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'''Diabetes mellitus Main page'''
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Patient Information
: [[Diabetes mellitus type 1 (patient information)|Type 1]]
: [[Diabetes mellitus type 2 (patient information)|Type 2]]
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[[Diabetes mellitus#Overview|Overview]]
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[[Diabetes mellitus#Classification|Classification]]
: [[Diabetes mellitus type 1]]
: [[Diabetes mellitus type 2]]
: [[Gestational diabetes]]
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[[Diabetes mellitus#Differential diagnosis|Differential Diagnosis]]
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[[Diabetes mellitus#Complications|Complications]]
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[[Diabetes mellitus#Screening|Screening]]
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[[Diabetes mellitus#Diagnosis|Diagnosis]]
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[[Diabetes mellitus#Prevention|Prevention]]
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| {{#ev:youtube|https://https://www.youtube.com/watch?v=zucxZw069kw|350}}
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__NOTOC__
__NOTOC__


{{CMG}}; {{AE}} {{MJ}}
{{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====
 
{{#ev:youtube|CqSyj4cVZPE}}
 
 
====Chronic glomerulonephritis====
 
{{#ev:youtube|eA1vYarRAWo}}
 
===Images===
 
[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]
 
<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>
 
<div align="left">
<gallery heights="175" widths="175">
Image:Glomerulonephritis case 3.jpg|This is a higher-power photomicrograph of hyalinized glomeruli (1) and glomeruli with thickened basement membranes (2).
Image:Glomerulonephritis case 4.jpg|This is a photomicrograph of interstitial and vascular lesions in end stage renal disease.
</gallery>
</div>
 
<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>
 
<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>
 
<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>
 
===Images:===
 
*[http://www.pathologyatlas.ro/Crescentic%20Glomerulonephritis.html Crescentic GN]
 
*[http://www.pathologyatlas.ro/Chronic%20Glomerulonephritis1.html Chronic GN]


{{SI}}
==References==
{{Reflist|2}}


==Overview==
[[Category:Disease]]
[[Category:Organ disorders]]
[[Category:Inflammations]]
[[Category:Kidney diseases]]
 
[[Category:Needs overview]]
 
{{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]]


==Historical Perspective==
3 beta-hydroxysteroid dehydrogenase deficiency first time described in 1962, a patient with ambiguous genitalia and salt wasting.<ref name="pmid13968789">{{cite journal |vauthors=BONGIOVANNI AM |title=The adrenogenital syndrome with deficiency of 3 beta-hydroxysteroid dehydrogenase |journal=J. Clin. Invest. |volume=41 |issue= |pages=2086–92 |year=1962 |pmid=13968789 |pmc=291138 |doi=10.1172/JCI104666 |url=}}</ref>


==Classification==
--------------------------------------
There are three types of 3 beta-hydroxysteroid dehydrogenase deficiency: the salt-wasting, non-salt-wasting, and non-classic types.
==Pathophysiology==
*The pathogenesis of 3 beta-hydroxysteroid dehydrogenase deficiency is characterized by impaired pathway biosynthesis of progestins, mineralocorticoids, glucocorticoids, and androgens (therefore estrogen. As a result of [[cortisol]] absence, [[corticotropin]] ([[ACTH]]) secretion increases leads to produce 3-hydroxy-delta-5-steroids pregnenolone, 17-hydroxypregnenolone, and dehydroepiandrosterone (DHEA), also their sulfates.<ref name="pmid13968789">{{cite journal |vauthors=BONGIOVANNI AM |title=The adrenogenital syndrome with deficiency of 3 beta-hydroxysteroid dehydrogenase |journal=J. Clin. Invest. |volume=41 |issue= |pages=2086–92 |year=1962 |pmid=13968789 |pmc=291138 |doi=10.1172/JCI104666 |url=}}</ref>
==Causes==
* 3 beta-hydroxysteroid dehydrogenase deficiency is caused by a mutation in the HSD3B2 gene.
==Differentiating [disease name] from other Diseases==
* 3 beta-hydroxysteroid dehydrogenase deficiency must be differentiated from other diseases that cause ambiguous genitalia such as:
* [[21-hydroxylase deficiency]]
* [[11-β hydroxylase deficiency]]
* [[17-α hydroxylase deficiency]]
* Gestational [[hyperandrogenism]]
* [[P450-oxidoreductase deficiency]]
==Epidemiology and Demographics==
* The prevalence of 3 beta-hydroxysteroid dehydrogenase deficiency is unknown. At least 60 affected individuals have been reported.<ref name="url3-beta-hydroxysteroid dehydrogenase deficiency - Genetics Home Reference">{{cite web |url=https://ghr.nlm.nih.gov/condition/3-beta-hydroxysteroid-dehydrogenase-deficiency#statistics |title=3-beta-hydroxysteroid dehydrogenase deficiency - Genetics Home Reference |format= |work= |accessdate=}}</ref>
==Risk Factors==
*Common risk factors in the development of 3 beta-hydroxysteroid dehydrogenase deficiency is family history of this disease.


== Diagnosis ==
__NOTOC__
=== Symptoms ===
* Symptoms of 3 beta-hydroxysteroid dehydrogenase deficiency may include the following:<ref name="pmid7626445">{{cite journal |vauthors=Simard J, Rheaume E, Mebarki F, Sanchez R, New MI, Morel Y, Labrie F |title=Molecular basis of human 3 beta-hydroxysteroid dehydrogenase deficiency |journal=J. Steroid Biochem. Mol. Biol. |volume=53 |issue=1-6 |pages=127–38 |year=1995 |pmid=7626445 |doi= |url=}}</ref>
Symptoms of both cortisol and aldosterone deficiency:
:* Feeding difficulties
:* [[Vomiting]]
:* [[Volume depletion]]
:* [[Muscle weakness]]


* Undervirilization in newborn males.
{{Glomerulonephritis}}
* Mild virilization and clitoromegaly in newborn female because of peripheral conversion of DHEA sulfate (DHEAS) to testosterone.
{{CMG}}; {{AE}}{{HK}}
=== Physical Examination ===
*Physical examination may be remarkable for:
Undervirilization in newborn males and mild virilization and clitoromegaly in newborn female.


=== Laboratory Findings ===
==Overview==
Hormonal criteria described for 3 beta-hydroxysteroid dehydrogenase deficiency based on delta-5-17-hydroxypregnenolone levels as following:<ref name="pmid12050224">{{cite journal |vauthors=Lutfallah C, Wang W, Mason JI, Chang YT, Haider A, Rich B, Castro-Magana M, Copeland KC, David R, Pang S |title=Newly proposed hormonal criteria via genotypic proof for type II 3beta-hydroxysteroid dehydrogenase deficiency |journal=J. Clin. Endocrinol. Metab. |volume=87 |issue=6 |pages=2611–22 |year=2002 |pmid=12050224 |doi=10.1210/jcem.87.6.8615 |url=}}</ref>
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.  
* Neonates ≥12,600 ng/dL
* Tanner stage I children ≥5490 ng/dL
* Children with premature pubarche ≥9790 ng/dL
* Adults ≥9620 ng/dL


Other laboratory findings include:
==Differential Diagnosis==
* [Hyponatremia]
The following table differentiates between various types of glomerulonephritides:
* [Hyperkalemia]
{| 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>
|}


== Treatment ==
=== Medical Therapy ===
*The mainstay of therapy for 3 beta-hydroxysteroid dehydrogenase deficiency is [[hydrocortisone]] and [[fludrocortisone acetate]].
* Gender-appropriate replacement of androgens or estrogens with progestins is necessary at the puberty time.
=== Surgery ===
The reconstruction surgery for ambiguous genitalia in genetically male patients may be applied.
==References==
==References==
{{Reflist|2}}
{{Reflist|2}}


{{WikiDoc Help Menu}}
{{WH}}
{{WikiDoc Sources}}
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[[Category:Needs content]]
 
[[Category:Disease]]
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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

Template:WH Template:WS