Minimal change disease differential diagnosis: Difference between revisions

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__NOTOC__
__NOTOC__
{{Minimal change disease}}
[[Image:Home_logo1.png|right|250px|link=https://www.wikidoc.org/index.php/Minimal_change_disease]]
{{CMG}}; {{AE}} [[User:YazanDaaboul|Yazan Daaboul]], [[User:Sergekorjian|Serge Korjian]]
{{CMG}}; {{AE}} {{MJ}}, {{HK}}


==Overview==
==Overview==
Line 7: Line 7:


==Differential Diagnosis==
==Differential Diagnosis==
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.  
Minimal change disease should be differentiated from other glomerular diseases. The various types of glomerular diseases may 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. The following table differentiates between various types of glumerular diseases:
The following table differentiates between various types of glomerulonephritides:<ref name="pmid17195422">{{cite journal |vauthors=Saha TC, Singh H |title=Minimal change disease: a review |journal=South. Med. J. |volume=99 |issue=11 |pages=1264–70 |date=November 2006 |pmid=17195422 |doi=10.1097/01.smj.0000243183.87381.c2 |url=}}</ref><ref name="pmid27092244">{{cite journal |vauthors=Saleem MA, Kobayashi Y |title=Cell biology and genetics of minimal change disease |journal=F1000Res |volume=5 |issue= |pages= |date=2016 |pmid=27092244 |pmc=4821284 |doi=10.12688/f1000research.7300.1 |url=}}</ref><ref name="pmid26064510">{{cite journal |vauthors=Keskar V, Jamale TE, Kulkarni MJ, Kiggal Jagadish P, Fernandes G, Hase N |title=Minimal-change disease in adolescents and adults: epidemiology and therapeutic response |journal=Clin Kidney J |volume=6 |issue=5 |pages=469–72 |date=October 2013 |pmid=26064510 |pmc=4438390 |doi=10.1093/ckj/sft063 |url=}}</ref><ref name="pmid21974967">{{cite journal |vauthors=Chugh SS, Clement LC, Macé C |title=New insights into human minimal change disease: lessons from animal models |journal=Am. J. Kidney Dis. |volume=59 |issue=2 |pages=284–92 |date=February 2012 |pmid=21974967 |pmc=3253318 |doi=10.1053/j.ajkd.2011.07.024 |url=}}</ref><ref name="pmid28242845">{{cite journal |vauthors=Rosenberg AZ, Kopp JB |title=Focal Segmental Glomerulosclerosis |journal=Clin J Am Soc Nephrol |volume=12 |issue=3 |pages=502–517 |date=March 2017 |pmid=28242845 |pmc=5338705 |doi=10.2215/CJN.05960616 |url=}}</ref><ref name="pmid25168829">{{cite journal |vauthors=Jefferson JA, Shankland SJ |title=The pathogenesis of focal segmental glomerulosclerosis |journal=Adv Chronic Kidney Dis |volume=21 |issue=5 |pages=408–16 |date=September 2014 |pmid=25168829 |pmc=4149756 |doi=10.1053/j.ackd.2014.05.009 |url=}}</ref><ref name="pmid2429634">{{cite journal |vauthors=Gephardt GN, Tubbs RR, Popowniak KL, McMahon JT |title=Focal and segmental glomerulosclerosis. Immunohistologic study of 20 renal biopsy specimens |journal=Arch. Pathol. Lab. Med. |volume=110 |issue=10 |pages=902–5 |date=October 1986 |pmid=2429634 |doi= |url=}}</ref><ref name="pmid25558821">{{cite journal |vauthors=Lai WL, Yeh TH, Chen PM, Chan CK, Chiang WC, Chen YM, Wu KD, Tsai TJ |title=Membranous nephropathy: a review on the pathogenesis, diagnosis, and treatment |journal=J. Formos. Med. Assoc. |volume=114 |issue=2 |pages=102–11 |date=February 2015 |pmid=25558821 |doi=10.1016/j.jfma.2014.11.002 |url=}}</ref><ref name="pmid10495797">{{cite journal |vauthors=Wasserstein AG |title=Membranous glomerulonephritis |journal=J. Am. Soc. Nephrol. |volume=8 |issue=4 |pages=664–74 |date=April 1997 |pmid=10495797 |doi= |url=}}</ref><ref name="pmid21949093">{{cite journal |vauthors=Suzuki H, Kiryluk K, Novak J, Moldoveanu Z, Herr AB, Renfrow MB, Wyatt RJ, Scolari F, Mestecky J, Gharavi AG, Julian BA |title=The pathophysiology of IgA nephropathy |journal=J. Am. Soc. Nephrol. |volume=22 |issue=10 |pages=1795–803 |date=October 2011 |pmid=21949093 |pmc=3892742 |doi=10.1681/ASN.2011050464 |url=}}</ref><ref name="pmid23782179">{{cite journal |vauthors=Wyatt RJ, Julian BA |title=IgA nephropathy |journal=N. Engl. J. Med. |volume=368 |issue=25 |pages=2402–14 |date=June 2013 |pmid=23782179 |doi=10.1056/NEJMra1206793 |url=}}</ref><ref name="pmid22373436">{{cite journal |vauthors=He S, Wu Z |title=Gene-based Higher Criticism methods for large-scale exonic single-nucleotide polymorphism data |journal=BMC Proc |volume=5 Suppl 9 |issue= |pages=S65 |date=November 2011 |pmid=22373436 |pmc=3287904 |doi=10.1186/1753-6561-5-S9-S65 |url=}}</ref><ref name="pmid8746284">{{cite journal |vauthors=Higgins RM, Goldsmith DJ, Connolly J, Scoble JE, Hendry BM, Ackrill P, Venning MC |title=Vasculitis and rapidly progressive glomerulonephritis in the elderly |journal=Postgrad Med J |volume=72 |issue=843 |pages=41–4 |date=January 1996 |pmid=8746284 |pmc=2398323 |doi= |url=}}</ref><ref name="pmid12631105">{{cite journal |vauthors=Jennette JC |title=Rapidly progressive crescentic glomerulonephritis |journal=Kidney Int. |volume=63 |issue=3 |pages=1164–77 |date=March 2003 |pmid=12631105 |doi=10.1046/j.1523-1755.2003.00843.x |url=}}</ref><ref name="pmid8914046">{{cite journal |vauthors=Bolton WK |title=Goodpasture's syndrome |journal=Kidney Int. |volume=50 |issue=5 |pages=1753–66 |date=November 1996 |pmid=8914046 |doi= |url=}}</ref><ref name="pmid1090223">{{cite journal |vauthors=Mathew TH, Hobbs JB, Kalowski S, Sutherland PW, Kincaid-Smith P |title=Goodpasture's syndrome: normal renal diagnostic findings |journal=Ann. Intern. Med. |volume=82 |issue=2 |pages=215–8 |date=February 1975 |pmid=1090223 |doi= |url=}}</ref><ref name="pmid18172777">{{cite journal |vauthors=Renaudineau Y, Le Meur Y |title=Renal involvement in Wegener's granulomatosis |journal=Clin Rev Allergy Immunol |volume=35 |issue=1-2 |pages=22–9 |date=October 2008 |pmid=18172777 |doi=10.1007/s12016-007-8066-6 |url=}}</ref><ref name="pmid6384024">{{cite journal |vauthors=Weiss MA, Crissman JD |title=Renal biopsy findings in Wegener's granulomatosis: segmental necrotizing glomerulonephritis with glomerular thrombosis |journal=Hum. Pathol. |volume=15 |issue=10 |pages=943–56 |date=October 1984 |pmid=6384024 |doi= |url=}}</ref><ref name="pmid16632015">{{cite journal |vauthors=Sinico RA, Di Toma L, Maggiore U, Tosoni C, Bottero P, Sabadini E, Giammarresi G, Tumiati B, Gregorini G, Pesci A, Monti S, Balestrieri G, Garini G, Vecchio F, Buzio C |title=Renal involvement in Churg-Strauss syndrome |journal=Am. J. Kidney Dis. |volume=47 |issue=5 |pages=770–9 |date=May 2006 |pmid=16632015 |doi=10.1053/j.ajkd.2006.01.026 |url=}}</ref><ref name="pmid21325353">{{cite journal |vauthors=Cartin-Ceba R, Keogh KA, Specks U, Sethi S, Fervenza FC |title=Rituximab for the treatment of Churg-Strauss syndrome with renal involvement |journal=Nephrol. Dial. Transplant. |volume=26 |issue=9 |pages=2865–71 |date=September 2011 |pmid=21325353 |pmc=3218640 |doi=10.1093/ndt/gfq852 |url=}}</ref><ref name="pmid20688249">{{cite journal |vauthors=Chung SA, Seo P |title=Microscopic polyangiitis |journal=Rheum. Dis. Clin. North Am. |volume=36 |issue=3 |pages=545–58 |date=August 2010 |pmid=20688249 |pmc=2917831 |doi=10.1016/j.rdc.2010.04.003 |url=}}</ref><ref name="pmid18524109">{{cite journal |vauthors=Pagnoux C |title=[Wegener's granulomatosis and microscopic polyangiitis] |language=French |journal=Rev Prat |volume=58 |issue=5 |pages=522–32 |date=March 2008 |pmid=18524109 |doi= |url=}}</ref><ref name="pmid19908070">{{cite journal |vauthors=Alchi B, Jayne D |title=Membranoproliferative glomerulonephritis |journal=Pediatr. Nephrol. |volume=25 |issue=8 |pages=1409–18 |date=August 2010 |pmid=19908070 |pmc=2887509 |doi=10.1007/s00467-009-1322-7 |url=}}</ref><ref name="pmid657595">{{cite journal |vauthors=Davis AE, Schneeberger EE, Grupe WE, McCluskey RT |title=Membranoproliferative glomerulonephritis (MPGN type I) and dense deposit disease (DDD) in children |journal=Clin. Nephrol. |volume=9 |issue=5 |pages=184–93 |date=May 1978 |pmid=657595 |doi= |url=}}</ref>


{| class="wikitable"
{| class="wikitable"
! rowspan="3" align="center" style="background:#4479BA; color: #FFFFFF;" + |Glomerulonephritis
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Glomerular diseases
! rowspan="3" align="center" style="background:#4479BA; color: #FFFFFF;" + |Sub-entity
! colspan="2" rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Disease
! rowspan="3" align="center" style="background:#4479BA; color: #FFFFFF;" + |Causes and associations
! colspan="9" align="center" style="background:#4479BA; color: #FFFFFF;" + |History and Symtoms
! colspan="7" rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |History and Symtoms
! colspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Laboratory Findings
! colspan="9" align="center" style="background:#4479BA; color: #FFFFFF;" + |Laboratory Findings
! colspan="3" align="center" style="background:#4479BA; color: #FFFFFF;" + |Pathology
|-
! 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;" + |History
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Systemic symptoms
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hemeturia
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Proteinuria
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hypertension
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Pitting edema
! 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;" + |Oliguria
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Peri-orbital edema
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephrotic features
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephritic features
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hyperlipidemia and hypercholesterolemia
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Auto-antibodies,
Complements
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Light microscope
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Electron microscope
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Immunoflourescence pattern
|-
|-
| rowspan="3" align="center" style="background:#4479BA; color: #FFFFFF;" + |Non-proliferative
! rowspan="13" align="center" style="background:#4479BA; color: #FFFFFF;" + |Acute Nephritic Syndromes
![[Minimal change disease]]
! colspan="2" |[[Poststreptococcal glomerulonephritis|Poststreptococcal Glomerulonephritis]]<ref name="pmid13022878">{{cite journal| author=GERMUTH FG| title=A comparative histologic and immunologic study in rabbits of induced hypersensitivity of the serum sickness type. | journal=J Exp Med | year= 1953 | volume= 97 | issue= 2 | pages= 257-82 | pmid=13022878 | doi= | pmc=PMC2136196 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13022878 }}</ref><ref name="pmid5031005">{{cite journal| author=Germuth FG, Senterfit LB, Dreesman GR| title=Immune complex disease. V. The nature of the circulating complexes associated with glomerular alterations in the chronic BSA-rabbit system. | journal=Johns Hopkins Med J | year= 1972 | volume= 130 | issue= 6 | pages= 344-57 | pmid=5031005 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=5031005 }}</ref><ref name="pmid22895519">{{cite journal| author=Radhakrishnan J, Cattran DC| title=The KDIGO practice guideline on glomerulonephritis: reading between the (guide)lines--application to the individual patient. | journal=Kidney Int | year= 2012 | volume= 82 | issue= 8 | pages= 840-56 | pmid=22895519 | doi=10.1038/ki.2012.280 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22895519 }}</ref>
|
* [[Streptococcal infections|Streptococcal]] [[skin]] [[infections]]
* [[Streptococcus|Streptococcal]] [[pharyngitis]]
* 2-3 weeks after [[infection]]
|
|
* [[Idiopathic]]
* [[Fever]]
* [[Protein]] [[Protein tyrosine phosphatase|tyrosine phosphatase]] receptor type O (glomerular epithelial protein 1- GLEPP1)
* [[Fatigue]]
* Skin [[rash]]
|<nowiki>+/-</nowiki>
| +
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|
|
* Young children
* [[Anti-dsDNA antibody|Anti-dsDNA antibodies]]
* Recent [[infection]] and [[immunization]]
* Anti-C1q antibodies
* [[Atopy]]
* [[Antineutrophil cytoplasmic antibodies]] ([[ANCA]])  
* [[Hodgkin's lymphoma|Hodgkin lymphoma]]
* [[Thrombosis]] (due to [[Urinary system|urinary]] loss of [[Antithrombin III|antithrombin-III]])
|
|
+
* Hypercellular and [[inflamed]] [[glomeruli]]
|
|
-
* Sub-[[epithelial]] [[immune complex]] deposits
* Obliteration of epithelial cell foot processes
|
|
-
* [[Immune]] complex GN
* Granular deposit
|-
! colspan="2" |[[Renal]] disease due to [[Endocarditis|Subacute Bacterial Endocarditis]], or [[cardiac shunt]] (Atrioventricular)<ref name="pmid6380288">{{cite journal |vauthors=Neugarten J, Baldwin DS |title=Glomerulonephritis in bacterial endocarditis |journal=Am. J. Med. |volume=77 |issue=2 |pages=297–304 |date=August 1984 |pmid=6380288 |doi= |url=}}</ref><ref name="pmid6831779">{{cite journal |vauthors=Arze RS, Rashid H, Morley R, Ward MK, Kerr DN |title=Shunt nephritis: report of two cases and review of the literature |journal=Clin. Nephrol. |volume=19 |issue=1 |pages=48–53 |date=January 1983 |pmid=6831779 |doi= |url=}}</ref>
|
|
-
* History of infective endocarditis mostly due to ''[[Staphylococcus aureus|S. aureus]]''
* [[Cardiac shunt]]
|
|
+/-
* [[Fever]]
* [[Fatigue]]
* Weight loss
|<nowiki>+/-</nowiki>
| +
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|
|
-
* [[Myeloperoxidase (MPO)|ANCA (myeloperoxidase)]] positive in 1/3
* Activation of the [[alternative complement pathway]] (Decreased [[C3 (complement)|C3]], C4)
* Positive [[RF]]
* Positive [[Anti-glomerular basement membrane antibody|anti-GBM autoantibodies]]
|
|
+
* [[Rapidly progressive glomerulonephritis|Crescentic]] GN is the most common pathological features
 
* [[Membranoproliferative glomerulonephritis|Diffuse membranoproliferative glomerulonephritis]] features
* Focal proliferative GN
* Mesangial proliferative GN 
|
|
+
* [[Mesangial cell|Mesangial]] deposits,
* Subendothelial deposits
* Subepithelial "humps," in minority of cases
|
|
-
* Pauci-immune GN
|-
! colspan="2" |[[Lupus nephritis|Lupus Nephritis]]<ref name="pmid14717922">{{cite journal |vauthors=Weening JJ, D'Agati VD, Schwartz MM, Seshan SV, Alpers CE, Appel GB, Balow JE, Bruijn JA, Cook T, Ferrario F, Fogo AB, Ginzler EM, Hebert L, Hill G, Hill P, Jennette JC, Kong NC, Lesavre P, Lockshin M, Looi LM, Makino H, Moura LA, Nagata M |title=The classification of glomerulonephritis in systemic lupus erythematosus revisited |journal=Kidney Int. |volume=65 |issue=2 |pages=521–30 |date=February 2004 |pmid=14717922 |doi=10.1111/j.1523-1755.2004.00443.x |url=}}</ref>
|
|
-
* History of [[SLE]] features
|
|
-
* [[Systemic lupus erythematosus|Lupus]] criteria:
** [[Malar rash]]
** [[Arthritis]]
** [[Arthralgia]]
** [[Anemia]]
** Easy bruising
|<nowiki>+/-</nowiki>
| +
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|
|
-
* Anti-C1q antibodies
* [[Anti-dsDNA antibody|Anti-dsDNA]]
|
|
* Normal
* Differs based on the disease classification
|
|
* Fusion of [[podocytes]]
* Differs based on the disease classification
|
|
-
* Differs based on the disease classification, mostly immune complex GN
* Granular deposit
|-
|-
![[Focal segmental glomerulosclerosis]]
! colspan="2" |[[Goodpasture syndrome|Antiglomerular Basement Membrane Disease]] [[Goodpasture syndrome|(Goodpasture's syndrome)]]<ref name="pmid8914046">{{cite journal |vauthors=Bolton WK |title=Goodpasture's syndrome |journal=Kidney Int. |volume=50 |issue=5 |pages=1753–66 |date=November 1996 |pmid=8914046 |doi= |url=}}</ref><ref name="pmid1090223">{{cite journal |vauthors=Mathew TH, Hobbs JB, Kalowski S, Sutherland PW, Kincaid-Smith P |title=Goodpasture's syndrome: normal renal diagnostic findings |journal=Ann. Intern. Med. |volume=82 |issue=2 |pages=215–8 |date=February 1975 |pmid=1090223 |doi= |url=}}</ref>
|
|
* Idiopathic
* Young adults
* [[Human Immunodeficiency Virus (HIV)|HIV]]
* [[Heroine hydrochloride|Heroine]] use
* [[Sickle-cell disease|Sickle cell disease]]
* [[Interferon]]
* Severe [[obesity]]
* [[Cryoglobulinemia|Mixed cryoglobulinemia]] ([[Hepatitis C]])
|
|
* Adults
* Dry [[cough]]
* [[Hemoptysis]]
* [[Malaise]] 
* [[Fever]] and chills
* [[Arthralgia]] 
* [[Fatigue]]
* [[Lethargy]]
* [[Pallor]]
* [[Anorexia]]
* Easy bruising
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>-</nowiki>
| +
| +
| +
|<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]])
* [[Myeloperoxidase (MPO)|ANCA (myeloperoxidase)]]
* Positive [[Anti-glomerular basement membrane antibody|anti-GBM autoantibodies]]
|
* Hypercellular and [[inflamed]] [[glomeruli]] (Crescent formation) 
|Diffuse thickening of the [[glomerular basement membrane]] with absence of sub-[[Epithelial cells|epithelial]] and sub-[[endothelial]] deposits 
|
|
* Effacement of [[podocytes]]
* Immune complex GN
|<nowiki>-</nowiki>
* Linear deposit
|-
|-
![[Membranous glomerulonephritis]]
! colspan="2" |[[IgA nephropathy|IgA Nephropathy]]<ref name="pmid21949093">{{cite journal |vauthors=Suzuki H, Kiryluk K, Novak J, Moldoveanu Z, Herr AB, Renfrow MB, Wyatt RJ, Scolari F, Mestecky J, Gharavi AG, Julian BA |title=The pathophysiology of IgA nephropathy |journal=J. Am. Soc. Nephrol. |volume=22 |issue=10 |pages=1795–803 |date=October 2011 |pmid=21949093 |pmc=3892742 |doi=10.1681/ASN.2011050464 |url=}}</ref><ref name="pmid23782179">{{cite journal |vauthors=Wyatt RJ, Julian BA |title=IgA nephropathy |journal=N. Engl. J. Med. |volume=368 |issue=25 |pages=2402–14 |date=June 2013 |pmid=23782179 |doi=10.1056/NEJMra1206793 |url=}}</ref>
|
|
* [[Idiopathic]]
* Young children
* [[Hepatitis B]] and [[Hepatitis C|C]]
* History of [[mucosal]] [[infections]] (e.g. [[gastroenteritis]]) and [[upper respiratory tract infection]]
* [[Solid tumors]]
* 2-3 days after [[infection]] (synpharyngitic)
* [[Systemic lupus erythematosus]]
* Drugs ([[NSAIDS]], pencilamine, [[gold]], [[captopril]])
|
|
* Low grade [[fever]]
* [[Flank pain]]
|<nowiki>+</nowiki>
| +/-
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
| -
|
* Immune complex deposition
|
* Crescent formation
|
* [[Mesangial cell|Mesangial]] proliferation
|
* Immune complex GN, granular deposite
|-
! colspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Disease
! align="center" style="background:#4479BA; color: #FFFFFF;" + |History
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Systemic symptoms
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hemeturia
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Proteinuria
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hypertension
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Pitting edema
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Oliguria
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephrotic features
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephritic features
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hyperlipidemia and hypercholesterolemia
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Auto-antibodies,
Complements
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Light microscope
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Electron microscope
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Immunoflourescence pattern
|-
! rowspan="3" |[[Vasculitis|ANCA Small-Vessel Vasculitis]]<ref name="pmid8746284">{{cite journal |vauthors=Higgins RM, Goldsmith DJ, Connolly J, Scoble JE, Hendry BM, Ackrill P, Venning MC |title=Vasculitis and rapidly progressive glomerulonephritis in the elderly |journal=Postgrad Med J |volume=72 |issue=843 |pages=41–4 |date=January 1996 |pmid=8746284 |pmc=2398323 |doi= |url=}}</ref><ref name="pmid12631105">{{cite journal |vauthors=Jennette JC |title=Rapidly progressive crescentic glomerulonephritis |journal=Kidney Int. |volume=63 |issue=3 |pages=1164–77 |date=March 2003 |pmid=12631105 |doi=10.1046/j.1523-1755.2003.00843.x |url=}}</ref>
! colspan="1" |[[Granulomatosis with polyangiitis|Granulomatosis with Polyangiitis (Wegener's)]]<ref name="pmid18172777">{{cite journal |vauthors=Renaudineau Y, Le Meur Y |title=Renal involvement in Wegener's granulomatosis |journal=Clin Rev Allergy Immunol |volume=35 |issue=1-2 |pages=22–9 |date=October 2008 |pmid=18172777 |doi=10.1007/s12016-007-8066-6 |url=}}</ref><ref name="pmid6384024">{{cite journal |vauthors=Weiss MA, Crissman JD |title=Renal biopsy findings in Wegener's granulomatosis: segmental necrotizing glomerulonephritis with glomerular thrombosis |journal=Hum. Pathol. |volume=15 |issue=10 |pages=943–56 |date=October 1984 |pmid=6384024 |doi= |url=}}</ref><ref name="pmid18524109">{{cite journal |vauthors=Pagnoux C |title=[Wegener's granulomatosis and microscopic polyangiitis] |language=French |journal=Rev Prat |volume=58 |issue=5 |pages=522–32 |date=March 2008 |pmid=18524109 |doi= |url=}}</ref>
|
* Middle age male
|
* Constitutional symptoms
* [[Dyspnea]]
* [[Purpura]]
* [[Arthralgia|Arthralgias]]
* Neurologic dysfunction
* [[Rhinosinusitis|Sinusitis]]
* [[Otitis media]]
* [[Epistaxis]].
|<nowiki>+</nowiki>
| +
| +
| +
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
| -
|
|
* Thick [[glomerular basement membrane]]
* [[ANCA]]
|
|
* Sub-[[Epithelial cells|epithelial]] [[immune complex]] depositis with 'spike and dome' appearance
* [[Necrotizing]] and [[Crescentic glomerulonephritis|crescentic]] glomerulonephritis
|<nowiki>-</nowiki>
|-
| rowspan="7" align="center" style="background:#4479BA; color: #FFFFFF;" + |Proliferative
![[IgA nephropathy]]
|
|
* [[Idiopathic]]
* Subendothelial [[edema]]
* [[Viral infections]]  
 
* Microthrombosis
* [[Degranulation]] of [[neutrophils]]
|
|
* Young children
* Pauci-immune GN
* History of [[mucosal]] [[infections]] (e.g. [[gastroenteritis]]) and [[upper respiratory tract infection]]
|-
* 2-3 days after [[infection]] (synpharyngitic)
! colspan="1" |[[Microscopic polyangiitis|Microscopic Polyangiitis]]<ref name="pmid20688249">{{cite journal |vauthors=Chung SA, Seo P |title=Microscopic polyangiitis |journal=Rheum. Dis. Clin. North Am. |volume=36 |issue=3 |pages=545–58 |date=August 2010 |pmid=20688249 |pmc=2917831 |doi=10.1016/j.rdc.2010.04.003 |url=}}</ref>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|
* Constitutional symptoms
* [[Dyspnea]]
* [[Purpura]]
* [[Arthralgia|Arthralgias]]
* Neurologic dysfunction
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
| +
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+/-</nowiki>
| -
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
| +
|
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| +
|
|
* Crescent formation
* [[P-ANCA]]
|
|
* [[Mesangial cell|Mesangial]] proliferation
* Hypercellular and [[inflamed]] [[glomeruli]] (Crescent formation)
|<nowiki>-</nowiki>
|-
! rowspan="5" |[[Rapidly progressive glomerulonephritis]]
|
|
* [[Goodpasture syndrome]]
* Hypercellular and [[inflamed]] [[glomeruli]] (Crescent formation)
|
|
* Young adults
* Pauci-immune GN
|-
! colspan="1" |[[Eosinophilic granulomatosis with polyangiitis|Churg-Strauss Syndrome]]<ref name="pmid16632015">{{cite journal |vauthors=Sinico RA, Di Toma L, Maggiore U, Tosoni C, Bottero P, Sabadini E, Giammarresi G, Tumiati B, Gregorini G, Pesci A, Monti S, Balestrieri G, Garini G, Vecchio F, Buzio C |title=Renal involvement in Churg-Strauss syndrome |journal=Am. J. Kidney Dis. |volume=47 |issue=5 |pages=770–9 |date=May 2006 |pmid=16632015 |doi=10.1053/j.ajkd.2006.01.026 |url=}}</ref>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|
*  [[Asthma]]
* [[Rhinosinusitis|Sinusitis]]
* [[Myalgia]] 
* [[Arthralgia]]
* [[Purpura]]
* [[Cardiac arrhythmia|Arrythmias]]
* [[Peripheral neuropathy]]
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
| +
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</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>
* Hypercellular and [[inflamed]] [[glomeruli]] (Crescent formation)
|
|
* Hypercellular and [[inflamed]] [[glomeruli]] (Crescent formation)
* Hypercellular and [[inflamed]] [[glomeruli]] (Crescent formation)
|
|
*  Diffuse thickening of the [[glomerular basement membrane]] with absence of sub-[[Epithelial cells|epithelial]] and sub-[[endothelial]] deposits 
* Pauci-immune GN
|<nowiki>+ (Linear)</nowiki>
|-
|-
! colspan="2" |[[Membranoproliferative glomerulonephritis|Membranoproliferative Glomerulonephritis]]<ref name="pmid19908070">{{cite journal |vauthors=Alchi B, Jayne D |title=Membranoproliferative glomerulonephritis |journal=Pediatr. Nephrol. |volume=25 |issue=8 |pages=1409–18 |date=August 2010 |pmid=19908070 |pmc=2887509 |doi=10.1007/s00467-009-1322-7 |url=}}</ref><ref name="pmid657595">{{cite journal |vauthors=Davis AE, Schneeberger EE, Grupe WE, McCluskey RT |title=Membranoproliferative glomerulonephritis (MPGN type I) and dense deposit disease (DDD) in children |journal=Clin. Nephrol. |volume=9 |issue=5 |pages=184–93 |date=May 1978 |pmid=657595 |doi= |url=}}</ref>
|
|
* [[Poststreptococcal glomerulonephritis|Post infectious glomerulonephritis]]
* [[Idiopathic]]
* [[Hepatitis B]] and [[Hepatitis C|C]] (Type 1)
* C3 nepritic factor (Type2)
|
|
* [[Streptococcal infections|Streptococcal]] [[skin]] [[infections]]  
* [[Hematuria]]
* [[Streptococcus|Streptococcal]] [[pharyngitis]]
* [[Oliguria]]
* 2-3 weeks after [[infection]]
* [[Periorbital edema]]
|<nowiki>+/-</nowiki>
* [[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>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|
|
* Hypercellular and [[inflamed]] [[glomeruli]]
* Thick [[glomerular basement membrane]] (Tram-track appearance)
|
* [[Mesangial cell|Mesangial]] proliferation
* [[Leukocytes|Leukocyte]] infiltration
|
|
* Sub-[[epithelial]] [[immune complex]] deposits
* Immune complex GN
| + (Granular)
* Granular deposite
|-
|-
! colspan="2" |[[Henoch-Schönlein purpura]] <ref name="pmid8023818">{{cite journal |vauthors=Jennette JC, Falk RJ |title=The pathology of vasculitis involving the kidney |journal=Am. J. Kidney Dis. |volume=24 |issue=1 |pages=130–41 |date=July 1994 |pmid=8023818 |doi= |url=}}</ref>
|
|
* [[Granulomatosis with polyangiitis|Granulomatosis with polyangitis]] ([[Wegener's granulomatosis|Wegner's granulomatosis]])
* Most common in young male, following [[Upper respiratory tract|upper respiratory]] infections
|
|
* [[Necrotizing]] [[granulomas]] ([[Nasopharynx]], [[lungs]], [[kidneys]])
* '''Skin manifestations-''' Palpable [[purpura]] on buttocks
* [[Conjunctivitis]]
* '''Gastrointestinal''' '''manifestations-'''
* Ulceration of the [[cornea]]
** [[Abdominal pain]]
* [[Episcleritis]]
** [[Melena]]
* [[Peripheral neuropathy]]
** [[Dysentery|Bloody diarrhea]]
|<nowiki>+/-</nowiki>
** [[Hematemesis]]
* '''Joints'''  '''manifestations-'''
** [[Arthralgia]]
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
| +
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| -
|
* Diffuse mesangial IgA deposits often associated with mesangial hypercellularity
|
* Diffuse mesangial IgA deposits often associated with mesangial hypercellularity
|
* Immune complex GN, granular deposite
|-
! colspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Disease
! align="center" style="background:#4479BA; color: #FFFFFF;" + |History
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Systemic symptoms
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hemeturia
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Proteinuria
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hypertension
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Pitting edema
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Oliguria
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephrotic features
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephritic features
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hyperlipidemia and hypercholesterolemia
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Auto-antibodies,
Complements
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Light microscope
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Electron microscope
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Immunoflourescence pattern
|-
! colspan="2" |[[Cryoglobulinemia]]<ref name="pmid26802335">{{cite journal |vauthors=Fogo AB, Lusco MA, Najafian B, Alpers CE |title=AJKD Atlas of Renal Pathology: Cryoglobulinemic Glomerulonephritis |journal=Am. J. Kidney Dis. |volume=67 |issue=2 |pages=e5–7 |date=February 2016 |pmid=26802335 |doi=10.1053/j.ajkd.2015.12.007 |url=}}</ref>
|Patients having cryoglobulinemia may have positive history of:
* [[Hepatitis C|Hepatitis C infection]]
* [[Hepatitis B|Hepatitis B infection]]
* Leg ulcers
* Recurrent [[thrombosis]]
|'''Pulmonary symptoms:'''
* [[Difficulty breathing]]
* Cough
'''Cutaneous symptoms:'''
* [[Purpura]] 
* [[Skin ulcer]]
'''Gastrointestinal symptoms:'''
* Abdominal pain
'''General symptoms:'''
* Fever
* [[Arthralgia]],
* [[Myalgia]]
* [[Fatigue]]
* [[Blurred vision|Blurring]]/loss of vision
* [[Diplopia]]
* [[Confusion]]
|<nowiki>+/-</nowiki>
| +
|<nowiki>+/-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|
* [[Membranoproliferative glomerulonephritis]]
|
* [[Mesangial cell|Mesangial]] and subendothelial deposits
|
* Prominent [[IgM]] and C3
|-
! rowspan="9" align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephrotic Syndrome
! colspan="2" |[[Minimal change disease|Minimal Change Disease]]<ref name="pmid17195422">{{cite journal |vauthors=Saha TC, Singh H |title=Minimal change disease: a review |journal=South. Med. J. |volume=99 |issue=11 |pages=1264–70 |date=November 2006 |pmid=17195422 |doi=10.1097/01.smj.0000243183.87381.c2 |url=}}</ref><ref name="pmid27092244">{{cite journal |vauthors=Saleem MA, Kobayashi Y |title=Cell biology and genetics of minimal change disease |journal=F1000Res |volume=5 |issue= |pages= |date=2016 |pmid=27092244 |pmc=4821284 |doi=10.12688/f1000research.7300.1 |url=}}</ref>
| colspan="2" |
* Young children
* Recent [[infection]] and [[immunization]]
* [[Atopy]]
* [[Hodgkin's lymphoma|Hodgkin lymphoma]]
* [[Thrombosis]] (due to [[Urinary system|urinary]] loss of [[Antithrombin III|antithrombin-III]])
| -
| +
| -
| +
| +/-
| +
| -
| +
|
|
* Normal
|
* Foot process [[effacement]]
* Fusion of [[podocytes]]
|
* Often unremarkable
* Few cases stain positively for [[IgM]] antibodies and C3.
|-
! colspan="2" |[[Focal segmental glomerulosclerosis|Focal Segmental Glomerulosclerosis]]<ref name="pmid28242845">{{cite journal |vauthors=Rosenberg AZ, Kopp JB |title=Focal Segmental Glomerulosclerosis |journal=Clin J Am Soc Nephrol |volume=12 |issue=3 |pages=502–517 |date=March 2017 |pmid=28242845 |pmc=5338705 |doi=10.2215/CJN.05960616 |url=}}</ref><ref name="pmid25168829">{{cite journal |vauthors=Jefferson JA, Shankland SJ |title=The pathogenesis of focal segmental glomerulosclerosis |journal=Adv Chronic Kidney Dis |volume=21 |issue=5 |pages=408–16 |date=September 2014 |pmid=25168829 |pmc=4149756 |doi=10.1053/j.ackd.2014.05.009 |url=}}</ref><ref name="pmid2429634">{{cite journal |vauthors=Gephardt GN, Tubbs RR, Popowniak KL, McMahon JT |title=Focal and segmental glomerulosclerosis. Immunohistologic study of 20 renal biopsy specimens |journal=Arch. Pathol. Lab. Med. |volume=110 |issue=10 |pages=902–5 |date=October 1986 |pmid=2429634 |doi= |url=}}</ref>
| colspan="2" |
* Idiopathic
* [[Human Immunodeficiency Virus (HIV)|HIV]]
* [[Heroine hydrochloride|Heroine]] use
* [[Sickle-cell disease|Sickle cell disease]]
* [[Interferon]]
* Severe [[obesity]]
* [[Cryoglobulinemia|Mixed cryoglobulinemia]] ([[Hepatitis C]])
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| +
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
| + ([[C-ANCA]])
|<nowiki>+/-</nowiki>
| +
|<nowiki>-</nowiki>
| +
|
|
* Focal (some [[glomeruli]]) and segmental (only part of [[glomerulus]])
|
* Effacement of [[podocytes]]
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|-
! colspan="2" |[[Membranous glomerulonephritis|Membranous Glomerulonephritis]]<ref name="pmid25558821">{{cite journal |vauthors=Lai WL, Yeh TH, Chen PM, Chan CK, Chiang WC, Chen YM, Wu KD, Tsai TJ |title=Membranous nephropathy: a review on the pathogenesis, diagnosis, and treatment |journal=J. Formos. Med. Assoc. |volume=114 |issue=2 |pages=102–11 |date=February 2015 |pmid=25558821 |doi=10.1016/j.jfma.2014.11.002 |url=}}</ref><ref name="pmid10495797">{{cite journal |vauthors=Wasserstein AG |title=Membranous glomerulonephritis |journal=J. Am. Soc. Nephrol. |volume=8 |issue=4 |pages=664–74 |date=April 1997 |pmid=10495797 |doi= |url=}}</ref>
| colspan="2" |
* [[Idiopathic]]
* [[Hepatitis B]] and [[Hepatitis C|C]]
* [[Solid tumors]]
* [[Systemic lupus erythematosus]]
* Drugs ([[NSAIDS]], pencilamine, [[gold]], [[captopril]])
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|
| +
* Hypercellular and [[inflamed]] [[glomeruli]] (Crescent formation)
|<nowiki>-</nowiki>
|<nowiki>-  (pauci-immune)</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|-
| +
|<nowiki>-</nowiki>
| +
|Immune complex deposition
|
|
* [[Churg-Strauss syndrome|Churg Strauss syndrome]]
* Thick [[glomerular basement membrane]]
|
|
* [[Necrotizing]] [[granulomas]] ([[Lungs]] and [[kidneys]])
* Sub-[[Epithelial cells|epithelial]] [[immune complex]] depositis with 'spike and dome' appearance
* [[Asthma]]
|Immune complex GN, granular deposite
* [[Peripheral neuropathy]]
|-
|<nowiki>+/-</nowiki>
! colspan="2" |[[Diabetic nephropathy|Diabetic Nephropathy]]<ref name="pmid11978659">{{cite journal| author=Drummond K, Mauer M, International Diabetic Nephropathy Study Group| title=The early natural history of nephropathy in type 1 diabetes: II. Early renal structural changes in type 1 diabetes. | journal=Diabetes | year= 2002 | volume= 51 | issue= 5 |pages= 1580-7 | pmid=11978659 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11978659  }}</ref><ref name="pmid3699305">{{cite journal| author=Hørlyck A, Gundersen HJ, Osterby R| title=The cortical distribution pattern of diabetic glomerulopathy. | journal=Diabetologia | year= 1986 | volume= 29| issue= 3 | pages= 146-50 | pmid=3699305 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3699305  }}</ref><ref name="pmid21422926">{{cite journal| author=Alpers CE, Hudkins KL| title=Mouse models of diabetic nephropathy. | journal=Curr Opin Nephrol Hypertens | year= 2011 | volume= 20 | issue= 3 |pages= 278-84 | pmid=21422926 | doi=10.1097/MNH.0b013e3283451901 | pmc=PMC3658822 |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21422926  }}</ref><ref name="pmid19970254">{{cite journal| author=Kimmelstiel P, Wilson C| title=Intercapillary Lesions in the Glomeruli of the Kidney. | journal=Am J Pathol | year= 1936 | volume= 12 | issue= 1 |pages= 83-98.7 | pmid=19970254 | doi= | pmc=PMC1911022 |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19970254  }}</ref><ref name="pmid2766585">{{cite journal| author=Alpers CE, Biava CG| title=Idiopathic lobular glomerulonephritis (nodular mesangial sclerosis): a distinct diagnostic entity. | journal=Clin Nephrol | year= 1989 | volume= 32 | issue= 2 | pages= 68-74 | pmid=2766585 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2766585  }}</ref><ref name="pmid17536064">{{cite journal| author=Toyoda M, Najafian B, Kim Y, Caramori ML, Mauer M| title=Podocyte detachment and reduced glomerular capillary endothelial fenestration in human type 1 diabetic nephropathy. | journal=Diabetes | year= 2007 | volume= 56 | issue= 8 | pages= 2155-60 |pmid=17536064 | doi=10.2337/db07-0019 | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17536064  }}</ref><ref name="pmid16565248">{{cite journal| author=Najafian B, Crosson JT, Kim Y, Mauer M| title=Glomerulotubular junction abnormalities are associated with proteinuria in type 1 diabetes. | journal=J Am Soc Nephrol | year= 2006 | volume= 17 | issue= 4 Suppl 2 | pages= S53-60| pmid=16565248 | doi=10.1681/ASN.2005121342 | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16565248  }}</ref><ref name="pmid12660325">{{cite journal| author=Najafian B, Kim Y, Crosson JT, Mauer M| title=Atubular glomeruli and glomerulotubular junction abnormalities in diabetic nephropathy. | journal=J Am Soc Nephrol | year= 2003 | volume= 14 | issue= 4 | pages= 908-17 | pmid=12660325 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12660325  }}</ref><ref name="pmid21659756">{{cite journal| author=Najafian B, Alpers CE, Fogo AB| title=Pathology of human diabetic nephropathy. |journal=Contrib Nephrol | year= 2011 | volume= 170 | issue=  | pages= 36-47 | pmid=21659756 |doi=10.1159/000324942 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21659756  }}</ref><ref name="pmid216597562">{{cite journal| author=Najafian B, Alpers CE, Fogo AB| title=Pathology of human diabetic nephropathy. |journal=Contrib Nephrol | year= 2011 | volume= 170 | issue=  | pages= 36-47 | pmid=21659756 |doi=10.1159/000324942 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21659756  }}</ref>
|<nowiki>+</nowiki>
| colspan="2" |'''''For more information on diabetes [[Diabetes mellitus|click here]]'''.''
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| +
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+/-</nowiki>
| +
|<nowiki>-</nowiki>
| +
|
|
* Diffuse [[Mesangial cell|mesangial]] matrix expansion (nodular glomerulosclerosis)
* Increased [[Mesangial cell|mesangial]] hypercellularity
* Prominent glomerular basement membranes
* Thick [[basement membrane]] without any deposit
|
|
+ ([[C-ANCA]])
* Nodular glomerulosclerosis
| -
|-
! colspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Disease
! align="center" style="background:#4479BA; color: #FFFFFF;" + |History
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Systemic symptoms
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hemeturia
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Proteinuria
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hypertension
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Pitting edema
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Oliguria
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephrotic features
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephritic features
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hyperlipidemia and hypercholesterolemia
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Auto-antibodies,
Complements
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Light microscope
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Electron microscope
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Immunoflourescence pattern
|-
! rowspan="4" | [[Glomerular deposition disease|Glomerular Deposition Diseases]] 
![[Light chain nephropathy|Light Chain Deposition Disease]]<ref name="pmid21511832">{{cite journal |vauthors=Hutchison CA, Cockwell P, Stringer S, Bradwell A, Cook M, Gertz MA, Dispenzieri A, Winters JL, Kumar S, Rajkumar SV, Kyle RA, Leung N |title=Early reduction of serum-free light chains associates with renal recovery in myeloma kidney |journal=J. Am. Soc. Nephrol. |volume=22 |issue=6 |pages=1129–36 |date=June 2011 |pmid=21511832 |pmc=3103732 |doi=10.1681/ASN.2010080857 |url=}}</ref>
|
* Occurs in the setting of high tumor burden
| -
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| +
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+/-</nowiki>
| +
|<nowiki>-</nowiki>
| +
| -
|
* Light-chain deposits
|
* Granular deposits on electron microscopy
|
|
* Hypercellular and [[inflamed]] [[glomeruli]] (Crescent formation)
* Detection of light chain deposits using anti–light chain antibody
|<nowiki>- (pauci-immune)</nowiki>
|<nowiki>-</nowiki>
|-
|-
![[Amyloidosis|Renal Amyloidosis]]<ref name="pmid23227278">{{cite journal |vauthors=Baker KR, Rice L |title=The amyloidoses: clinical features, diagnosis and treatment |journal=Methodist Debakey Cardiovasc J |volume=8 |issue=3 |pages=3–7 |date=2012 |pmid=23227278 |pmc=3487569 |doi= |url=}}</ref><ref name="pmid23979488">{{cite journal |vauthors=Gillmore JD, Hawkins PN |title=Pathophysiology and treatment of systemic amyloidosis |journal=Nat Rev Nephrol |volume=9 |issue=10 |pages=574–86 |date=October 2013 |pmid=23979488 |doi=10.1038/nrneph.2013.171 |url=}}</ref><ref name="pmid26155101">{{cite journal |vauthors=Jerzykowska S, Cymerys M, Gil LA, Balcerzak A, Pupek-Musialik D, Komarnicki MA |title=Primary systemic amyloidosis as a real diagnostic challenge - case study |journal=Cent Eur J Immunol |volume=39 |issue=1 |pages=61–6 |date=2014 |pmid=26155101 |pmc=4439975 |doi=10.5114/ceji.2014.42126 |url=}}</ref><ref name="pmid16409147">{{cite journal |vauthors=Pepys MB |title=Amyloidosis |journal=Annu. Rev. Med. |volume=57 |issue= |pages=223–41 |date=2006 |pmid=16409147 |doi=10.1146/annurev.med.57.121304.131243 |url=}}</ref>
|
|
* [[Microscopic polyangiitis]]
* For the secondary causes of amloidosis:
* [[Tuberculosis]]
* [[Familial mediterranean fever|Familial Mediterranean fever]]
* [[Rheumatoid arthritis]]
* [[Multiple myeloma]]  
|
|
* [[Necrotizing]] [[vasculitis]] (no [[granuloma]])
* [[Dyspnea]]
* [[Lethargy]]
* Weight loss
 
* [[Hemorrhagic diathesis|Bleeding tendency]]
|<nowiki>-</nowiki>
| +
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+</nowiki>
| +
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| +
| -
|
* Diffuse glomerular deposition of amorphous hyaline material (nodular pattern), in mesangium (weakly staining with periodic acid-Schiff (PAS)
|
* Nodular deposit
|
* AA amyloidosis type: negative for immunoglobulins and complement
* AL amyloidosis type: Positive for lambda or kappa light chains
|-
!Fibrillary-Immunotactoid Glomerulopathy<ref name="pmid1996564">{{cite journal |vauthors=Korbet SM, Schwartz MM, Lewis EJ |title=Immunotactoid glomerulopathy |journal=Am. J. Kidney Dis. |volume=17 |issue=3 |pages=247–57 |date=March 1991 |pmid=1996564 |doi= |url=}}</ref>
|
* [[Malignancy]]
* [[Monoclonal gammopathy]]
* [[Autoimmunity|Autoimmune]] disease
| -
|<nowiki>+/-</nowiki>
| +
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
| +
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
| -
|
* Diffuse sclerosing glomerulonephritis
* Diffuse proliferative glomerulonephritis
* Membranoproliferative glomerulonephritis
* Mesangioproliferative/sclerosing disease
* Membranous glomerulonephritis
|
* Large fibrillar deposits in the mesangium randomly
* Glomerular capillary walls different from amloidosis
* No staining with Congo red or thioflavine-T or with antibodies to a specific type
|
* Positive for immunoglobulin G (IgG), C3
* [[Light chain|Kappa]] and lambda (ie, polyclonal) light chains
|-
![[Fabry's disease|Fabry's Disease]]<ref name="pmid12068025">{{cite journal |vauthors=Alroy J, Sabnis S, Kopp JB |title=Renal pathology in Fabry disease |journal=J. Am. Soc. Nephrol. |volume=13 Suppl 2 |issue= |pages=S134–8 |date=June 2002 |pmid=12068025 |doi= |url=}}</ref><ref name="pmid9918480">{{cite journal |author=Meikle PJ, Hopwood JJ, Clague AE, Carey WF |title=Prevalence of lysosomal storage disorders |journal=[[JAMA : the Journal of the American Medical Association]] |volume=281 |issue=3 |pages=249–54 |year=1999 |month=January |pmid=9918480 |doi= |url=}}</ref><ref name="pmid11889412">{{cite journal |author=Branton MH, Schiffmann R, Sabnis SG, ''et al.'' |title=Natural history of Fabry renal disease: influence of alpha-galactosidase A activity and genetic mutations on clinical course |journal=[[Medicine]] |volume=81 |issue=2 |pages=122–38 |year=2002 |month=March |pmid=11889412 |doi= |url=}}</ref>
|
* [[Family history]] suggestive of the disorder
|
* [[Anhidrosis]] or decreased sweating
* [[Fatigue (medical)|Fatigue]]
* [[Angiokeratoma|Angiokeratomas]]
* Burning pain of the extremities
* Corneal opacities.
* [[Dysphagia]]
* [[Abdominal pain]]
* [[Steatorrhea]]
* [[Delayed puberty]]
* [[Raynaud's phenomenon]]
* [[Hearing loss]]
* [[Telangiectasis]]
* [[Ataxia]]
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| +
| +
|
+ ([[P-ANCA]])
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+/-</nowiki>
| +
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| +
| -
|
* Vacuolization of visceral glomerular epithelial cells (podocytes) and distal tubular epithelial cells
* Glycolipid accumulation
|
|
* Hypercellular and [[inflamed]] [[glomeruli]] (Crescent formation)
* Myeloid or zebra bodies: Gb3 deposition within enlarged secondary lysosomes as lamellated membrane structures
|<nowiki>- (pauci-immune)</nowiki>
* Inclusions, composed of concentric layers (onion skin appearance)
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|-
|-
![[Membranoproliferative glomerulonephritis]]
! rowspan="4" align="center" style="background:#4479BA; color: #FFFFFF;" + |Basement Membrane Syndrome
! colspan="2" |[[Alport syndrome|Alport's Syndrome]]<ref name="pmid111374282">{{cite journal| author=McCarthy PA, Maino DM| title=Alport syndrome: a review. | journal=Clin Eye Vis Care | year= 2000 | volume= 12 | issue= 3-4 | pages= 139-150 | pmid=11137428 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11137428 }}</ref><ref name="pmid84141532">{{cite journal| author=Chugh KS, Sakhuja V, Agarwal A, Jha V, Joshi K, Datta BN et al.| title=Hereditary nephritis (Alport's syndrome)--clinical profile and inheritance in 28 kindreds. | journal=Nephrol Dial Transplant | year= 1993 | volume= 8 | issue= 8 | pages= 690-5 | pmid=8414153 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8414153 }}</ref><ref name="pmid8414153">{{cite journal| author=Chugh KS, Sakhuja V, Agarwal A, Jha V, Joshi K, Datta BN et al.| title=Hereditary nephritis (Alport's syndrome)--clinical profile and inheritance in 28 kindreds. | journal=Nephrol Dial Transplant | year= 1993 | volume= 8 | issue= 8 | pages= 690-5 | pmid=8414153 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8414153 }}</ref><ref name="pmid11137428">{{cite journal| author=McCarthy PA, Maino DM| title=Alport syndrome: a review. | journal=Clin Eye Vis Care | year= 2000 | volume= 12 | issue= 3-4 | pages= 139-150 | pmid=11137428 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11137428 }}</ref><ref name="pmid7819734">{{cite journal| author=Amari F, Segawa K, Ando F| title=Lens coloboma and Alport-like glomerulonephritis. | journal=Eur J Ophthalmol | year= 1994 | volume= 4 | issue= 3 | pages= 181-3 | pmid=7819734 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7819734 }}</ref><ref name="pmid6871140">{{cite journal| author=Govan JA| title=Ocular manifestations of Alport's syndrome: a hereditary disorder of basement membranes? | journal=Br J Ophthalmol | year= 1983 | volume= 67 | issue= 8 | pages= 493-503 | pmid=6871140 | doi= | pmc=PMC1040106 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6871140 }}</ref>
|
|
* [[Idiopathic]]
* Positive family history
* [[Hepatitis B]] and [[Hepatitis C|C]] (Type 1)
|'''Auditary:'''
* C3 nepritic factor (Type2)
*Early [[Tinnitus]]
|
*[[Vertigo]]
* [[Hematuria]]
*High-frequency progressive bilateral [[Hearing impairment|hearing loss]]
* [[Oliguria]]
 
* [[Periorbital edema]]
'''Occular problems:'''
* [[Hypertension]]
* Refractory Error
|<nowiki>+/-</nowiki>
 
|<nowiki>+</nowiki>
*Arcus
|<nowiki>+</nowiki>
*[[Glaucoma]]
|<nowiki>+</nowiki>
*Band Keratopathy
|<nowiki>+</nowiki>
*[[Lenticonus]]
|<nowiki>+</nowiki>
*[[Weill-Marchesani syndrome|Spherophakia]]
*[[Cataract|Cataracts]]  
|<nowiki>-</nowiki>
| +
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+/-</nowiki>
| +
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| +
| -
|
* Early stage: unremarkable
* Late stages: [[glomerulosclerosis]], [[interstitial fibrosis]], and interstitial [[foam cells]] (due to prolonged [[proteinuria]]).
|
* Within [[glomerular basement membrane]] ([[GBM]]): longitudinal splitting of the lamina densa
|
* Absence of staining of the alpha-3, alpha-4, and alpha-5 (IV) chains in the [[glomerular basement membrane]]
* Minimal binding to a glomerulus in indirect [[immunofluorescence]] microscopy with [[Anti-glomerular basement membrane antibody|anti-glomerular basement membrane]] antibodies
|-
! colspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Disease
! align="center" style="background:#4479BA; color: #FFFFFF;" + |History
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Systemic symptoms
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hemeturia
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Proteinuria
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hypertension
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Pitting edema
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Oliguria
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephrotic features
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephritic features
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hyperlipidemia and hypercholesterolemia
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Auto-antibodies,
Complements
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Light microscope
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Electron microscope
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Immunoflourescence pattern
|-
! colspan="2" |[[Thin basement membrane disease|Thin Basement Membrane Disease]]<ref name="pmid12969134">{{cite journal |author=Savige J, Rana K, Tonna S, Buzza M, Dagher H, Wang YY |title=Thin basement membrane nephropathy |journal=Kidney Int. |volume=64 |issue=4 |pages=1169–78 |year=2003 |month=October |pmid=12969134 |doi=10.1046/j.1523-1755.2003.00234.x}}</ref><ref name="pmid17726307">{{cite journal |author=Hou P, Chen Y, Ding J, Li G, Zhang H |title=A novel mutation of COL4A3 presents a different contribution to Alport syndrome and thin basement membrane nephropathy |journal=Am. J. Nephrol. |volume=27 |issue=5 |pages=538–44 |year=2007 |pmid=17726307 |doi=10.1159/000107666 |url=http://content.karger.com/produktedb/produkte.asp?typ=fulltext&file=000107666}}</ref>
|
* Positive family history
* Gross [[hematuria]] following [[upper respiratory tract infection]]
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| -
| +
| -/+
| -
|<nowiki>-/+</nowiki>
| -
| -/+
| -
| -
| -
|Diffuse thinning of the [[Glomerular basement membrane|glomerular basement membranes]] (GBM)
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|-
! colspan="2" |[[Nail-patella syndrome|Nail-Patella Syndrome]]<ref name="pmid28941488">{{cite journal |vauthors=Najafian B, Smith K, Lusco MA, Alpers CE, Fogo AB |title=AJKD Atlas of Renal Pathology: Nail-Patella Syndrome-Associated Nephropathy |journal=Am. J. Kidney Dis. |volume=70 |issue=4 |pages=e19–e20 |date=October 2017 |pmid=28941488 |doi=10.1053/j.ajkd.2017.08.001 |url=}}</ref><ref name="pmid1960197">{{cite journal |vauthors=Guidera KJ, Satterwhite Y, Ogden JA, Pugh L, Ganey T |title=Nail patella syndrome: a review of 44 orthopaedic patients |journal=J Pediatr Orthop |volume=11 |issue=6 |pages=737–42 |date=1991 |pmid=1960197 |doi= |url=}}</ref>
|
* Positive family history
|
* Poorly developed fingernails, toe nails, and patellae (kneecaps).
* [[Elbow]] deformities
* Abnormally shaped [[pelvis]] bone ([[hip]] bone)
* [[Knee]] may be small, deformed or absent
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
| +
| -
| -
| -
| -
| -
| -
| -
|
|
* Thick [[glomerular basement membrane]] (Tram-track appearance)
* Mostly unremarkable changes
* Secondary FSGS
* Late stages:
 
** Global glomerulosclerosis,
** Tubulointerstitial fibrosis
|
* [[Glomerular basement membrane|Glomerular basement membranes (GBMs)]]: Focal or diffuse irregular thickening with electron-lucent areas (moth-eaten appearance) containing type III collagen bundles.
* Similar collagen fibrils can be seen in mesangial matrix.
* Podocytes: Segmental effacement of foot processes.
|
* [[Immunofluorescence]] studies are typically negative.
 
* Nonspecific [[IgM]] and C3 deposition may be seen in sclerotic glomeruli.
|-
! rowspan="6" align="center" style="background:#4479BA; color: #FFFFFF;" + | Glomerular-Vascular Syndromes 
! colspan="2" |[[Hypertensive nephropathy|Hypertensive Nephrosclerosis]]<ref name="pmid24327566">{{cite journal |vauthors=Hughson MD, Puelles VG, Hoy WE, Douglas-Denton RN, Mott SA, Bertram JF |title=Hypertension, glomerular hypertrophy and nephrosclerosis: the effect of race |journal=Nephrol. Dial. Transplant. |volume=29 |issue=7 |pages=1399–409 |date=July 2014 |pmid=24327566 |pmc=4071048 |doi=10.1093/ndt/gft480 |url=}}</ref>
|Chronic [[hypertension]]
|
* [[Hypertensive retinopathy|Hypertensive retinal]] changes.
 
* High [[jugular venous pressure]]
 
* [[Rales]] from [[pulmonary edema]] on auscultation
* .Signs of [[left ventricular hypertrophy]]
 
* [[Left ventricle|Left ventricular]] heave
* Shifting of apex towards the left
 
* [[S3]] and [[gallop rhythm]]
* Loud S2
 
* [[Ascites]]
 
* [[Paralysis]] from [[stroke]] secondary to [[hypertension]]
 
* Inferior limb [[edema]]
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
| +
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
| -
| +/-
| -
| colspan="3" |
* Interstitial [[fibrosis]] and atrophy
* Medial thickening and intimal fibrosis of medium-sized and larger vessels
* Arteriolar thickening, and hyalinosis
* Chronic stages:
** Global sclerosis
** Focal segmental [[sclerosis]]
|-
! colspan="2" |[[Cholesterol emboli syndrome|Cholesterol Emboli]]<ref name="pmid27012950">{{cite journal |vauthors=Lusco MA, Najafian B, Alpers CE, Fogo AB |title=AJKD Atlas of Renal Pathology: Cholesterol Emboli |journal=Am. J. Kidney Dis. |volume=67 |issue=4 |pages=e23–4 |date=April 2016 |pmid=27012950 |doi=10.1053/j.ajkd.2016.02.034 |url=}}</ref>
|
* Atherosclerotic cardiovascular disease
* Anticoagulation therapy
* Cardiopulmonary resuscitation
* [[Hypertension]]
* [[Aortic aneurysm]]
* [[Hypercholesterolemia]]
* Smoking history
* Male sex
* Age over 55 years
* [[Vascular]] procedures
* Invasive [[angiography]]
* [[Aortic aneurysm]] rupture or surgery
* [[Vascular]] surgery
|
* Depends on the organ involved
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
| +
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
| -
| +/-
| -
|
* Atheroemboli are seen in interlobular and arcuate arteries, as lance-shaped clefts, due to dissolution of [[cholesterol]] crystals
* Acute lesions:
** Atheroemboli are surrounded by red blood cells, fibrin, and leukocytes, with multinucleated giant cell reactions 
* Chronic lesions:
** Cholesterol clefts are surrounded by intimal fibrosis
** Vessel recanalization of chronic lesions can occur.
* Global and segmental sclerosis of glomeruli may be present.
|
* Extensive foot process effacement can be seen
|
* Not specific changes
|-
! colspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Disease
! align="center" style="background:#4479BA; color: #FFFFFF;" + |History
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Systemic symptoms
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hemeturia
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Proteinuria
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hypertension
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Pitting edema
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Oliguria
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephrotic features
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephritic features
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hyperlipidemia and hypercholesterolemia
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Auto-antibodies,
Complements
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Light microscope
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Electron microscope
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Immunoflourescence pattern
|-
! colspan="2" |[[Sickle-cell disease|Sickle Cell Disease]]<ref name="pmid12028473">{{cite journal |vauthors=Wesson DE |title=The initiation and progression of sickle cell nephropathy |journal=Kidney Int. |volume=61 |issue=6 |pages=2277–86 |date=June 2002 |pmid=12028473 |doi=10.1046/j.1523-1755.2002.00363.x |url=}}</ref>
|
* Positive family history
|
* [[Pain and nociception|Pain]] and/or [[bone pain]]
* [[Dactylitis]]
* [[Blurry vision]]
* [[Priapism|Persistent and painful erection]]
* [[Numbness]]
* [[Tingling]]
* Motor skill loss
* [[Aphasia|Speech deficits]]
* [[Gait disturbance]]
* Leg ulceration
* [[Jaundice]]
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
| +/-
| -
| -
| -
| -
| -
| -
| colspan="3" |
* [[Glomerulus|Glomerular]] hypertrophy
* [[Hemosiderin]] deposits
* Focal areas of hemorrhage or necrosis
* Chronic stage: interstitial inflammation, edema, fibrosis, tubular atrophy, and [[papillary]] infarcts
 
* Glomerular enlargement and focal segmental glomerulosclerosis ([[Focal segmental glomerulosclerosis|FSGS]])
|-
! colspan="2" |[[Thrombotic microangiopathies|Thrombotic Microangiopathies]]<ref name="pmid27884283">{{cite journal |vauthors=Lusco MA, Fogo AB, Najafian B, Alpers CE |title=AJKD Atlas of Renal Pathology: Thrombotic Microangiopathy |journal=Am. J. Kidney Dis. |volume=68 |issue=6 |pages=e33–e34 |date=December 2016 |pmid=27884283 |doi=10.1053/j.ajkd.2016.10.006 |url=}}</ref>
| colspan="2" |'''''Click for more information on [[Thrombotic microangiopathies|Thrombotic Microangiopathies]].'''''
| +
|<nowiki>+/-</nowiki>
| +
| +/-
| +/-
| +/-
| -
| -
| -
|
* Acute stage:
** Inravasculr fibrin thrombi
* Chronic stage:
** Endocapillary hypercellularity.
** Intimal proliferation of [[Arteriole|arterioles]]
|
* Swollen glomerular endothelial cells with loss of [[Fenestration|fenestrations]]
* Chronic stage: interposed cells with new [[GBM]] matrix material deposition.
|
* [[Thrombus|Thrombi]] stain positive for [[fibrinogen]]
|-
! colspan="2" |[[Antiphospholipid syndrome|Antiphospholipid Antibody Syndrome]] <ref name="pmid24684307">{{cite journal| author=Jayakody Arachchillage D, Greaves M| title=The chequered history of the antiphospholipid syndrome. | journal=Br J Haematol | year= 2014 | volume= 165 | issue= 5 | pages= 609-17 | pmid=24684307 | doi=10.1111/bjh.12848 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24684307  }}</ref><ref name="pmid246843072">{{cite journal| author=Jayakody Arachchillage D, Greaves M| title=The chequered history of the antiphospholipid syndrome. | journal=Br J Haematol | year= 2014 | volume= 165 | issue= 5 | pages= 609-17 | pmid=24684307 | doi=10.1111/bjh.12848 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24684307  }}</ref><ref name="pmid18714484">{{cite journal| author=Popa A, Voinea L, Pop M, Stana D, Dascalu AM, Alexandrescu C et al.| title=[Primary antiphospholipid syndrome]. | journal=Oftalmologia | year= 2008 | volume= 52 | issue= 1 | pages= 13-7 | pmid=18714484 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18714484  }}</ref>
|
* [[Thrombosis]]
* [[Miscarriage]] 
* History of [[nephropathy]]
* History of [[Hematology|hematologic]] abnormalities
* Nonthrombotic neurologic symptoms, such as [[migraine]] headaches
* [[Pulmonary hypertension]]
|
*Fatigue
*Fever
*Weight loss
 
*[[Venous thrombosis]]
*[[Arterial thrombosis]]
*[[Thrombocytopenia]]
*Recurrent fetal loss     
| +
|<nowiki>+/-</nowiki>
| +
| +/-
| +/-
| +/-
| -
| -
| -
|
* Acute stage:
** Inravasculr fibrin [[Thrombus|thrombi]]
* Chronic stage:
** [[Endocapillary proliferative glomerulonephritis|Endocapillary]] hypercellularity.
** Intimal proliferation of [[Arteriole|arterioles]]
|
* Swollen glomerular endothelial cells with loss of fenestrations
* Chronic stage: interposed cells with new GBM matrix material deposition.
|
|
* [[Mesangial cell|Mesangial]] proliferation and [[Leukocytes|leukocyte]] infiltration
* [[Thrombus|Thrombi]] stain positive for [[fibrinogen]]
|<nowiki>+ (Granular)</nowiki>
|}
|}
<small>
'''Some infectious diseases such as [[HIV]], [[Hepatitis B virus|HBV]], [[Hepatitis C|HCV]], [[syphilis]], [[leprosy]], [[malaria]], and [[schistosomiasis]] may cause glomerular diseases.'''


==Other differentials==
==Other differentials==

Latest revision as of 21:48, 13 February 2019

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mehrian Jafarizade, M.D [2], Syed Hassan A. Kazmi BSc, MD [3]

Overview

The differential diagnosis of minimal change disease must always include other renal etiologies of nephrotic syndrome, such as focal segmental glomerulosclerosis (FSGS) and IgM nephropathy, and causes of peripheral edema and hypoalbuminemia, such as congestive heart failure, liver cirrhosis, and protein-losing enteropathy.

Differential Diagnosis

Minimal change disease should be differentiated from other glomerular diseases. The various types of glomerular diseases may 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. The following table differentiates between various types of glumerular diseases:

Glomerular diseases Disease History and Symtoms Laboratory Findings Pathology
History Systemic symptoms Hemeturia Proteinuria Hypertension Pitting edema Oliguria Nephrotic features Nephritic features Hyperlipidemia and hypercholesterolemia Auto-antibodies,

Complements

Light microscope Electron microscope Immunoflourescence pattern
Acute Nephritic Syndromes Poststreptococcal Glomerulonephritis[1][2][3] +/- + +/- +/- +/- +/- +/- +/-
  • Immune complex GN
  • Granular deposit
Renal disease due to Subacute Bacterial Endocarditis, or cardiac shunt (Atrioventricular)[4][5] +/- + +/- +/- +/- +/- +/- +/-
  • Crescentic GN is the most common pathological features
  • Mesangial deposits,
  • Subendothelial deposits
  • Subepithelial "humps," in minority of cases
  • Pauci-immune GN
Lupus Nephritis[6]
  • History of SLE features
+/- + +/- +/- +/- +/- +/- +/-
  • Differs based on the disease classification
  • Differs based on the disease classification
  • Differs based on the disease classification, mostly immune complex GN
  • Granular deposit
Antiglomerular Basement Membrane Disease (Goodpasture's syndrome)[7][8]
  • Young adults
+ + + + + + - - Diffuse thickening of the glomerular basement membrane with absence of sub-epithelial and sub-endothelial deposits 
  • Immune complex GN
  • Linear deposit
IgA Nephropathy[9][10] + +/- + +/- + - + -
  • Immune complex deposition
  • Crescent formation
  • Immune complex GN, granular deposite
Disease History Systemic symptoms Hemeturia Proteinuria Hypertension Pitting edema Oliguria Nephrotic features Nephritic features Hyperlipidemia and hypercholesterolemia Auto-antibodies,

Complements

Light microscope Electron microscope Immunoflourescence pattern
ANCA Small-Vessel Vasculitis[11][12] Granulomatosis with Polyangiitis (Wegener's)[13][14][15]
  • Middle age male
+ + + +/- + - + -
  •  Pauci-immune GN
Microscopic Polyangiitis[16] +/- + + + + + + -
  •  Pauci-immune GN
Churg-Strauss Syndrome[17] +/- + + + + + + -
  •  Pauci-immune GN
Membranoproliferative Glomerulonephritis[18][19] + + + +/- + + - - -
  • Immune complex GN
  • Granular deposite
Henoch-Schönlein purpura [20] + + + +/- + + - - -
  • Diffuse mesangial IgA deposits often associated with mesangial hypercellularity
  • Diffuse mesangial IgA deposits often associated with mesangial hypercellularity
  • Immune complex GN, granular deposite
Disease History Systemic symptoms Hemeturia Proteinuria Hypertension Pitting edema Oliguria Nephrotic features Nephritic features Hyperlipidemia and hypercholesterolemia Auto-antibodies,

Complements

Light microscope Electron microscope Immunoflourescence pattern
Cryoglobulinemia[21] Patients having cryoglobulinemia may have positive history of: Pulmonary symptoms:
  • Cough

Cutaneous symptoms:

Gastrointestinal symptoms:

  • Abdominal pain

General symptoms:

+/- + +/- + +/- +/- +/- +/- +/-
  • Prominent IgM and C3
Nephrotic Syndrome Minimal Change Disease[22][23] - + - + +/- + - +
  • Normal
  • Often unremarkable
  • Few cases stain positively for IgM antibodies and C3.
Focal Segmental Glomerulosclerosis[24][25][26] - + - + +/- + - + -
Membranous Glomerulonephritis[27][28] - + - + +/- + - + Immune complex deposition Immune complex GN, granular deposite
Diabetic Nephropathy[29][30][31][32][33][34][35][36][37][38] For more information on diabetes click here. - + - + +/- + - +
  • Diffuse mesangial matrix expansion (nodular glomerulosclerosis)
  • Increased mesangial hypercellularity
  • Prominent glomerular basement membranes
  • Thick basement membrane without any deposit
  • Nodular glomerulosclerosis
-
Disease History Systemic symptoms Hemeturia Proteinuria Hypertension Pitting edema Oliguria Nephrotic features Nephritic features Hyperlipidemia and hypercholesterolemia Auto-antibodies,

Complements

Light microscope Electron microscope Immunoflourescence pattern
 Glomerular Deposition Diseases  Light Chain Deposition Disease[39]
  • Occurs in the setting of high tumor burden
- - + - + +/- + - + -
  • Light-chain deposits
  • Granular deposits on electron microscopy
  • Detection of light chain deposits using anti–light chain antibody
Renal Amyloidosis[40][41][42][43] - + - + +/- + - + -
  • Diffuse glomerular deposition of amorphous hyaline material (nodular pattern), in mesangium (weakly staining with periodic acid-Schiff (PAS)
  • Nodular deposit
  • AA amyloidosis type: negative for immunoglobulins and complement
  • AL amyloidosis type: Positive for lambda or kappa light chains
Fibrillary-Immunotactoid Glomerulopathy[44] - +/- + +/- +/- +/- + +/- +/- -
  • Diffuse sclerosing glomerulonephritis
  • Diffuse proliferative glomerulonephritis
  • Membranoproliferative glomerulonephritis
  • Mesangioproliferative/sclerosing disease
  • Membranous glomerulonephritis
  • Large fibrillar deposits in the mesangium randomly
  • Glomerular capillary walls different from amloidosis
  • No staining with Congo red or thioflavine-T or with antibodies to a specific type
  • Positive for immunoglobulin G (IgG), C3
  • Kappa and lambda (ie, polyclonal) light chains
Fabry's Disease[45][46][47] - + - + +/- + - + -
  • Vacuolization of visceral glomerular epithelial cells (podocytes) and distal tubular epithelial cells
  • Glycolipid accumulation
  • Myeloid or zebra bodies: Gb3 deposition within enlarged secondary lysosomes as lamellated membrane structures
  • Inclusions, composed of concentric layers (onion skin appearance)
-
Basement Membrane Syndrome Alport's Syndrome[48][49][50][51][52][53]
  • Positive family history
Auditary:

Occular problems:

  • Refractory Error
- + - + +/- + - + -
  • Early stage: unremarkable
Disease History Systemic symptoms Hemeturia Proteinuria Hypertension Pitting edema Oliguria Nephrotic features Nephritic features Hyperlipidemia and hypercholesterolemia Auto-antibodies,

Complements

Light microscope Electron microscope Immunoflourescence pattern
Thin Basement Membrane Disease[54][55]
  • Positive family history
- - + -/+ - -/+ - -/+ - - - Diffuse thinning of the glomerular basement membranes (GBM) -
Nail-Patella Syndrome[56][57]
  • Positive family history
  • Poorly developed fingernails, toe nails, and patellae (kneecaps).
  • Elbow deformities
  • Abnormally shaped pelvis bone (hip bone)
  • Knee may be small, deformed or absent
+ + - - - - - - -
  • Mostly unremarkable changes
  • Secondary FSGS
  • Late stages:
    • Global glomerulosclerosis,
    • Tubulointerstitial fibrosis
  • Glomerular basement membranes (GBMs): Focal or diffuse irregular thickening with electron-lucent areas (moth-eaten appearance) containing type III collagen bundles.
  • Similar collagen fibrils can be seen in mesangial matrix.
  • Podocytes: Segmental effacement of foot processes.
  • Nonspecific IgM and C3 deposition may be seen in sclerotic glomeruli.
 Glomerular-Vascular Syndromes  Hypertensive Nephrosclerosis[58] Chronic hypertension +/- +/- + +/- +/- +/- - +/- -
  • Interstitial fibrosis and atrophy
  • Medial thickening and intimal fibrosis of medium-sized and larger vessels
  • Arteriolar thickening, and hyalinosis
  • Chronic stages:
Cholesterol Emboli[59]
  • Depends on the organ involved
+/- +/- + +/- +/- +/- - +/- -
  • Atheroemboli are seen in interlobular and arcuate arteries, as lance-shaped clefts, due to dissolution of cholesterol crystals
  • Acute lesions:
    • Atheroemboli are surrounded by red blood cells, fibrin, and leukocytes, with multinucleated giant cell reactions
  • Chronic lesions:
    • Cholesterol clefts are surrounded by intimal fibrosis
    • Vessel recanalization of chronic lesions can occur.
  • Global and segmental sclerosis of glomeruli may be present.
  • Extensive foot process effacement can be seen
  • Not specific changes
Disease History Systemic symptoms Hemeturia Proteinuria Hypertension Pitting edema Oliguria Nephrotic features Nephritic features Hyperlipidemia and hypercholesterolemia Auto-antibodies,

Complements

Light microscope Electron microscope Immunoflourescence pattern
Sickle Cell Disease[60]
  • Positive family history
+/- +/- +/- - - - - - -
  • Glomerular hypertrophy
  • Hemosiderin deposits
  • Focal areas of hemorrhage or necrosis
  • Chronic stage: interstitial inflammation, edema, fibrosis, tubular atrophy, and papillary infarcts
  • Glomerular enlargement and focal segmental glomerulosclerosis (FSGS)
Thrombotic Microangiopathies[61] Click for more information on Thrombotic Microangiopathies. + +/- + +/- +/- +/- - - -
  • Acute stage:
    • Inravasculr fibrin thrombi
  • Chronic stage:
    • Endocapillary hypercellularity.
    • Intimal proliferation of arterioles
  • Swollen glomerular endothelial cells with loss of fenestrations
  • Chronic stage: interposed cells with new GBM matrix material deposition.
Antiphospholipid Antibody Syndrome [62][63][64]
  • Fatigue
  • Fever
  • Weight loss
+ +/- + +/- +/- +/- - - -
  • Swollen glomerular endothelial cells with loss of fenestrations
  • Chronic stage: interposed cells with new GBM matrix material deposition.


Some infectious diseases such as HIV, HBV, HCV, syphilis, leprosy, malaria, and schistosomiasis may cause glomerular diseases.

Other differentials

References

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