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{{Minimal change disease}}
{{Minimal change disease}}
{{CMG}}; {{AE}} [[User:YazanDaaboul|Yazan Daaboul]], [[User:Sergekorjian|Serge Korjian]]
{{CMG}}; {{AE}} [[User:YazanDaaboul|Yazan Daaboul]], [[User:Sergekorjian|Serge Korjian]]; {{VKG}}


==Overview==
==Overview==
Minimal change disease can be classified based on the underlying clinical etiology of disease into primary and secondary. Minimal change disease currently has no pathological classification system.  Based on the proposed Columbia classification, minimal change disease was considered an entity within the spectrum of [[focal segmental glomerulonephritis]] ([[FSGS]]).<ref name="pmid14750104">{{cite journal| author=D'Agati VD, Fogo AB, Bruijn JA, Jennette JC| title=Pathologic classification of focal segmental glomerulosclerosis: a working proposal. | journal=Am J Kidney Dis | year= 2004 | volume= 43 | issue= 2 | pages= 368-82 | pmid=14750104 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14750104  }} </ref>
[[Minimal change disease]] can be classified based on the underlying clinical [[etiology]] of disease into primary and secondary. Minimal change disease currently has no [[pathological]] classification system.  Based on the proposed Columbia classification, minimal change disease was considered an entity within the spectrum of [[focal segmental glomerulonephritis]] ([[FSGS]]).


==Classification==
==Classification==
* [[Minimal change disease]] may be classified into the following variants with only minor changes on [[light microscopy]] and these variants may represent MCD or [[focal segmental glomerulosclerosis]] ([[Focal segmental glomerulosclerosis|FSGS]])
** [[Idiopathic]] [[mesangial proliferative glomerulonephritis]].
** [[Immunoglobulin]] M ([[IgM]]) [[nephropathy]].
** C1q [[nephropathy]].
==== IDIOPATHIC MESANGIAL PROLIFERATIVE GLOMERULONEPHRITIS ====
* Focal(<50% of [[glomeruli]] are involved) or [[diffuse]](>50% of glomeruli are involved) is an non specific sign for [[glomerular]] injury.
* IDIOPATHIC MESANGIAL PROLIFERATIVE GLOMERULONEPHRITIS is seen in <ref name="pmid4795879">{{cite journal |vauthors=Sagel I, Treser G, Ty A, Yoshizawa N, Kleinberger H, Yuceoglu AM, Wasserman E, Lange K |title=Occurrence and nature of glomerular lesions after group A streptococci infections in children |journal=Ann. Intern. Med. |volume=79 |issue=4 |pages=492–9 |date=October 1973 |pmid=4795879 |doi= |url=}}</ref>
** [[lupus nephritis]]
** [[IgA nephropathy]]
** [[Post-streptococcal glomerulonephritis|Postinfectious glomerulonephritis]]
* No [[immune]] deposits are found in [[idiopathic]] [[mesangial proliferative glomerulonephritis]].
==== IGM NEPHROPATHY ====
* In IGM [[nephropathy]] patients present with deposits of [[IgM]] and [[complement]] with [[electron]] dense deposits in the [[mesangium]].<ref name="pmid1852859">{{cite journal |vauthors=O'Donoghue DJ, Lawler W, Hunt LP, Acheson EJ, Mallick NP |title=IgM-associated primary diffuse mesangial proliferative glomerulonephritis: natural history and prognostic indicators |journal=Q. J. Med. |volume=79 |issue=288 |pages=333–50 |date=April 1991 |pmid=1852859 |doi= |url=}}</ref>
* Patients who are presenting with [[IgM]] [[nephropathy]] are less much likely to respond to [[Immunosuppression|immunosuppressive]] agents than those with MCD.
==== C1Q NEPHROPATHY ====
* [[Mesangial cell|Mesangial]] deposits on [[electron microscopy]] and C1q deposits on [[immunofluorescence]] microscopy are noed in patients with C1Q [[nephropathy]].<ref name="pmid16247648">{{cite journal |vauthors=Kersnik Levart T, Kenda RB, Avgustin Cavić M, Ferluga D, Hvala A, Vizjak A |title=C1Q nephropathy in children |journal=Pediatr. Nephrol. |volume=20 |issue=12 |pages=1756–61 |date=December 2005 |pmid=16247648 |doi=10.1007/s00467-005-2040-4 |url=}}</ref><ref name="pmid3875286">{{cite journal |vauthors=Jennette JC, Hipp CG |title=C1q nephropathy: a distinct pathologic entity usually causing nephrotic syndrome |journal=Am. J. Kidney Dis. |volume=6 |issue=2 |pages=103–10 |date=August 1985 |pmid=3875286 |doi= |url=}}</ref>
* C1Q [[nephropathy]] is a subgroup of primary [[focal segmental glomerulosclerosis]].<ref name="pmid1928065">{{cite journal |vauthors=Iskandar SS, Browning MC, Lorentz WB |title=C1q nephropathy: a pediatric clinicopathologic study |journal=Am. J. Kidney Dis. |volume=18 |issue=4 |pages=459–65 |date=October 1991 |pmid=1928065 |doi= |url=}}</ref>


===Clinical Classification===
===Clinical Classification===
The clinical classification of minimal change disease is based on the underlying etiology of the disease.
* The clinical classification of [[minimal change disease]] is based on the underlying [[etiology]] of the disease.


====Primary====
====Primary====
In primary (idiopathic) cases, the underlying cause is not known.
* In primary ([[idiopathic]]) cases, the underlying cause is not known.


====Secondary====
====Secondary====
Secondary forms of minimal change disease are associated with certain environmental exposures, such as [[allergies]] ([[bee sting]]), [[malignancies]] ([[lymphoma]]s and [[leukemia]]s), [[medication]]s ([[NSAID]], [[penicillamine]], [[ampicillin]]), and other toxins (gold, mercury)
* Secondary forms of [[minimal change disease]] are associated with certain environmental exposures, such as [[allergies]] ([[bee sting]]), [[malignancies]] ([[lymphoma]]s and [[leukemia]]s), [[medication]]s ([[NSAID]], [[penicillamine]], [[ampicillin]]), and other [[Toxin|toxins]] ([[gold]], [[Mercury (element)|mercury]]).<ref name="pmid16864010">{{cite journal |vauthors=Habib GS, Saliba W, Nashashibi M, Armali Z |title=Penicillamine and nephrotic syndrome |journal=Eur. J. Intern. Med. |volume=17 |issue=5 |pages=343–8 |date=August 2006 |pmid=16864010 |doi=10.1016/j.ejim.2006.03.001 |url=}}</ref>


===Pathological Classification===
===Pathological Classification===
Minimal change disease currently has no classification system. Early observations noted that a small number of patients with minimal change disease have focal tip lesions.<ref name="pmid12046027">{{cite journal| author=Haas M, Yousefzadeh N| title=Glomerular tip lesion in minimal change nephropathy: a study of autopsies before 1950. | journal=Am J Kidney Dis | year= 2002 | volume= 39 | issue= 6 | pages= 1168-75 | pmid=12046027 | doi=10.1053/ajkd.2002.33386 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12046027  }} </ref> Based on the proposed Columbia classification by D’Agati and colleagues<ref name="pmid14750104">{{cite journal| author=D'Agati VD, Fogo AB, Bruijn JA, Jennette JC| title=Pathologic classification of focal segmental glomerulosclerosis: a working proposal. | journal=Am J Kidney Dis | year= 2004 | volume= 43 | issue= 2 | pages= 368-82 | pmid=14750104 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14750104  }} </ref> in 2004, minimal change disease was considered an entity within the spectrum of [[focal segmental glomerulonephritis]] ([[FSGS]]) and may have a clinical course similar to those with “tip lesion” subtype of FSGS.
* [[Minimal change disease]] currently has no classification system.
 
* Early observations noted that a small number of patients with minimal change disease have focal tip lesions.<ref name="pmid12046027">{{cite journal| author=Haas M, Yousefzadeh N| title=Glomerular tip lesion in minimal change nephropathy: a study of autopsies before 1950. | journal=Am J Kidney Dis | year= 2002 | volume= 39 | issue= 6 | pages= 1168-75 | pmid=12046027 | doi=10.1053/ajkd.2002.33386 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12046027  }} </ref>  
* Based on the proposed Columbia classification by D’Agati and colleagues in 2004, minimal change disease was considered an entity within the spectrum of [[focal segmental glomerulonephritis]] ([[FSGS]]) and may have a clinical course similar to those with “tip lesion” subtype of [[Focal segmental glomerulosclerosis|FSGS]].<ref name="pmid14750104">{{cite journal| author=D'Agati VD, Fogo AB, Bruijn JA, Jennette JC| title=Pathologic classification of focal segmental glomerulosclerosis: a working proposal. | journal=Am J Kidney Dis | year= 2004 | volume= 43 | issue= 2 | pages= 368-82 | pmid=14750104 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14750104  }} </ref>
{| border="1" style="border-collapse:collapse; text-align:left;" cellpadding="5" align="center"
{| border="1" style="border-collapse:collapse; text-align:left;" cellpadding="5" align="center"
|+ '''''Pathological Classification of Focal Segmental Glomerulosclerosis<ref name="pmid14750104">{{cite journal| author=D'Agati VD, Fogo AB, Bruijn JA, Jennette JC| title=Pathologic classification of focal segmental glomerulosclerosis: a working proposal. | journal=Am J Kidney Dis | year= 2004 |volume= 43 | issue= 2 | pages= 368-82 | pmid=14750104 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14750104  }} </ref>'''''
|+ '''''Pathological Classification of Focal Segmental Glomerulosclerosis<ref name="pmid14750104">{{cite journal |vauthors=D'Agati VD, Fogo AB, Bruijn JA, Jennette JC |title=Pathologic classification of focal segmental glomerulosclerosis: a working proposal |journal=Am. J. Kidney Dis. |volume=43 |issue=2 |pages=368–82 |date=February 2004 |pmid=14750104 |doi= |url=}}</ref>'''''
| bgcolor="#d9ff54"|'''Variant''' || bgcolor="#d9ff54"|'''Location of Lesion'''|| bgcolor="#d9ff54"|'''Distribution of Lesion'''|| bgcolor="#d9ff54"|'''Characteristic Features'''
| bgcolor="#d9ff54" |'''Variant''' || bgcolor="#d9ff54" |'''Location of Lesion'''|| bgcolor="#d9ff54" |'''Distribution of Lesion'''|| bgcolor="#d9ff54" |'''Characteristic Features'''
|-
|-
| bgcolor="#ececec"|'''Not Otherwise Specified (NOS)''' || Anywhere|| Segmental|| Capillary lumen abolished by the segmental increase in [[matrix]].
| bgcolor="#ececec" |'''Not Otherwise Specified (NOS)''' || Anywhere|| Segmental|| [[Capillary]] lumen abolished by the segmental increase in [[matrix]].
|-
|-
| bgcolor="#ececec"|'''Perihilar Variant''' || Perihilar||Segmental|| Presence of one or more [[glomeruli]] containing [[hyalinosis]] in the perihilar regions with or without [[sclerosis]]. Within each [[glomerulus]], the segmental lesions must contain > 50% perihilar hyalinosis and/or [[sclerosis]].
| bgcolor="#ececec" |'''Perihilar Variant''' || Perihilar||Segmental|| Presence of one or more [[glomeruli]] containing hyalinosis in the perihilar regions with or without [[sclerosis]]. Within each [[glomerulus]], the segmental lesions must contain > 50% perihilar hyalinosis and/or [[sclerosis]].
|-
|-
| bgcolor="#ececec"|'''Cellular Variant''' || Anywhere|| Segmental|| Presence of one or more [[glomerulus]] with segmental hypercellularity of the capillary [[endothelium]] that blocks the [[capillary]] lumen, with or without foam cells and/or karryohexis.
| bgcolor="#ececec" |'''Cellular Variant''' || Anywhere|| Segmental|| Presence of one or more [[glomerulus]] with segmental hypercellularity of the capillary [[endothelium]] that blocks the [[capillary]] lumen, with or without foam cells and/or karryohexis.
|-
|-
| bgcolor="#ececec"|'''Tip Variant''' || At tip domain|| Segmental|| One or more segmental lesions, that include tip domains. Lesions must have adhesions/confluence of [[podocyte]]s with parietal or tubular cells. Tip domains are defined as 25% of tuft adjacent to the origin of the proximal tubule.  Sclerosing lesions shuld be <25% of tuft, while cellular lesions should be < 50% of tuft. No perihilar sclerosis should be observed.
| bgcolor="#ececec" |'''Tip Variant''' || At tip domain|| Segmental|| One or more segmental lesions, that include tip domains. Lesions must have adhesions/confluence of [[podocyte]]s with parietal or tubular cells. Tip domains are defined as 25% of tuft adjacent to the origin of the proximal tubule.  Sclerosing lesions shuld be <25% of tuft, while cellular lesions should be < 50% of tuft. No perihilar sclerosis should be observed.
|-
|-
|bgcolor="#ececec"|'''Collapsing Variant''' || Anywhere|| Segmental or global|| One or more [[glomeruli]] with collapse with evidence of [[podocyte]] [[hypertrophy]] and [[hyperplasia]].
| bgcolor="#ececec" |'''Collapsing Variant''' || Anywhere|| Segmental or global|| One or more [[glomeruli]] with collapse with evidence of [[podocyte]] [[hypertrophy]] and [[hyperplasia]].
|}
|}<sup>
 
<sup><center>Adapted from D’Agati VD, Fogo AB, Bruijn JA, and Jennette JC. Pathological classification of focal segmental glomerulosclerosis. A working proposal. ''Am J of Kidney Dis''. 2004; 43(2):368-382.</center></sup>


==References==
==References==

Latest revision as of 14:23, 13 June 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yazan Daaboul, Serge Korjian; Vamsikrishna Gunnam M.B.B.S [2]

Overview

Minimal change disease can be classified based on the underlying clinical etiology of disease into primary and secondary. Minimal change disease currently has no pathological classification system. Based on the proposed Columbia classification, minimal change disease was considered an entity within the spectrum of focal segmental glomerulonephritis (FSGS).

Classification

IDIOPATHIC MESANGIAL PROLIFERATIVE GLOMERULONEPHRITIS

IGM NEPHROPATHY

C1Q NEPHROPATHY

Clinical Classification

Primary

  • In primary (idiopathic) cases, the underlying cause is not known.

Secondary

Pathological Classification

  • Minimal change disease currently has no classification system.
  • Early observations noted that a small number of patients with minimal change disease have focal tip lesions.[7]
  • Based on the proposed Columbia classification by D’Agati and colleagues in 2004, minimal change disease was considered an entity within the spectrum of focal segmental glomerulonephritis (FSGS) and may have a clinical course similar to those with “tip lesion” subtype of FSGS.[8]
Pathological Classification of Focal Segmental Glomerulosclerosis[8]
Variant Location of Lesion Distribution of Lesion Characteristic Features
Not Otherwise Specified (NOS) Anywhere Segmental Capillary lumen abolished by the segmental increase in matrix.
Perihilar Variant Perihilar Segmental Presence of one or more glomeruli containing hyalinosis in the perihilar regions with or without sclerosis. Within each glomerulus, the segmental lesions must contain > 50% perihilar hyalinosis and/or sclerosis.
Cellular Variant Anywhere Segmental Presence of one or more glomerulus with segmental hypercellularity of the capillary endothelium that blocks the capillary lumen, with or without foam cells and/or karryohexis.
Tip Variant At tip domain Segmental One or more segmental lesions, that include tip domains. Lesions must have adhesions/confluence of podocytes with parietal or tubular cells. Tip domains are defined as 25% of tuft adjacent to the origin of the proximal tubule. Sclerosing lesions shuld be <25% of tuft, while cellular lesions should be < 50% of tuft. No perihilar sclerosis should be observed.
Collapsing Variant Anywhere Segmental or global One or more glomeruli with collapse with evidence of podocyte hypertrophy and hyperplasia.

References

  1. Sagel I, Treser G, Ty A, Yoshizawa N, Kleinberger H, Yuceoglu AM, Wasserman E, Lange K (October 1973). "Occurrence and nature of glomerular lesions after group A streptococci infections in children". Ann. Intern. Med. 79 (4): 492–9. PMID 4795879.
  2. O'Donoghue DJ, Lawler W, Hunt LP, Acheson EJ, Mallick NP (April 1991). "IgM-associated primary diffuse mesangial proliferative glomerulonephritis: natural history and prognostic indicators". Q. J. Med. 79 (288): 333–50. PMID 1852859.
  3. Kersnik Levart T, Kenda RB, Avgustin Cavić M, Ferluga D, Hvala A, Vizjak A (December 2005). "C1Q nephropathy in children". Pediatr. Nephrol. 20 (12): 1756–61. doi:10.1007/s00467-005-2040-4. PMID 16247648.
  4. Jennette JC, Hipp CG (August 1985). "C1q nephropathy: a distinct pathologic entity usually causing nephrotic syndrome". Am. J. Kidney Dis. 6 (2): 103–10. PMID 3875286.
  5. Iskandar SS, Browning MC, Lorentz WB (October 1991). "C1q nephropathy: a pediatric clinicopathologic study". Am. J. Kidney Dis. 18 (4): 459–65. PMID 1928065.
  6. Habib GS, Saliba W, Nashashibi M, Armali Z (August 2006). "Penicillamine and nephrotic syndrome". Eur. J. Intern. Med. 17 (5): 343–8. doi:10.1016/j.ejim.2006.03.001. PMID 16864010.
  7. Haas M, Yousefzadeh N (2002). "Glomerular tip lesion in minimal change nephropathy: a study of autopsies before 1950". Am J Kidney Dis. 39 (6): 1168–75. doi:10.1053/ajkd.2002.33386. PMID 12046027.
  8. 8.0 8.1 D'Agati VD, Fogo AB, Bruijn JA, Jennette JC (2004). "Pathologic classification of focal segmental glomerulosclerosis: a working proposal". Am J Kidney Dis. 43 (2): 368–82. PMID 14750104.

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