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{{Membranoproliferative glomerulonephritis}}
{{Membranoproliferative glomerulonephritis}}
{{CMG}}; '''Associate Editor-In-Chief:''' {{CZ}}
{{CMG}} {{APM}}; '''Associate Editor-In-Chief:''' {{OO}}{{CZ}} {{N.F}}{{JSS}} [https://www.wikidoc.org/index.php?title=L.Farrukh&action=edit&redlink=1 <nowiki>L.Farrukh [6]</nowiki>]


==Overview==
==[[Membranoproliferative glomerulonephritis overview|Overview]]==


'''Membranoproliferative glomerulonephritis''' or MPGN is a type of [[glomerulonephritis]] caused by immune complexes depositing in the kidney glomerular mesangium and basement membrane ([[GBM]]), activating [[complement system|complement]] and damaging the glomeruli.  The GBM is rebuilt ontop of the deposits, causing a "tram-tracking" appearance under the microscope.
==[[Membranoproliferative glomerulonephritis historical perspective|Historical Perspective]]==
==[[Membranoproliferative glomerulonephritis classification|Classification]]==


==Diagnosis==
==[[Membranoproliferative glomerulonephritis pathophysiology|Pathophysiology]]==


==Other Diagnostic Procedures==
==[[Membranoproliferative glomerulonephritis causes|Causes]]==


* Kidney biopsy for definitive diagnosis.
==[[Membranoproliferative glomerulonephritis differential diagnosis|Differentiating Membranoproliferative glomerulonephritis from other Diseases]]==


==Histologic Findings==
==[[Membranoproliferative glomerulonephritis epidemiology and demographics|Epidemiology and Demographics]]==
==[[Membranoproliferative glomerulonephritis risk factors|Risk Factors]]==


===Light microscopy===
==[[Membranoproliferative glomerulonephritis natural history, complications and prognosis|Natural History, Complications and Prognosis]]==


Glomeruli generally are enlarged and hypercellular, with an increase in mesangial cellularity and matrix. Mesangial increase, when generalized throughout the glomeruli, causes an exaggeration of their lobular form, giving rise to the alternative name of lobular nephritis. Infiltrating neutrophils and monocytes contribute to glomerular hypercellularity.
| [[Membranoproliferative glomerulonephritis electrocardiogram|Electrocardiogram]] | [[Membranoproliferative glomerulonephritis chest x ray|Chest X Ray]] | [[Membranoproliferative glomerulonephritis CT|CT]] | [[Membranoproliferative glomerulonephritis MRI|MRI]] | [[Membranoproliferative glomerulonephritis echocardiography or ultrasound|Echocardiography or Ultrasound]] | [[Membranoproliferative glomerulonephritis other imaging findings|Other Imaging Findings]] | [[Membranoproliferative glomerulonephritis other diagnostic studies|Other Diagnostic Studies]]


The capillary basement membranes are thickened by interposition of mesangial cells and matrix into the capillary wall. This gives rise to the tram-track or double-contoured appearance of the capillary wall, best appreciated with the methenamine silver stain or the periodic acid-Schiff reagent.
==Treatment==


Crescents may be visible in 10% of patient biopsy specimens. Interstitial changes, including inflammation, interstitial fibrosis, and tubular atrophy, are observed in patients with progressive decline in GFR.
[[Membranoproliferative glomerulonephritis medical therapy|Medical Therapy]] | [[Membranoproliferative glomerulonephritis surgery|Surgery]] | [[Membranoproliferative glomerulonephritis primary prevention|Primary Prevention]] | [[Membranoproliferative glomerulonephritis secondary prevention|Secondary Prevention]] | [[Membranoproliferative glomerulonephritis cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Membranoproliferative glomerulonephritis future or investigational therapies|Future or Investigational Therapies]]


===Membranoproliferative glomerulonephritis type I===
==Case Studies==


On electron microscopy, electron dense deposits in subendothelial sites are characteristic of this disease. Mesangial and occasional subepithelial deposits also may be present. Irregular new basement membrane material is formed around the subendothelial deposits and mesangial projections, producing the tram-track appearance on light microscopy.
By immunofluorescence, prominent C3 deposition in a granular pattern is noted in the capillary walls, with variable mesangial C3 deposits. Early components of complement, immunoglobulin G (IgG), and, less commonly, immunoglobulin M (IgM) may be found in a distribution similar to C3.
===Membranoproliferative glomerulonephritis type II or dense deposit disease===
The basement membranes of the glomerulus, Bowman capsule, tubules, and peritubular capillaries are thickened. The basement membrane appears irregular and ribbonlike on special stains (eg, periodic acid-Schiff, thioflavine-T, toluidine blue).
On electron microscopy, the basement membrane is thickened by discontinuous, amorphous electron dense deposits that reside in the lamina densa layer, hence the alternative name of dense deposit disease. Mesangial and subepithelial dense deposits may be noted.
Immunofluorescence reveals complement component C3 deposited in an irregular granular pattern in the basement membranes on either side but not within the dense deposits or in nodular ring forms in the mesangium. Little or no deposition of immunoglobulins occurs in the glomeruli.
===Membranoproliferative glomerulonephritis type III===
This variant of MPGN, also called the Burkholder variant, displays combined features of MPGN type I and membranous nephropathy.
Subepithelial, subendothelial, and mesangial deposits are present on electron microscopy. Successive generations of subendothelial and subepithelial deposits disrupt the basement membrane, and concurrent formation of new lamina densa material is present, giving the basement membrane a complex laminated appearance.
Immunohistology shows granular deposition of C3, C5, properdin, IgG, and IgM, predominantly in the capillary walls.
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{{Nephrology}}
{{Nephrology}}


[[Category:Nephrology]]
[[Category:Nephrology]]
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Latest revision as of 15:18, 6 September 2020

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Membranoproliferative glomerulonephritis
ICD-10 N00-N08 with .2 suffix
ICD-9 581.2, 582.2, 583.2
MeSH D015432

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Ali Poyan Mehr, M.D. [2]; Associate Editor-In-Chief: Olufunmilola Olubukola M.D.[3]Cafer Zorkun, M.D., Ph.D. [4] Nazia Fuad M.D. Jogeet Singh Sekhon, M.D. [5] L.Farrukh [6]

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