA, Crissman JD (October 1984). “Renal biopsy findings in Wegener’s granulomatosis: segmental necrotizing glomerulonephritis with glomerular thrombosis”. Hum. Pathol. 15 (10): 943–56. PMID 6384024.
  15. ↑ Pagnoux C (March 2008). “[Wegener’s granulomatosis and microscopic polyangiitis]”. Rev Prat (in French). 58 (5): 522–32. PMID 18524109.
  16. ↑ Chung SA, Seo P (August 2010). “Microscopic polyangiitis”. Rheum. Dis. Clin. North Am. 36 (3): 545–58. doi:10.1016/j.rdc.2010.04.003. PMC 2917831. PMID 20688249.
  17. ↑ Sinico RA, Di Toma L, Maggiore U, Tosoni C, Bottero P, Sabadini E, Giammarresi G, Tumiati B, Gregorini G, Pesci A, Monti S, Balestrieri G, Garini G, Vecchio F, Buzio C (May 2006). “Renal involvement in Churg-Strauss syndrome”. Am. J. Kidney Dis. 47 (5): 770–9. doi:10.1053/j.ajkd.2006.01.026. PMID 16632015.
  18. ↑ Alchi B, Jayne D (August 2010). “Membranoproliferative glomerulonephritis”. Pediatr. Nephrol. 25 (8): 1409–18. doi:10.1007/s00467-009-1322-7. PMC 2887509. PMID 19908070.
  19. ↑ Davis AE, Schneeberger EE, Grupe WE, McCluskey RT (May 1978). “Membranoproliferative glomerulonephritis (MPGN type I) and dense deposit disease (DDD) in children”. Clin. Nephrol. 9 (5): 184–93. PMID 657595.
  20. ↑ Jennette JC, Falk RJ (July 1994). “The pathology of vasculitis involving the kidney”. Am. J. Kidney Dis. 24 (1): 130–41. PMID 8023818.
  21. ↑ Fogo AB, Lusco MA, Najafian B, Alpers CE (February 2016). “AJKD Atlas of Renal Pathology: Cryoglobulinemic Glomerulonephritis”. Am. J. Kidney Dis. 67 (2): e5–7. doi:10.1053/j.ajkd.2015.12.007. PMID 26802335.
  22. ↑ Saha TC, Singh H (November 2006). “Minimal change disease: a review”. South. Med. J. 99 (11): 1264–70. doi:10.1097/01.smj.0000243183.87381.c2. PMID 17195422.
  23. ↑ Saleem MA, Kobayashi Y (2016). “Cell biology and genetics of minimal change disease”. F1000Res. 5. doi:10.12688/f1000research.7300.1. PMC 4821284. PMID 27092244.
  24. ↑ Rosenberg AZ, Kopp JB (March 2017). “Focal Segmental Glomerulosclerosis”. Clin J Am Soc Nephrol. 12 (3): 502–517. doi:10.2215/CJN.05960616. PMC 5338705. PMID 28242845.
  25. ↑ Jefferson JA, Shankland SJ (September 2014). “The pathogenesis of focal segmental glomerulosclerosis”. Adv Chronic Kidney Dis. 21 (5): 408–16. doi:10.1053/j.ackd.2014.05.009. PMC 4149756. PMID 25168829.
  26. ↑ Gephardt GN, Tubbs RR, Popowniak KL, McMahon JT (October 1986). “Focal and segmental glomerulosclerosis. Immunohistologic study of 20 renal biopsy specimens”. Arch. Pathol. Lab. Med. 110 (10): 902–5. PMID 2429634.
  27. ↑ Lai WL, Yeh TH, Chen PM, Chan CK, Chiang WC, Chen YM, Wu KD, Tsai TJ (February 2015). “Membranous nephropathy: a review on the pathogenesis, diagnosis, and treatment”. J. Formos. Med. Assoc. 114 (2): 102–11. doi:10.1016/j.jfma.2014.11.002. PMID 25558821.
  28. ↑ Wasserstein AG (April 1997). “Membranous glomerulonephritis”. J. Am. Soc. Nephrol. 8 (4): 664–74. PMID 10495797.
  29. ↑ Drummond K, Mauer M, International Diabetic Nephropathy Study Group (2002). “The early natural history of nephropathy in type 1 diabetes: II. Early renal structural changes in type 1 diabetes”. Diabetes. 51 (5): 1580–7. PMID 11978659.
  30. ↑ Hørlyck A, Gundersen HJ, Osterby R (1986). “The cortical distribution pattern of diabetic glomerulopathy”. Diabetologia. 29 (3): 146–50. PMID 3699305.
  31. ↑ Alpers CE, Hudkins KL (2011). “Mouse models of diabetic nephropathy”. Curr Opin Nephrol Hypertens. 20 (3): 278–84. doi:10.1097/MNH.0b013e3283451901. PMC 3658822. PMID 21422926.
  32. ↑ Kimmelstiel P, Wilson C (1936). “Intercapillary Lesions in the Glomeruli of the Kidney”. Am J Pathol. 12 (1): 83–98.7. PMC 1911022. PMID 19970254.
  33. ↑ Alpers CE, Biava CG (1989). “Idiopathic lobular glomerulonephritis (nodular mesangial sclerosis): a distinct diagnostic entity”. Clin Nephrol. 32 (2): 68–74. PMID 2766585.
  34. ↑ Toyoda M, Najafian B, Kim Y, Caramori ML, Mauer M (2007). “Podocyte detachment and reduced glomerular capillary endothelial fenestration in human type 1 diabetic nephropathy”. Diabetes. 56 (8): 2155–60. doi:10.2337/db07-0019. PMID 17536064.
  35. ↑ Najafian B, Crosson JT, Kim Y, Mauer M (2006). “Glomerulotubular junction abnormalities are associated with proteinuria in type 1 diabetes”. J Am Soc Nephrol. 17 (4 Suppl 2): S53–60. doi:10.1681/ASN.2005121342. PMID 16565248.
  36. ↑ Najafian B, Kim Y, Crosson JT, Mauer M (2003). “Atubular glomeruli and glomerulotubular junction abnormalities in diabetic nephropathy”. J Am Soc Nephrol. 14 (4): 908–17. PMID 12660325.
  37. ↑ Najafian B, Alpers CE, Fogo AB (2011). “Pathology of human diabetic nephropathy”. Contrib Nephrol. 170: 36–47. doi:10.1159/000324942. PMID 21659756.
  38. ↑ Najafian B, Alpers CE, Fogo AB (2011). “Pathology of human diabetic nephropathy”. Contrib Nephrol. 170: 36–47. doi:10.1159/000324942. PMID 21659756.
  39. ↑ Hutchison CA, Cockwell P, Stringer S, Bradwell A, Cook M, Gertz MA, Dispenzieri A, Winters JL, Kumar S, Rajkumar SV, Kyle RA, Leung N (June 2011). “Early reduction of serum-free light chains associates with renal recovery in myeloma kidney”. J. Am. Soc. Nephrol. 22 (6): 1129–36. doi:10.1681/ASN.2010080857. PMC 3103732. PMID 21511832.
  40. ↑ Baker KR, Rice L (2012). “The amyloidoses: clinical features, diagnosis and treatment”. Methodist Debakey Cardiovasc J. 8 (3): 3–7. PMC 3487569. PMID 23227278.
  41. ↑ Gillmore JD, Hawkins PN (October 2013). “Pathophysiology and treatment of systemic amyloidosis”. Nat Rev Nephrol. 9 (10): 574–86. doi:10.1038/nrneph.2013.171. PMID 23979488.
  42. ↑ Jerzykowska S, Cymerys M, Gil LA, Balcerzak A, Pupek-Musialik D, Komarnicki MA (2014). “Primary systemic amyloidosis as a real diagnostic challenge – case study”. Cent Eur J Immunol. 39 (1): 61–6. doi:10.5114/ceji.2014.42126. PMC 4439975. PMID 26155101.
  43. ↑ Pepys MB (2006). “Amyloidosis”. Annu. Rev. Med. 57: 223–41. doi:10.1146/annurev.med.57.121304.131243. PMID 16409147.
  44. ↑ Korbet SM, Schwartz MM, Lewis EJ (March 1991). “Immunotactoid glomerulopathy”. Am. J. Kidney Dis. 17 (3): 247–57. PMID 1996564.
  45. ↑ Alroy J, Sabnis S, Kopp JB (June 2002). “Renal pathology in Fabry disease”. J. Am. Soc. Nephrol. 13 Suppl 2: S134–8. PMID 12068025.
  46. ↑ Meikle PJ, Hopwood JJ, Clague AE, Carey WF (1999). “Prevalence of lysosomal storage disorders”. JAMA : the Journal of the American Medical Association. 281 (3): 249–54. PMID 9918480. Unknown parameter |month= ignored (help)
  47. ↑ Branton MH, Schiffmann R, Sabnis SG; et al. (2002). “Natural history of Fabry renal disease: influence of alpha-galactosidase A activity and genetic mutations on clinical course”. Medicine. 81 (2): 122–38. PMID 11889412. Unknown parameter |month= ignored (help)
  48. ↑ McCarthy PA, Maino DM (2000). “Alport syndrome: a review”. Clin Eye Vis Care. 12 (3–4): 139–150. PMID 11137428.
  49. ↑ Chugh KS, Sakhuja V, Agarwal A, Jha V, Joshi K, Datta BN; et al. (1993). “Hereditary nephritis (Alport’s syndrome)–clinical profile and inheritance in 28 kindreds”. Nephrol Dial Transplant. 8 (8): 690–5. PMID 8414153.
  50. ↑ Chugh KS, Sakhuja V, Agarwal A, Jha V, Joshi K, Datta BN; et al. (1993). “Hereditary nephritis (Alport’s syndrome)–clinical profile and inheritance in 28 kindreds”. Nephrol Dial Transplant. 8 (8): 690–5. PMID 8414153.
  51. ↑ McCarthy PA, Maino DM (2000). “Alport syndrome: a review”. Clin Eye Vis Care. 12 (3–4): 139–150. PMID 11137428.
  52. ↑ Amari F, Segawa K, Ando F (1994). “Lens coloboma and Alport-like glomerulonephritis”. Eur J Ophthalmol. 4 (3): 181–3. PMID 7819734.
  53. ↑ Govan JA (1983). “Ocular manifestations of Alport’s syndrome: a hereditary disorder of basement membranes?”. Br J Ophthalmol. 67 (8): 493–503. PMC 1040106. PMID 6871140.
  54. ↑ Savige J, Rana K, Tonna S, Buzza M, Dagher H, Wang YY (2003). “Thin basement membrane nephropathy”. Kidney Int. 64 (4): 1169–78. doi:10.1046/j.1523-1755.2003.00234.x. PMID 12969134. Unknown parameter |month= ignored (help)
  55. ↑ Hou P, Chen Y, Ding J, Li G, Zhang H (2007). “A novel mutation of COL4A3 presents a different contribution to Alport syndrome and thin basement membrane nephropathy”. Am. J. Nephrol. 27 (5): 538–44. doi:10.1159/000107666. PMID 17726307.
  56. ↑ Najafian B, Smith K, Lusco MA, Alpers CE, Fogo AB (October 2017). “AJKD Atlas of Renal Pathology: Nail-Patella Syndrome-Associated Nephropathy”. Am. J. Kidney Dis. 70 (4): e19–e20. doi:10.1053/j.ajkd.2017.08.001. PMID 28941488.
  57. ↑ Guidera KJ, Satterwhite Y, Ogden JA, Pugh L, Ganey T (1991). “Nail patella syndrome: a review of 44 orthopaedic patients”. J Pediatr Orthop. 11 (6): 737–42. PMID 1960197.
  58. ↑ Hughson MD, Puelles VG, Hoy WE, Douglas-Denton RN, Mott SA, Bertram JF (July 2014). “Hypertension, glomerular hypertrophy and nephrosclerosis: the effect of race”. Nephrol. Dial. Transplant. 29 (7): 1399–409. doi:10.1093/ndt/gft480. PMC 4071048. PMID 24327566.
  59. ↑ Lusco MA, Najafian B, Alpers CE, Fogo AB (April 2016). “AJKD Atlas of Renal Pathology: Cholesterol Emboli”. Am. J. Kidney Dis. 67 (4): e23–4. doi:10.1053/j.ajkd.2016.02.034. PMID 27012950.
  60. ↑ Wesson DE (June 2002). “The initiation and progression of sickle cell nephropathy”. Kidney Int. 61 (6): 2277–86. doi:10.1046/j.1523-1755.2002.00363.x. PMID 12028473.
  61. ↑ Lusco MA, Fogo AB, Najafian B, Alpers CE (December 2016). “AJKD Atlas of Renal Pathology: Thrombotic Microangiopathy”. Am. J. Kidney Dis. 68 (6): e33–e34. doi:10.1053/j.ajkd.2016.10.006. PMID 27884283.
  62. ↑ Jayakody Arachchillage D, Greaves M (2014). “The chequered history of the antiphospholipid syndrome”. Br J Haematol. 165 (5): 609–17. doi:10.1111/bjh.12848. PMID 24684307.
  63. ↑ Jayakody Arachchillage D, Greaves M (2014). “The chequered history of the antiphospholipid syndrome”. Br J Haematol. 165 (5): 609–17. doi:10.1111/bjh.12848. PMID 24684307.
  64. ↑ Popa A, Voinea L, Pop M, Stana D, Dascalu AM, Alexandrescu C; et al. (2008). “[Primary antiphospholipid syndrome]”. Oftalmologia. 52 (1): 13–7. PMID 18714484.

Template:WH Template:WS

Epidemiology and Demographics

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Ahsan Hussain, M.D.[2]

Overview

The incidence rate of membranous glomerulonephritis is 27 per 100.000. The prevalence rate of membranous glomerulonephritis is 690 per 100,000. The prevalence of membranous glomerulonephritis is approximately 690 per 100,000 individuals worldwide. In 2001, the mortality rate of membranous glomerulonephritis is approximately 380 per 100,000. The incidence of membranous glomerulonephritis increases with age; the median age at diagnosis is 40 years. Membranous glomerulopathy usually affects individuals of the caucasian race and chinese population. Membranous glomerulonephritis affects men and women equally. Membranous glomerulonephritis tends to affect Caucasian population and Chinese population.

Epidemiology and Demographics

  • The membranous glomerulonephritis is a rare disease.[1][2]

Incidence

  • The incidence of membranous glomerulopathy is approximately 27 per 100,000 individuals worldwide.[1]

Prevalence

  • The prevalence of membranous glomerulonephritis is approximately 690 per 100,000 individuals worldwide.[1][3]

Mortality rate

  • In 2001, the mortality rate of membranous glomerulonephritis is approximately 380 per 100,000[1][3][4]

Age

  • Patients of all age groups may develop membranous glomerulonephritis
  • The incidence of membranous glomerulonephritis increases with age; the median age at diagnosis is 40 years[5]

Race

  • Membranous glomerulopathy usually affects individuals of the caucasian race and chinese population.[3][5]

Gender

  • Membranous glomerulonephritis affects men and women equally.[3]

Region

  • Membranous glomerulonephritis tends to affect Caucasian population and Chinese population.[3][5]\

References

  1. ↑ 1.0 1.1 1.2 1.3 McGrogan, A.; Franssen, C. F. M.; de Vries, C. S. (2010). “The incidence of primary glomerulonephritis worldwide: a systematic review of the literature”. Nephrology Dialysis Transplantation. 26 (2): 414–430. doi:10.1093/ndt/gfq665. ISSN 0931-0509.
  2. ↑ Cattran DC, Brenchley PE (March 2017). “Membranous nephropathy: integrating basic science into improved clinical management”. Kidney Int. 91 (3): 566–574. doi:10.1016/j.kint.2016.09.048. PMID 28065518.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 Debiec H, Ronco P (July 2014). “Immunopathogenesis of membranous nephropathy: an update”. Semin Immunopathol. 36 (4): 381–97. doi:10.1007/s00281-014-0423-y. PMID 24715030.
  4. ↑ Xu X, Wang G, Chen N, Lu T, Nie S, Xu G, Zhang P, Luo Y, Wang Y, Wang X, Schwartz J, Geng J, Hou FF (December 2016). “Long-Term Exposure to Air Pollution and Increased Risk of Membranous Nephropathy in China”. J. Am. Soc. Nephrol. 27 (12): 3739–3746. doi:10.1681/ASN.2016010093. PMC 5118492. PMID 27365535.
  5. ↑ 5.0 5.1 5.2 Tang, Lijun; Yao, Jing; Kong, Xianglei; Sun, Qing; Wang, Zunsong; Zhang, Ying; Wang, Ping; Liu, Yipeng; Li, Wenbin; Cui, Meiyu; Zhen, Junhui; Xu, Dongmei (2017). “Increasing prevalence of membranous nephropathy in patients with primary glomerular diseases: A cross-sectional study in China”. Nephrology. 22 (2): 168–173. doi:10.1111/nep.12739. ISSN 1320-5358.

Template:WH Template:WS

Risk Factors

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Ahsan Hussain, M.D.[2]

Overview

The most common risk factors of membranous glomerulonephritis include SLE and drugs like captopril, penicilliamine.

Risk Factors

Common Risk Factors

Less Common Risk Factors

References

  1. ↑ 1.0 1.1 Wasserstein AG (April 1997). “Membranous glomerulonephritis”. J. Am. Soc. Nephrol. 8 (4): 664–74. PMID 10495797.
  2. ↑ Reichert, LJ; Koene, RA; Wetzels, JF (1998). “Prognostic factors in idiopathic membranous nephropathy”. American Journal of Kidney Diseases. 31 (1): 1–11. doi:10.1053/ajkd.1998.v31.pm9428445. ISSN 0272-6386.
  3. ↑ Troyanov, S.; Roasio, L.; Pandes, M.; Herzenberg, A.M.; Cattran, D.C. (2006). “Renal pathology in idiopathic membranous nephropathy: A new perspective”. Kidney International. 69 (9): 1641–1648. doi:10.1038/sj.ki.5000289. ISSN 0085-2538.
  4. ↑ Reichert, LJ; Koene, RA; Wetzels, JF (1998). “Prognostic factors in idiopathic membranous nephropathy”. American Journal of Kidney Diseases. 31 (1): 1–11. doi:10.1053/ajkd.1998.v31.pm9428445. ISSN 0272-6386.

Template:WH Template:WS

Screening

Screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Ahsan Hussain, M.D.[2]

Overview

There is insufficient evidence to recommend routine screening for membranous glomerulonephritis.

Screening

There is insufficient evidence to recommend routine screening for membranous glomerulonephritis.

References

Template:WH Template:WS

Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Ahsan Hussain, M.D.[2]

Overview

The symptoms of membranous glomerulonephritis usually develop in the fourth decade of life in males. Approximately 5-30% patients with MN have spontanous remission. Common complications of membranous glomerulonephritis include renal failure, hypertension, proteinuria, dyslipidemia, hypercoagulable state leading to thromboembolism, Increased risk of infection. Prognosis is generally good, and 1 year mortality rate of patients with membranous glomerulonephritis is approximately 0.38%. The presence of proteinuria and baseline renal insuffiency are associated with a particularly poor prognosis among patients with membranous glomerulonephritis. Membranous glomerulonephritis caused by NSAIDS is associated with the most favorable prognosis.

Natural History

  • The natural history of membranous glomerulonephritis (MN) is given below:[1][2]
    • The symptoms of MN usually develop in the fourth decade of life in males.
    • The presence of symptoms of MN young female is suggestive of lupus.
    • Approximately 5-30% patients with MN have spontanous remission.

Complications

Prognosis

  • The prognostic factors of membranous glomerulonephritis are given below:[5][6]
    • Prognosis is generally good, and 1 year mortality rate of patients with membranous glomerulonephritis is approximately 0.38%.
    • Depending on the extent of the membranous glomerulonephritis at the time of diagnosis, the prognosis may vary. However, the prognosis is generally regarded as good.
    • The presence of proteinuria and baseline renal insuffiency are associated with a particularly poor prognosis among patients with membranous glomerulonephritis.
    • Membranous glomerulonephritis caused by NSAIDS is associated with the most favorable prognosis.
    • The prognosis of membranous glomerulonephritis associated with hepatitis B has less favorable prognosis.

References

  1. ↑ Kerjaschki D (2000). “Pathogenetic concepts of membranous glomerulopathy (MGN)”. J. Nephrol. 13 Suppl 3: S96–100. PMID 11132040.
  2. ↑ Schieppati A, Mosconi L, Perna A, Mecca G, Bertani T, Garattini S, Remuzzi G (July 1993). “Prognosis of untreated patients with idiopathic membranous nephropathy”. N. Engl. J. Med. 329 (2): 85–9. doi:10.1056/NEJM199307083290203. PMID 8510707.
  3. ↑ Debiec H, Ronco P (July 2014). “Immunopathogenesis of membranous nephropathy: an update”. Semin Immunopathol. 36 (4): 381–97. doi:10.1007/s00281-014-0423-y. PMID 24715030.
  4. ↑ Barbour S, Reich H, Cattran D (2013). “Short-term complications of membranous nephropathy”. Contrib Nephrol. 181: 143–51. doi:10.1159/000349976. PMID 23689576.
  5. ↑ Wasserstein AG (April 1997). “Membranous glomerulonephritis”. J. Am. Soc. Nephrol. 8 (4): 664–74. PMID 10495797.
  6. ↑ McGrogan, A.; Franssen, C. F. M.; de Vries, C. S. (2010). “The incidence of primary glomerulonephritis worldwide: a systematic review of the literature”. Nephrology Dialysis Transplantation. 26 (2): 414–430. doi:10.1093/ndt/gfq665. ISSN 0931-0509.

Template:WH Template:WS

Diagnosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | Renal Biopsy | Light Microscopy | CT | Immunofluorescence Microscopy | Ultrasound | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

Case #1

Template:Nephrology

Template:WikiDoc Sources

Looking for the patient version?

Back to the patient-friendly article

Imprint

Privacy Policy

Terms and Conditions

© 2026 MyEClinic – IFTM Institut für Telematik in der Medizin GmbH