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__NOTOC__
{| class="infobox bordered" style="width: 15em; text-align: left; font-size: 90%; background:AliceBlue"
{{SI}}
|-
{{CMG}}; {{AE}} {{CZ}}; {{Ammu}}
| colspan="1" style="text-align:center; background:LightGrey" |


{{SK}} CAH; Adrenogenital syndrome
'''Diabetes mellitus Main page'''
|- bgcolor="LightGrey"
!


==Overview==
|- bgcolor="Pink"
Congenital adrenal hyperplasia is a group of [[autosome|autosomal]] [[recessive]] [[disease]]s that result from multiple [[genetic]] mutations. The genes encode a number of enzymes that mediate the adrenal glands [[steroidogenesis]] pathway. As a result, mutations in such genes will result in various enzyme deficiencies that lead to a disequilibrium of the biochemical reactions mediating the production of cortisol, aldesterone, and androgens.<ref name="Warrell2005">{{cite book|author=David A. Warrell|title=Oxford textbook of medicine: Sections 18-33|url=https://books.google.com/books?id=hL1NKQJlY1IC&pg=PA261|accessdate=14 June 2010|year=2005|publisher=Oxford University Press|isbn=978-0-19-856978-7|pages=261–}}</ref> The outcome of congenital adrenal hyperplasia is either an excessive or deficient production of the aforementioned hormones, which alters the development of both [[primary sex characteristic|primary]] and [[secondary sex characteristic]]s among affected patients.<ref name="MilunskyMilunsky2010">{{cite book|author1=Aubrey Milunsky|author2=Jeff Milunsky|title=Genetic Disorders and the Fetus: Diagnosis, Prevention and Treatment|url=https://books.google.com/books?id=oKCmA4dOYtMC&pg=PA600|accessdate=14 June 2010|date=29 January 2010|publisher=John Wiley and Sons|isbn=978-1-4051-9087-9|pages=600–}}</ref> Congenital adrenal hyperplasia may be classified according to
!
biochemical enzyme deficiency into commonly five subtypes: [[lipoid congenital adrenal hyperplasia]], [[congenital adrenal hyperplasia due to 21-hydroxylase deficiency]], [[congenital adrenal hyperplasia due to 17 alpha-hydroxylase deficiency]], [[congenital adrenal hyperplasia due to 3 beta-hydroxysteroid dehydrogenase deficiency]], and [[congenital adrenal hyperplasia due to 11β-hydroxylase deficiency]].
Patient Information
===Congenital Adrenal Hyperplasia===
: [[Diabetes mellitus type 1 (patient information)|Type 1]]
* The figure below illustrates the biochemical reactions of the adrenal glands [[steroidogenesis]] pathway:
: [[Diabetes mellitus type 2 (patient information)|Type 2]]
<br>
|-
[[Image:DHEA1_svg.png|thumb|center|800px|Production of DHEA from Cholesterol. ([[Cortisol]] is a [[glucocorticoid]].)]]
!


==Historical Perspective==
|- bgcolor="Pink"
!
[[Diabetes mellitus#Overview|Overview]]
|-
!


==Classification==
|- bgcolor="Pink"
* Congenital adrenal hyperplasia may be classified according to biochemical enzyme deficiency into commonly the following types:
!
<br>
[[Diabetes mellitus#Classification|Classification]]
{{Familytree/start}}
: [[Diabetes mellitus type 1]]
{{Familytree|boxstyle=background: #E0FFFF;| | | | | | | | | | | | | | A01 | | | | | | | | | | | | | | | | | | |A01=<div style="width: 20em; padding:0.5em;">'''Congenital Adrenal Hyperplasia'''</div>}}
: [[Diabetes mellitus type 2]]
{{Familytree|boxstyle=background: #E0FFFF;| | | | |,|-|-|-|-|v|-|-|-|-|+|-|-|-|-|v|-|-|-|-|.| | | | | | | | | | | | | |}}
: [[Gestational diabetes]]
{{Familytree|boxstyle=background: #E0FFFF;| | | | B01 | | | B02 | | | B03 | | | B04 | | | B05 | | | | | | | | | | | |B01= <div style="width: 15em; padding:0.5em;">[[Lipoid congenital adrenal hyperplasia]]</div>|B02= <div style="width: 15em; padding:0.5em;">[[Congenital adrenal hyperplasia due to 21-hydroxylase deficiency]]</div>|B03=  <div style="width: 15em; padding:0.5em;"> [[Congenital adrenal hyperplasia due to 17 alpha-hydroxylase deficiency]]</div>|B04= <div style="width: 15em; padding:0.5em;"> [[Congenital adrenal hyperplasia due to 3 beta-hydroxysteroid dehydrogenase deficiency]] </div>|B05= <div style="width: 15em; padding:0.5em;"> [[Congenital adrenal hyperplasia due to 11β-hydroxylase deficiency]] </div>}}
|-  
{{Familytree/end}}
!
<br>
===Biochemistry===
* The table below lists the specific biochemical abnormalities present among the different types of congenital adrenal hyperplasia:
<br>
{| style="border: 0px; font-size: 90%; margin: 3px; width: 1000px"
|valign=top|
|+
! style="background: #4479BA; width: 200px; color: #FFFFFF;"|'''Common Medical Term'''


! style="background: #4479BA; width: 600px; color: #FFFFFF;"|'''OMIM Number'''
|- bgcolor="Pink"
!
[[Diabetes mellitus#Differential diagnosis|Differential Diagnosis]]
|-
!


! style="background: #4479BA; width: 200px; color: #FFFFFF;"|'''Enzyme'''
|- bgcolor="Pink"
!
[[Diabetes mellitus#Complications|Complications]]
|-
!


! style="background: #4479BA; width: 200px; color: #FFFFFF;"|'''Gene location'''
|- bgcolor="Pink"
!
[[Diabetes mellitus#Screening|Screening]]
|-
!


! style="background: #4479BA; width: 600px; color: #FFFFFF;"|'''Substrates'''
|- bgcolor="Pink"
!
[[Diabetes mellitus#Diagnosis|Diagnosis]]
|-
!


! style="background: #4479BA; width: 600px; color: #FFFFFF;"|'''Products'''
|- bgcolor="Pink"
!
[[Diabetes mellitus#Prevention|Prevention]]
|-
!
|}
---------------------------


<div style="-webkit-user-select: none;">
{| class="infobox" style="position: fixed; top: 65%; right: 10px; margin: 0 0 0 0; border: 0; float: right;"
|-
| {{#ev:youtube|https://https://www.youtube.com/watch?v=zucxZw069kw|350}}
|-
|-
|}
__NOTOC__
{{CMG}}
{{Glomerulonephritis}}
==Pathophysiology==
===Microscopic Pathology===
[http://www.peir.net Images shown below are courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
<div align="left">
<gallery heights="175" widths="175">
image:Acute GN 1.jpg|Glomerulonephritis: Micro H&E med mag; an excellent example of AGN with many neutrophils
image:Acute GN 2.jpg|Acute Glomerulonephritis: Micro H&E high mag; an  excellent example of acute exudative glomerulonephritis.
</gallery>
</div>
<br>
===Glomerulonephritis Videos===
====Rapidly progressive glomerulonephritis====


| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" align=center |
{{#ev:youtube|CqSyj4cVZPE}}
''' [[Congenital adrenal hyperplasia due to 21-hydroxylase deficiency|21-hydroxylase CAH]]'''
| style="padding: 5px 5px; background: #F5F5F5;"|
:{{OMIM|201910}}  
| style="padding: 5px 5px; background: #F5F5F5;"|
:P450c21
| style="padding: 5px 5px; background: #F5F5F5;"|
:6p21.3
| style="padding: 5px 5px; background: #F5F5F5;"|
:17OH-progesterone→ <br/>[[Progesterone]] 
| style="padding: 5px 5px; background: #F5F5F5;"|
:11-deoxycortisol→<br/>[[11-deoxycorticosterone|DOC]]


|-


| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" align=center |
====Chronic glomerulonephritis====
''' [[Lipoid congenital adrenal hyperplasia|lipoid CAH]]<br/>(20,22-desmolase)'''
| style="padding: 5px 5px; background: #F5F5F5;"|
:{{OMIM|201710}}
| style="padding: 5px 5px; background: #F5F5F5;"|
:StAR<br/>P450scc
| style="padding: 5px 5px; background: #F5F5F5;"|
:8p11.2<br/>15q23-q24
| style="padding: 5px 5px; background: #F5F5F5;"|
:Transport of [[cholesterol]]→<br/>[[cholesterol]]
| style="padding: 5px 5px; background: #F5F5F5;"|
:Into mitochondria→<br/>[[Pregnenolone]]
|-


| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" align=center |
{{#ev:youtube|eA1vYarRAWo}}
'''  [[Congenital adrenal hyperplasia due to 17 alpha-hydroxylase deficiency|17α-hydroxylase CAH]]'''
| style="padding: 5px 5px; background: #F5F5F5;"|
:{{OMIM|202110}}
| style="padding: 5px 5px; background: #F5F5F5;"|
:P450c17
| style="padding: 5px 5px; background: #F5F5F5;"|
:10q24.3
| style="padding: 5px 5px; background: #F5F5F5;"|
:[[pregnenolone]]→<br/>[[progesterone]]→<br/>17OH-pregnenolone→
| style="padding: 5px 5px; background: #F5F5F5;"|
:17OH-pregnenolone<br/>17OH-progesterone<br/>[[DHEA]]


|-
===Images===


| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" align=center |
[http://www.peir.net Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
'''[[Congenital adrenal hyperplasia due to 3 beta-hydroxysteroid dehydrogenase deficiency|3β-HSD CAH]]'''
| style="padding: 5px 5px; background: #F5F5F5;"|
:{{OMIM|201810}}
| style="padding: 5px 5px; background: #F5F5F5;"|
:3βHSD II
| style="padding: 5px 5px; background: #F5F5F5;"|
:1p13
| style="padding: 5px 5px; background: #F5F5F5;"|
:[[Pregnenolone]]→<br/>17OH-pregnenolone→<br/>[[DHEA]]→
| style="padding: 5px 5px; background: #F5F5F5;"|
:[[Progesterone]]<br/>17OH-progesterone<br/>[[androstenedione]]


|-
<div align="left">
<gallery heights="175" widths="175">
Image:Glomerulonephritis case 1.jpg|This is a low-power photomicrograph of a saggital section of end stage chronic glomerulonephritis (GN). Note the marked thinning of the cortex (arrow).
Image:Glomerulonephritis case 2.jpg|This is a higher-power photomicrograph of hyalinized glomeruli (arrows) and glomeruli with thick basement membranes.
</gallery>
</div>


| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" align=center |
<div align="left">
'''[[Congenital adrenal hyperplasia due to 11 beta-hydroxylase deficiency|11β-hydroxylase CAH]]'''
<gallery heights="175" widths="175">
| style="padding: 5px 5px; background: #F5F5F5;"|
Image:Glomerulonephritis case 3.jpg|This is a higher-power photomicrograph of hyalinized glomeruli (1) and glomeruli with thickened basement membranes (2).
:{{OMIM|202010}}
Image:Glomerulonephritis case 4.jpg|This is a photomicrograph of interstitial and vascular lesions in end stage renal disease.
| style="padding: 5px 5px; background: #F5F5F5;"|
</gallery>
:P450c11β
</div>
| style="padding: 5px 5px; background: #F5F5F5;"|
:8q21-22
| style="padding: 5px 5px; background: #F5F5F5;"|  
:11-deoxycortisol→<br/>DOC→
| style="padding: 5px 5px; background: #F5F5F5;"|
:[[Cortisol]]<br/>[[Corticosterone]]
|}


==Pathophysiology==
<div align="left">
<gallery heights="175" widths="175">
Image:Glomerulonephritis case 5.jpg|This is an immunofluorescent photomicrograph of granular membranous immunofluorescence (immune complex disease). The antibody used for these studies was specific for IgG.
Image:Glomerulonephritis case 6.jpg|This is an electron micrograph of subepithelial granular electron dense deposits (arrows) which correspond to the granular immunofluorescence seen in the previous image.
</gallery>
</div>


==Causes==
<div align="left">
<gallery heights="175" widths="175">
Image:Glomerulonephritis case 7.jpg|This is a photomicrograph of a glomerulus from another case with acute poststreptococcal glomerulonephritis. In this case the immune complex glomerular disease is ongoing with necrosis and accumulation of neutrophils in the glomerulus.
Image:Glomerulonephritis case 8.jpg|This immunofluorescent photomicrograph of a glomerulus from a case of acute poststreptococcal glomerulonephritis shows a granular immunofluorescence pattern consistent with immune complex disease. The primary antibody used for this staining was specific for IgG; however antibodies for complement would show a similar pattern.
</gallery>
</div>


==Differentiating {{PAGENAME}} from Other Diseases==
<div align="left">
<gallery heights="175" widths="175">
Image:Glomerulonephritis case 9.jpg|This electron micrograph demonstrates scattered subepithelial dense deposits (arrows) and a polymorphonuclear leukocyte in the lumen.
Image:Glomerulonephritis case 10.jpg|For comparison this is an immunofluorescent photomicrograph of a glomerulus from a patient with Goodpasture's syndrome. The linear (arrows) immunofluorescence is characteristic of Goodpasture's syndrome.
</gallery>
</div>


==Epidemiology and Demographics==
===Images:===


==Risk Factors==
*[http://www.pathologyatlas.ro/Crescentic%20Glomerulonephritis.html Crescentic GN]


==Screening==
*[http://www.pathologyatlas.ro/Chronic%20Glomerulonephritis1.html Chronic GN]


==Natural History, Complications, and Prognosis==
==References==
{{Reflist|2}}


==Diagnosis==
[[Category:Disease]]
===Diagnostic Criteria===
[[Category:Organ disorders]]
[[Category:Inflammations]]
[[Category:Kidney diseases]]


===History and Symptoms===
[[Category:Needs overview]]


===Physical Examination===
{{WH}}
{{WS}}
--------------------------------------------------
===Common Causes===
*[[Churg-strauss syndrome]]
*[[Cryoglobulinaemia]]
*[[Diabetes mellitus type 2]]
*[[Dibasic aminoaciduria type 2]]
*[[Endocarditis]]
*[[Glycogenosis type 1a]]
*[[Henoch-schönlein purpura ]]
*[[Hepatitis b]]
*[[Hereditary onycho-osteodysplasia]]
*[[Hypersensitivity vasculitis]]
*[[Iga nephropathy]]
*[[Lepromatous leprosy]]
*[[Mixed essential cryoglobulinaemia]]
*[[Myeloma]]
*[[Paraneoplastic syndrome]]
*[[Polyarteritis nodosa]]
*[[Radiotherapy]]
*[[Schimke immunoosseous dysplasia]]
*[[Secondary syphilis]]
*[[Serum sickness]]
*[[Sickle cell disease]]
*[[Systemic lupus erythematosus]]
*[[Vasculitis]]
*[[Wegener's granulomatosis]]
*[[Wiskott-aldrich syndrome]]


===Laboratory Findings===


===Imaging Findings===
--------------------------------------


===Other Diagnostic Studies===
__NOTOC__


==Treatment==
{{Glomerulonephritis}}
===Medical Therapy===
{{CMG}}; {{AE}}{{HK}}


===Surgery===
==Overview==
Glomerulonephritis may be proliferative or non-proliferative and may be associated with [[Nephrotic syndrome|nephrotic]] or [[Nephritic syndrome|nephritic]] features. The various types of glomerulonephritides should be differentiated from each other based on associations, presence of [[pitting edema]], hemeturia, [[hypertension]], [[hemoptysis]], [[oliguria]], peri-orbital edema, [[hyperlipidemia]], type of [[antibodies]], [[Light microscope|light]] and [[Electron microscopy|electron microscopic]] features.


===Prevention===
==Differential Diagnosis==
The following table differentiates between various types of glomerulonephritides:
{| class="wikitable"
! rowspan="3" align="center" style="background:#4479BA; color: #FFFFFF;" + |Glomerulonephritis
! rowspan="3" align="center" style="background:#4479BA; color: #FFFFFF;" + |Sub-entity
! rowspan="3" align="center" style="background:#4479BA; color: #FFFFFF;" + |Causes and associations
! colspan="7" rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |History and Symtoms
! colspan="9" align="center" style="background:#4479BA; color: #FFFFFF;" + |Laboratory Findings
|-
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Hyperlipidemia and hypercholesterolemia
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephrotic features
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephritic features
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |ANCA
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Anti-glomerular basement membrane antibody (Anti-GBM antibody)
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Immune complex formation
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Light microscope
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Electron microscope
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Immunoflourescence pattern
|-
! align="center" style="background:#4479BA; color: #FFFFFF;" + |History
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Pitting edema
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hemeturia (pre-dominantly microscopic)
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hypertension
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hemoptysis
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Oliguria
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Peri-orbital edema
|-
| rowspan="3" align="center" style="background:#4479BA; color: #FFFFFF;" + |Non-proliferative
!Minimal change disease
|
* Idiopathic
* Protein tyrosine phosphatase receptor type O (glomerular epithelial protein 1- GLEPP1)
|
* Young children
* Recent infection and immunization
* Atopy
* Hodgkin lymphoma
* Thrombosis (due to urinary loss of antithrombin-III)
|
+
|
-
|
-
|
-
|
+/-
|
-
|
+
|
+
|
-
|
-
|
-
|
-
|
* Normal
|
* Fusion of podocytes
|
-
|-
!Focal segmental glomerulosclerosis
|
* Idiopathic
* HIV
* Heroine use
* Sickle cell disease
* Interferon
* Severe obesity
* Mixed cryoglobunemia (Hepatitis C)
|
* Adults
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>-</nowiki>
| +
| +
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|
* Focal (some glomeruli) and segmental (only part of glomerulus)
|
* Effacement of podocytes
|<nowiki>-</nowiki>
|-
!Membranous glomerulonephritis
|
* Idiopathic
* Hepatitis B and C
* Solid tumors
* Systemic lupus erythmatosus
* Drugs (NSAIDS, penclliamine, gold, captopril)
|
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>-</nowiki>
| +
| +
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|
* Thick glomerular basement membrance
|
* Sub-epithelial immune complex depositis with 'spike and dome' appearance
|<nowiki>-</nowiki>
|-
| rowspan="7" align="center" style="background:#4479BA; color: #FFFFFF;" + |Proliferative
!IgA nephropathy
|
* Idiopathic
* Viral infections
|
* Young children
* History of mucosal infections (e.g. gastroenteritis) and upper respiratory tract infection
* 2-3 days after infection (synpharyngitic)
|<nowiki>+/-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+/-</nowiki>
| -
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| +
|
* Crescent formation
|
* Mesangial proliferation
|<nowiki>-</nowiki>
|-
! rowspan="5" |Rapidly progressive glomerulonephritis
|
* Goodpasture syndrome
|
* Young adults
|<nowiki>+/-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
| -
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|
* Hypercellular and inflamed glomeruli (Crescent formation)
|
*  Diffuse thickening of the glomerular basement membrane with absence of subepithelial and subendothelial deposits 
|<nowiki>+ (Linear)</nowiki>
|-
|
* Post infectious glomerulonephritis
|
* Streptococcal skin infections
* Streptococcal pharyngitis
* 2-3 weeks after infection
|<nowiki>+/-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|
* Hypercellular and inflamed glomeruli
|
* Sub-epithelial immune complex deposits
| + (Granular)
|-
|
* Granulomatosis with polyangitis (Wegner's granulomatosis)
|
* Necrotizing granulomas (Nasopharynx, lungs, kidneys)
* [[Conjunctivitis]]
* Ulceration of the [[cornea]]
* [[Episcleritis]]
* Peripheral neuropathy
|<nowiki>+/-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+ (C-ANCA)</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|
* Hypercellular and inflamed glomeruli (Crescent formation)
|<nowiki>-  (pauci-immune)</nowiki>
|<nowiki>+/-</nowiki>
|-
|
* Churg Strauss syndrome
|
* Necrotizing granulomas (Lungs and kidneys)
* Asthma
* Peripheral neuropathy
|<nowiki>+/-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|
+ (C-ANCA)
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|
* Hypercellular and inflamed glomeruli (Crescent formation)
|<nowiki>- (pauci-immune)</nowiki>
|<nowiki>-</nowiki>
|-
|
* Microscopic polyngitis
|
* Necrotizing vasculitis (no granuloma)
|<nowiki>+/-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| +
|
+ (P-ANCA)
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|
* Hypercellular and inflamed glomeruli (Crescent formation)
|<nowiki>- (pauci-immune)</nowiki>
|<nowiki>-</nowiki>
|-
!Membranoproliferative glomerulonephritis
|
* Idiopathic
* Hepatitis B and C (Type 1)
* C3 nepritic factor (Type2)
|
* Hemeturia
* Oliguria
* Periorbital edema
* Hypertension
|<nowiki>+/-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|
* Thick glomerular basement membrane (Tram-track appearance)
|
* Mesangial proliferation and leukocyte infiltration
|<nowiki>+ (Granular)</nowiki>
|}


==Reference==
==References==
{{Reflist|2}}
{{Reflist|2}}


[[Category:Endocrinology]]
{{WH}}
{{WS}}
 
[[Category:Needs content]]


{{WS}}
[[Category:Disease]]
{{WH}}
[[Category:Organ disorders]]
[[Category:Inflammations]]
[[Category:Kidney diseases]]

Latest revision as of 06:42, 28 July 2020

Diabetes mellitus Main page

Patient Information

Type 1
Type 2

Overview

Classification

Diabetes mellitus type 1
Diabetes mellitus type 2
Gestational diabetes

Differential Diagnosis

Complications

Screening

Diagnosis

Prevention


https://https://www.youtube.com/watch?v=zucxZw069kw%7C350}}


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Glomerulonephritis Main page

Glomerulonephritis patient information

Overview

Classification

[[]]
[[]]
[[]]

Pathophysiology

Differential Diagnosis

Screening

Diagnosis

Prevention

Pathophysiology

Microscopic Pathology

Images shown below are courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology


Glomerulonephritis Videos

Rapidly progressive glomerulonephritis

{{#ev:youtube|CqSyj4cVZPE}}


Chronic glomerulonephritis

{{#ev:youtube|eA1vYarRAWo}}

Images

Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

Images:

References

Template:WH Template:WS


Common Causes




Glomerulonephritis Main page

Glomerulonephritis patient information

Overview

Classification

[[]]
[[]]
[[]]

Pathophysiology

Differential Diagnosis

Screening

Diagnosis

Prevention

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

Overview

Glomerulonephritis may be proliferative or non-proliferative and may be associated with nephrotic or nephritic features. The various types of glomerulonephritides should be differentiated from each other based on associations, presence of pitting edema, hemeturia, hypertension, hemoptysis, oliguria, peri-orbital edema, hyperlipidemia, type of antibodies, light and electron microscopic features.

Differential Diagnosis

The following table differentiates between various types of glomerulonephritides:

Glomerulonephritis Sub-entity Causes and associations History and Symtoms Laboratory Findings
Hyperlipidemia and hypercholesterolemia Nephrotic features Nephritic features ANCA Anti-glomerular basement membrane antibody (Anti-GBM antibody) Immune complex formation Light microscope Electron microscope Immunoflourescence pattern
History Pitting edema Hemeturia (pre-dominantly microscopic) Hypertension Hemoptysis Oliguria Peri-orbital edema
Non-proliferative Minimal change disease
  • Idiopathic
  • Protein tyrosine phosphatase receptor type O (glomerular epithelial protein 1- GLEPP1)
  • Young children
  • Recent infection and immunization
  • Atopy
  • Hodgkin lymphoma
  • Thrombosis (due to urinary loss of antithrombin-III)

+

-

-

-

+/-

-

+

+

-

-

-

-

  • Normal
  • Fusion of podocytes

-

Focal segmental glomerulosclerosis
  • Idiopathic
  • HIV
  • Heroine use
  • Sickle cell disease
  • Interferon
  • Severe obesity
  • Mixed cryoglobunemia (Hepatitis C)
  • Adults
+ - - - +/- - + + - - - -
  • Focal (some glomeruli) and segmental (only part of glomerulus)
  • Effacement of podocytes
-
Membranous glomerulonephritis
  • Idiopathic
  • Hepatitis B and C
  • Solid tumors
  • Systemic lupus erythmatosus
  • Drugs (NSAIDS, penclliamine, gold, captopril)
+ - - - +/- - + + - - - +
  • Thick glomerular basement membrance
  • Sub-epithelial immune complex depositis with 'spike and dome' appearance
-
Proliferative IgA nephropathy
  • Idiopathic
  • Viral infections
  • Young children
  • History of mucosal infections (e.g. gastroenteritis) and upper respiratory tract infection
  • 2-3 days after infection (synpharyngitic)
+/- + + - + +/- - - + - - +
  • Crescent formation
  • Mesangial proliferation
-
Rapidly progressive glomerulonephritis
  • Goodpasture syndrome
  • Young adults
+/- + + + + + - - + - + +
  • Hypercellular and inflamed glomeruli (Crescent formation)
  •  Diffuse thickening of the glomerular basement membrane with absence of subepithelial and subendothelial deposits 
+ (Linear)
  • Post infectious glomerulonephritis
  • Streptococcal skin infections
  • Streptococcal pharyngitis
  • 2-3 weeks after infection
+/- + + + + + - - + - - +
  • Hypercellular and inflamed glomeruli
  • Sub-epithelial immune complex deposits
+ (Granular)
  • Granulomatosis with polyangitis (Wegner's granulomatosis)
+/- + + + + + - - + + (C-ANCA) - -
  • Hypercellular and inflamed glomeruli (Crescent formation)
- (pauci-immune) +/-
  • Churg Strauss syndrome
  • Necrotizing granulomas (Lungs and kidneys)
  • Asthma
  • Peripheral neuropathy
+/- + + + + + - - +

+ (C-ANCA)

- -
  • Hypercellular and inflamed glomeruli (Crescent formation)
- (pauci-immune) -
  • Microscopic polyngitis
  • Necrotizing vasculitis (no granuloma)
+/- + + + + + - - +

+ (P-ANCA)

- -
  • Hypercellular and inflamed glomeruli (Crescent formation)
- (pauci-immune) -
Membranoproliferative glomerulonephritis
  • Idiopathic
  • Hepatitis B and C (Type 1)
  • C3 nepritic factor (Type2)
  • Hemeturia
  • Oliguria
  • Periorbital edema
  • Hypertension
+/- + + + + + - + - - - +
  • Thick glomerular basement membrane (Tram-track appearance)
  • Mesangial proliferation and leukocyte infiltration
+ (Granular)

References

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