Wikipedia - Membranous Glomerulonephritis (CHECKED)

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6/28/15Membranous glomerulonephritis - Wikipedia, the free encyclopedia

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Membranous glomerulonephritis

Micrograph of membranous nephropathy showing prominent glomerular

basement membrane spikes. Jones' stain.

Classification and external resources

ICD-10 N03

(http://apps.who.int/classifications/icd10/browse/2015/en#/N03

ICD-9 583.1 (http://www.icd9data.com/getICD9Code.ashx?icd9=583

DiseasesDB 7970 (http://www.diseasesdatabase.com/ddb7970.htm)

eMedicine med/885 (http://www.emedicine.com/med/topic885.htm)

MeSH D015433 (https://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?

field=uid&term=D015433)

Membranous glomerulonephritisFrom Wikipedia, the free encyclopedia

Membranous glomerulonephritis

MGN) is a slowly progressive

disease of the kidney affecting mostly

patients between ages of 30 and 50years, usuallyCaucasian.

t is the second most common cause

of nephrotic syndrome in adults, with

focal segmental glomerulosclerosis

FSGS) being the most common.[1]

Contents

1Terminology2Signs and symptoms3 Causes and classification

3.1 Primary/idiopathic3.2 Secondary

4Pathogenesis5 Morphology6 Treatment

6.1 Immunosuppressive

therapy7 Prognosis8 References

Terminology

The closely related terms membranous nephropathy[2]and membranous glomerulopathy[3]both refer to a

similar constellation but without the assumption of inflammation.

Membranous nephritis (in which inflammation is implied, but the glomerulus not explicitly mentioned) is les

common, but the phrase is occasionally encountered.[4]These conditions are usually considered together.

By contrast, membranoproliferative glomerulonephritis has a similar name, but is considered a separate

condition with a distinctly different causality. Membranoproliferative glomerulonephritis involves the basem

membrane and mesangium, while membranous glomerulonephritis involves the basement membrane but not

mesangium. (Membranoproliferative glomerulonephritis has the alternate name "mesangiocapillary

glomerulonephritis", to emphasize its mesangial character.)
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Signs and symptoms

Some people may present as nephrotic syndrome with proteinuria, edema with or without renal failure. Othe

may be asymptomatic and may be picked up on screening or urinalysis as having proteinuria. A definitive

diagnosis of membranous nephropathy requires a kidney biopsy.

Causes and classificationPrimary/idiopathic

85% of MGN cases are classified asprimary membranous glomerulonephritisthat is to say, the cause of th

disease is idiopathic (of unknown origin or cause). This can also be referred to as idiopathic membranous

nephropathy. One study has identified antibodies to an M-type phospholipase A2receptor in 70% (26 of 37)

cases evaluated.[5]Other studies have implicated neutral endopeptidase and cationic bovine serum albumin a

antigens.[6]

Secondary

The remainder is secondary due to:

autoimmune conditions(e.g., systemic lupus erythematosus[7])infections(e.g., syphilis, malaria, hepatitis B, hepatitis C)drugs(e.g., captopril, NSAIDs, penicillamine, probenecid).inorganic salts(e.g. gold, mercury).tumors, frequently solid tumors of the lung and colon; hematological malignancies such as chronic

lymphocytic leukemia are less common.[8]

Pathogenesis

MGN 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 may be part of the

basement membrane, or deposited from elsewhere by the systemic circulation.

The immune complex serves as an activator that triggers a response from the C5b - C9 complements, which

form a membrane attack complex (MAC) on the glomerular epithelial cells. This, in turn, stimulates release

proteases and oxidants by the mesangial and epithelial cells, damaging the capillary walls and causing them become "leaky". In addition, the epithelial cells also seem to secrete an unknown mediator that reduces neph

synthesis and distribution.

Morphology

The defining point of MGN is the presence of subepithelial immunoglobulin-containing deposits along the

glomerular basement membrane (GBM).
https://en.wikipedia.org/wiki/Glomerular_basement_membranehttps://en.wikipedia.org/wiki/Nephrinhttps://en.wikipedia.org/wiki/Complement_membrane_attack_complexhttps://en.wikipedia.org/wiki/Glomerular_basement_membranehttps://en.wikipedia.org/wiki/Immune_complexhttps://en.wikipedia.org/wiki/Membranous_glomerulonephritis#cite_note-pmid15224365-8https://en.wikipedia.org/wiki/Chronic_lymphocytic_leukemiahttps://en.wikipedia.org/wiki/Colon_cancerhttps://en.wikipedia.org/wiki/Lung_cancerhttps://en.wikipedia.org/wiki/Tumorhttps://en.wikipedia.org/wiki/Mercury_(element)https://en.wikipedia.org/wiki/Goldhttps://en.wikipedia.org/wiki/Salthttps://en.wikipedia.org/wiki/Probenecidhttps://en.wikipedia.org/wiki/Penicillaminehttps://en.wikipedia.org/wiki/NSAIDshttps://en.wikipedia.org/wiki/Captoprilhttps://en.wikipedia.org/wiki/Drughttps://en.wikipedia.org/wiki/Hepatitis_Chttps://en.wikipedia.org/wiki/Hepatitis_Bhttps://en.wikipedia.org/wiki/Malariahttps://en.wikipedia.org/wiki/Syphilishttps://en.wikipedia.org/wiki/Infectionhttps://en.wikipedia.org/wiki/Membranous_glomerulonephritis#cite_note-urlRenal_Pathology2-7https://en.wikipedia.org/wiki/Systemic_lupus_erythematosushttps://en.wikipedia.org/wiki/Autoimmunehttps://en.wikipedia.org/wiki/Membranous_glomerulonephritis#cite_note-Ronco2012-6https://en.wikipedia.org/wiki/Albuminhttps://en.wikipedia.org/wiki/Neutral_endopeptidasehttps://en.wikipedia.org/wiki/Membranous_glomerulonephritis#cite_note-5https://en.wikipedia.org/wiki/Phospholipase_Ahttps://en.wikipedia.org/wiki/Idiopathichttps://en.wikipedia.org/wiki/Biopsyhttps://en.wikipedia.org/wiki/Proteinuriahttps://en.wikipedia.org/wiki/Urinalysishttps://en.wikipedia.org/wiki/Renal_failurehttps://en.wikipedia.org/wiki/Edemahttps://en.wikipedia.org/wiki/Proteinuriahttps://en.wikipedia.org/wiki/Nephrotic_syndrome


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Immune complexes (black) are

deposited in a thickened basement

membrane creating a "spike and

dome" appearance on electron

microscopy.

By light microscopy, the basement membrane is observed to be diffusely thickened. Using Jones' stainthe GBM appears to have a "spiked" or "holey" appearance.

On electron microscopy, subepithelial deposits that nestle against the glomerular basement membraneseems to be the cause of the thickening. Also, the podocytes lose their foot processes. As the diseaseprogresses, the deposits will eventually be cleared, leaving cavities in the basement membrane. Thesecavities will later be filled with basement membrane-like material, and if the disease continues evenfurther, the glomeruli will become sclerosed and finally hyalinized.

Immunoflourescence microscopy will reveal typical granular deposition of immunoglobulins and

complement along the basement membrane.[9]

Although it usually affects the entire glomerulus, it can affect parts of the glomerulus in some cases.[10]

Treatment

Treatment of secondary membranous nephropathy is guided by the

reatment of the original disease. For treatment of idiopathicmembranous nephropathy, the treatment options include

mmunosuppressive drugs and non-specific anti-proteinuric measures.

Recommended first line therapy often includes: cyclophosphamide

alternating with a corticosteroid.[11]

Immunosuppressive therapy

1. Corticosteroids: They have been tried with mixed results, with onestudy showing prevention of progression to renal failure without

improvement in proteinuria.2. Chlorambucil

3. Cyclosporine[12]

4. Tacrolimus5. Cyclophosphamide6. Mycophenolate mofetil

Perhaps the most difficult aspect of membranous glomerulonephritis is

deciding which people to treat with immunosuppressive therapy as

opposed to simple "background" or anti-proteinuric therapies. A large

part of this difficulty is due to a lack of ability to predict which peoplewill progress to end-stage renal disease, or renal disease severe enough

o require dialysis. Because the above medications carry risk, treatment

should not be initiated without careful consideration as to risk/benefit profile. Of note, corticosteroids (typica

Prednisone) alone are of little benefit. They should be combined with one of the other 5 medications, each of

which, along with prednisone, has shown some benefit in slowing down progression of membranous

nephropathy. It must be kept in mind, however, that each of the 5 medications also carry their own risks, on t

of prednisone.
https://en.wikipedia.org/wiki/Mycophenolate_mofetilhttps://en.wikipedia.org/wiki/Cyclophosphamidehttps://en.wikipedia.org/wiki/Tacrolimushttps://en.wikipedia.org/wiki/Membranous_glomerulonephritis#cite_note-pmid17389782-12https://en.wikipedia.org/wiki/Cyclosporinehttps://en.wikipedia.org/wiki/Chlorambucilhttps://en.wikipedia.org/wiki/Proteinuriahttps://en.wikipedia.org/wiki/Renal_failurehttps://en.wikipedia.org/wiki/Corticosteroidshttps://en.wikipedia.org/wiki/Membranous_glomerulonephritis#cite_note-11https://en.wikipedia.org/wiki/Corticosteroidhttps://en.wikipedia.org/wiki/Cyclophosphamidehttps://en.wikipedia.org/wiki/Immunosuppressivehttps://en.wikipedia.org/wiki/Membranous_glomerulonephritis#cite_note-pmid17699279-10https://en.wikipedia.org/wiki/Membranous_glomerulonephritis#cite_note-urlRenal_Pathology-9https://en.wikipedia.org/wiki/Immunoflourescencehttps://en.wikipedia.org/wiki/Hyalinehttps://en.wikipedia.org/wiki/Podocytehttps://en.wikipedia.org/wiki/Electron_microscopyhttps://en.wikipedia.org/wiki/Jones%27_stainhttps://en.wikipedia.org/wiki/Light_microscopyhttps://en.wikipedia.org/wiki/File:Membranous_Nephropathy_Pathology_Diagram.svg


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The twin aims of treating membranous nephropathy are first to induce a remission of the nephrotic syndrome

and second to prevent the development of endstage renal failure. A meta-analysis of four randomized contro

studies comparing treatments of membranous nephropathy showed that regimes comprising chlorambucil or

cyclophosphamide, either alone or with steroids, were more effective than symptomatic treatment or treatme

with steroids alone in inducing remission of the nephrotic syndrome.

Prognosis

About a third of patients have spontaneous remission, another third progress to require dialysis and the last th

continue to have proteinuria, without progression of renal failure.

References

1. Abeera Mansur, MD (May 2012). "Membranous Glomerulonephritis" (http://emedicine.medscape.com/article/23979

overview#a0199).

2. Passerini P, Ponticelli C (July 2003). "Corticosteroids, cyclophosphamide, and chlorambucil therapy of membranous

nephropathy" (http://journals.elsevierhealth.com/retrieve/pii/S0270929503000524). Semin. Nephrol.23(4): 35561.

doi:10.1016/S0270-9295(03)00052-4 (https://dx.doi.org/10.1016%2FS0270-9295%2803%2900052-4). PMID 12923

(https://www.ncbi.nlm.nih.gov/pubmed/12923723).

3. Markowitz GS (May 2001). "Membranous glomerulopathy: emphasis on secondary forms and disease variants"

(http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=1072-

4109&volume=8&issue=3&spage=119).Adv Anat Pathol8(3): 11925. doi:10.1097/00125480-200105000-00001

(https://dx.doi.org/10.1097%2F00125480-200105000-00001). PMID 11345236


4. Hallegua D, Wallace DJ, Metzger AL, Rinaldi RZ, Klinenberg JR (2000). "Cyclosporine for lupus membranous

nephritis: experience with ten patients and review of the literature" (http://openurl.ingenta.com/content/nlm?

genre=article&issn=0961-2033&volume=9&issue=4&spage=241&aulast=Hallegua).Lupus9(4): 24151.

doi:10.1191/096120300680198935 (https://dx.doi.org/10.1191%2F096120300680198935). PMID 10866094

(https://www.ncbi.nlm.nih.gov/pubmed/10866094).5. Beck, LH; Bonegio, RGB; Lambeau, G; Beck, DM; Powell, DW; Cummins, TD;, Klein, JB; Salant, DJ. (July 2, 200

"M-Type Phospholipase A2 Receptor as Target Antigen in Idiopathic Membranous Nephropathy"

(http://content.nejm.org/cgi/content/short/361/1/11). The New England Journal of Medicine361(1): 1121.

doi:10.1056/NEJMoa0810457 (https://dx.doi.org/10.1056%2FNEJMoa0810457). PMC 2762083

(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2762083). PMID 19571279


6. Ronco P, Debiec H (2012) Pathogenesis of membranous nephropathy: recent advances and future challenges. Nat Re

Nephrol doi:10.1038/nrneph.2012.35 (https://dx.doi.org/10.1038%2Fnrneph.2012.35).

7. "Renal Pathology" (http://library.med.utah.edu/WebPath/RENAHTML/RENAL088.html). Retrieved 2008-11-25.

8. Ziakas PD, Giannouli S, Psimenou E, Nakopoulou L, Voulgarelis M (July 2004). "Membranous glomerulonephritis i

chronic lymphocytic leukemia".Am. J. Hematol.76(3): 2714. doi:10.1002/ajh.20109(https://dx.doi.org/10.1002%2Fajh.20109). PMID 15224365 (https://www.ncbi.nlm.nih.gov/pubmed/15224365).

9. "Renal Pathology" (http://library.med.utah.edu/WebPath/RENAHTML/RENAL090.html). Retrieved 2008-11-25.

10. Obana M, Nakanishi K, Sako M et al. (July 2006). "Segmental membranous glomerulonephritis in children: compari

with global membranous glomerulonephritis" (http://cjasn.asnjournals.org/cgi/pmidlookup?

view=long&pmid=17699279). Clin J Am Soc Nephrol1(4): 7239. doi:10.2215/CJN.01211005

(https://dx.doi.org/10.2215%2FCJN.01211005). PMID 17699279 (https://www.ncbi.nlm.nih.gov/pubmed/17699279)
https://www.ncbi.nlm.nih.gov/pubmed/17699279https://en.wikipedia.org/wiki/PubMed_Identifierhttps://dx.doi.org/10.2215%2FCJN.01211005https://en.wikipedia.org/wiki/Digital_object_identifierhttp://cjasn.asnjournals.org/cgi/pmidlookup?view=long&pmid=17699279http://library.med.utah.edu/WebPath/RENAHTML/RENAL090.htmlhttps://www.ncbi.nlm.nih.gov/pubmed/15224365https://en.wikipedia.org/wiki/PubMed_Identifierhttps://dx.doi.org/10.1002%2Fajh.20109https://en.wikipedia.org/wiki/Digital_object_identifierhttp://library.med.utah.edu/WebPath/RENAHTML/RENAL088.htmlhttps://dx.doi.org/10.1038%2Fnrneph.2012.35https://en.wikipedia.org/wiki/Digital_object_identifierhttps://www.ncbi.nlm.nih.gov/pubmed/19571279https://en.wikipedia.org/wiki/PubMed_Identifierhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2762083https://en.wikipedia.org/wiki/PubMed_Centralhttps://dx.doi.org/10.1056%2FNEJMoa0810457https://en.wikipedia.org/wiki/Digital_object_identifierhttp://content.nejm.org/cgi/content/short/361/1/11https://www.ncbi.nlm.nih.gov/pubmed/10866094https://en.wikipedia.org/wiki/PubMed_Identifierhttps://dx.doi.org/10.1191%2F096120300680198935https://en.wikipedia.org/wiki/Digital_object_identifierhttp://openurl.ingenta.com/content/nlm?genre=article&issn=0961-2033&volume=9&issue=4&spage=241&aulast=Halleguahttps://www.ncbi.nlm.nih.gov/pubmed/11345236https://en.wikipedia.org/wiki/PubMed_Identifierhttps://dx.doi.org/10.1097%2F00125480-200105000-00001https://en.wikipedia.org/wiki/Digital_object_identifierhttp://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=1072-4109&volume=8&issue=3&spage=119https://www.ncbi.nlm.nih.gov/pubmed/12923723https://en.wikipedia.org/wiki/PubMed_Identifierhttps://dx.doi.org/10.1016%2FS0270-9295%2803%2900052-4https://en.wikipedia.org/wiki/Digital_object_identifierhttp://journals.elsevierhealth.com/retrieve/pii/S0270929503000524http://emedicine.medscape.com/article/239799-overview#a0199https://en.wikipedia.org/wiki/Renal_failurehttps://en.wikipedia.org/wiki/Dialysis


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11. Chen, Y; Schieppati, A; Chen, X; Cai, G; Zamora, J; Giuliano, GA; Braun, N; Perna, A (Oct 16, 2014).

"Immunosuppressive treatment for idiopathic membranous nephropathy in adults with nephrotic syndrome.". The

Cochrane database of systematic reviews10: CD004293. doi:10.1002/14651858.CD004293.pub3

(https://dx.doi.org/10.1002%2F14651858.CD004293.pub3). PMID 25318831


12. Goumenos DS, Katopodis KP, Passadakis P et al. (2007). "Corticosteroids and ciclosporin A in idiopathic membrano

nephropathy: higher remission rates of nephrotic syndrome and less adverse reactions than after traditional treatment

with cytotoxic drugs" (http://content.karger.com/produktedb/produkte.asp?typ=fulltext&file=000101367).Am. J.

Nephrol.27(3): 22631. doi:10.1159/000101367 (https://dx.doi.org/10.1159%2F000101367). PMID 17389782(https://www.ncbi.nlm.nih.gov/pubmed/17389782).

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Wikipedia - Membranous Glomerulonephritis (CHECKED)