Goodpasture syndrome differential diagnosis

Revision as of 21:55, 29 July 2020 by WikiBot (talk | contribs) (Bot: Removing from Primary care)
(diff) ← Older revision | Latest revision (diff) | Newer revision → (diff)
Jump to navigation Jump to search


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Ali Poyan Mehr, M.D. [2], Associate Editor(s)-in-Chief: Mehrian Jafarizade, M.D [3]

Overview

Goodpasture syndrome should be differentiated from other diseases presenting as fever, hematuria and hemoptysis. It should also be differentiated from other causes of small vessel vasculitis.

Differential Diagnosis

Goodpasture syndrome should be differentiated from other diseases presenting as fever, hematuria, hemoptysis. It should also be differentiated from other causes of small vessel vasculitis. The differentials include the following:

Diseases Clinical manifestations Para-clinical findings Gold standard Additional findings
Symptoms Physical examination
Lab Findings Imaging Histopathology
Headache Fever Weight loss Arthralgia Claudication Bruit HTN Focal neurological disorder Biomarker CBC ESR Other CT scan Angiography Ultrasound/ Echocardiography Other
Goodpasture syndrome or Anti-glomerular basement membrane disease[1] + +/- - - - - + - Anti-GBM antibodies Hypochromic microcytic anemia, Thrombocytopenia - ↓C3 level Pulmonary hemorrhage - Normal kidneys Alveolar infiltrates spreading from the hilum in CXR Cellular crescents in the glomeruli, Intra-alveolar hemorrhages Anti-GBM antibodies Hemoptysis, Hematuria
Small-Vessel Vasculitis ANCA-associated vasculitis Granulomatosis with polyangiitis (Wegener’s)[2] + +/- +/- - - - - + Anti-PR3 antibody (C-ANCA) (90%), Anti-MPO antibody (P-ANCA) (10%) Leukocytosis, Normochromic normocytic anemia ↑ ↑Cr or BUN, Hypoalbuminemia Consolidation, Patchy or diffuse ground-glass opacities Occlusion or stenosis of LAD and RCA in coronary angiography - Single or multiple nodules and masses with cavitation in CXR Parenchymal necrosis, Granulomatous inflammation Histological confirmation Conjunctivitis,

Episcleritis,

Uveitis,

Optic nerve vasculitis

Immune complex small-vessel vasculitis Cryoglobulinemic vasculitis[3] +/- +/- - + +/- - - - C4 component Leukocytosis, Anemia ↑ ANA, hypocomplementemia R/O underlying malignancy Stenosis or occlusions of the visceral arteries Bacterial endocarditis in echocardiography Interstitial involvement or pleural effusions in CXR HCV-associated proteins in vasculitic skin, Intraluminal cryoglobulin deposits  Histological confirmation Acrocyanosis, Retinal hemorrhage, Purpura
Hepatitis C virus-associated cryoglobulinemic vasculitis[4] +/- +/- + + - - + +/- HCV RNA, Cryoglobulins Leukocytosis, Anemia ↑ ↓Serum C4, Positive RF Increased hepatic echogenicity - Hepatomegaly, Splenomegaly Increased hepatic echogenicity in MRI Vasculitic skin, Antigen infilteration in lesions HCV RNA, Histological confirmation Palpable purpura, Microscopic hematuria
Gastrointestinal disease Acute mesenteric ischemia[5] - +/- - - - - - - I-FABP, Alpha-GST, Ischemia-modified albumin (IMA) Leukocytosis, ↑HCT -  ↑Amylase Bowel wall thickening, Intestinal pneumatosis, Portomesenteric thrombosis Mesenteric venous thrombosis  Arterial stenosis or occlusion of the celiac or superior mesenteric arteries in duplex ultrasound Ileus with distended loops of bowel, Bowel wall thickening in abdominal X-ray Superficial mucosal hemorrhage, edema and necrosis History and physical examination Abdominal pain, Distension, Absent bowel sounds
Cardiovascular disease Infective Endocarditis[6] + + + - - - - + NT-proBNP Normochromic-normocytic anemia ↑ Hyperglobulinemia, Cryoglobulinemia Metastatic infections, such as splenic infarct, renal infarcts, or psoas abscess - Vegetation, abscess, or new dehiscence of a prosthetic valvein echocardiography Vertebral osteomyelitis in MRI Vegetation or intracardiac abscess demonstrating active endocarditis Echocardiography (TTE) Janeway lesions, Osler nodes, Roth spots, Vertebral osteomyelitis
Pulmonary disease Non-Small Cell Lung Cancer[7] - +/- + - - - - +/- EGFR, ROS1, EML4-ALK,  PD-L1 Leukocytosis, Anemia ↑ Hypercalcemia, Hyponatremia Pulmonary lesion or mass - Pulmonary marginal lesions Staging and response to treatment in PET-CT Adenocarcinoma, Squamous cell carcinoma High resolution CT-scan Cough, Hemoptysis
Small Cell Lung Cancer[8] - +/- + - - - - +/- p53, Thyroid transcription factor-1 (TTF1) Anemia ↑ Hyponatremia Large hilar mass with bulky mediastinal adenopathy - Endobronchial ultrasound (EBUS) Standard staging Spindled cells with dark nuclei, scant cytoplasm, and fine, granular nuclear chromatin High resolution CT-scan Cough, Hemoptysis
Hematologic disease Hemolytic-Uremic Syndrome[9] + + - + - - + + C5b-9, ADAMTS13 Anemia, Thrombocytopenia, Reticulocytosis  ↑ ↑Lactate dehydrogenase (LDH), Hypercalcemia  Thalami, brainstem, or cerebellum abnormality Cerebral microangiopathy or hypertension Hypoechoic kidney  Abnormal hyperintensity in the brain cisterns in MRI Microthromboses include fibrin thrombi that may occlude the glomerular tuft Clinical findings coupled with laboratory abnormalities Hematuria, Proteinuria 
Chronic Lymphocytic Leukemia (CLL)[10] + + + + +/- - - +/- CD5, CD19, CD20, IgVH Absolute lymphocytosis, Smudge cells ↑ Flow cytometry Staging - - - Large atypical cells, cleaved cells, and prolymphocytes  Chromosomal and genetic testing Easy bruising
Hypereosinophilic Syndrome[11] +/- +/- - - - - - - IgE, CD117 with CD2 Eosinophilia - ↑Serum tryptase Lymphadenopathy and splenomegaly - Intracardiac thrombi in echocardiography - Reticulin stain for myelofibrosis and tryptase staining for mast cells Clinical findings coupled with laboratory abnormalities Splinter hemorrhages, Raynaud phenomenon
Non-Hodgkin Lymphoma[12] + + + + +/- +/- +/- +/- MYC, BCL2, BCL6, and TP53 Lymphocytosis, Anemia, Thrombocytopenia ↑ ↑Lactate dehydrogenase (LDH), Hypercalcemia  Enlarged lymph nodes, Hepatosplenomegaly, Filling defects in the liver and spleen - Hepatosplenomegaly Mediastinal lymphadenopathy Small cleaved or noncleaved, intermediate, or large cell with a follicular or diffuse pattern Surgically excised tissue biopsy Easy bruising, Testicular mass, Skin lesion
Serum Sickness[13] + + - +/- +/- - - +/- IL-1, IL-6, TNF Leukopenia  ↑ Polyclonal gammopathy, ↑Cr, Cryoglobulinemia - - - - Arteritic lesions are focal, necrotizing, and inflammatory involving all layers of the artery Clinical findings coupled with laboratory abnormalities Hematuria, Skin rash
Disseminated Intravascular Coagulation[14] +/- + - +/- - - + + Fibrin degradation product (FDP) Thrombocytopenia, Schistocytes ↑ ↑D-dimer, aPTT and PT Intracranial hemorrhage - - - Ischemia and necrosis due to fibrin deposition in small and medium-sized vessels Clinical findings coupled with laboratory abnormalities  Acral cyanosis, Hemorrhagic skin infarctions
Idiopathic Thrombocytopenic Purpura[15] + +/- - + - - - + FC gamma receptors (FCGR) IIb Anemia, Thrombocytopenia - HIV, ANA R/O other causes - R/O splenomegaly - Increased number of normal morphologic megakaryocytes Clinical findings coupled with thrombocytopenia Easy bruising, Purpura
Systemic disease Sarcoidosis[16] + + + + - - - +/-  IL-2 and IFN-γ Mild anemia ↑ ↑ACE, ↑1, 25-dihydroxyvitamin D Active alveolitis or fibrosis - Hepatosplenomegaly Bilateral hilar adenopathy Noncaseating granulomas (NCGs) Histological confirmation Heart block, Ocular lesion
Legionella Infection[17] + + + + - - - +/- Inflammatory cytokines Leukocytosis with left shift, Thrombocytosis ↑ ↑D-dimer, FDP, Hyponatremia Pleural effusion - - Nonspecific and indistinguishable CXR Intra-alveolar inflammation, Microabscesses in the parenchyma Sputum culture Cough, Diarrhea
Systemic lupus erythematosus[18] + + + + - - + + Anti dsDNA, ANA  Leukopenia, Lymphopenia, Anemia, Thrombocytopenia ↑ ↑Cr or BUN,

↑ALT or AST, Proteinuria

Interstitial lung disease, Pneumonitis, Pulmonary emboli, Alveolar hemorrhage Aneurysms Pericardial effusion, pulmonary hypertension, or verrucous Libman-Sacks endocarditis in echocardiography Central nervous system (CNS) lupus white-matter changes in MRI Staging lupus nephritis Anti-dsDNA antibody test Skin rashes or photosensitivity
Relapsing polychondritis[19] - +/- +/- + + - - - - Leukocytosis, Anemia - Cryoglobulins, ANA, C-ANCA Calcification of cartilaginous structures Aortic root dilatation Aortic root dilatation and degree of aortic regurgitation in echocardiography Tracheal stenosis in CXR Chondrolysis, Chondritis, Perichondritis Clinical findings coupled with imaging Ear pain and redness, Polyarthritis

Differentials Based On Renal Involvement

Goodpasture syndrome is associated with renal involvement in the form of rapidly progressive glomerulonephritis. The various types of glomerular diseases should be differentiated from each other based on associations, presence of pitting edema, hematuria, 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[20][21][22] +/- + +/- +/- +/- +/- +/- +/-
  • Immune complex GN
  • Granular deposit
Renal disease due to Subacute Bacterial Endocarditis, or cardiac shunt (Atrioventricular)[23][24] +/- + +/- +/- +/- +/- +/- +/-
  • Crescentic GN is the most common pathological features
  • Mesangial deposits,
  • Subendothelial deposits
  • Subepithelial "humps," in minority of cases
  • Pauci-immune GN
Lupus Nephritis[25]
  • 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)[26][27]
  • 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[28][29] + +/- + +/- + - + -
  • 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[30][31] Granulomatosis with Polyangiitis (Wegener's)[32][33][34]
  • Middle age male
 + + + +/- + - + -
  •  Pauci-immune GN
Microscopic Polyangiitis[35] +/- + + + + + + -
  •  Pauci-immune GN
Churg-Strauss Syndrome[36] +/- + + + + + + -
  •  Pauci-immune GN
Membranoproliferative Glomerulonephritis[37][38] + + + +/- + + - - -
  • Immune complex GN
  • Granular deposite
Henoch-Schönlein purpura [39] + + + +/- + + - - -
  • 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[40] 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[41][42] - + - + +/- + - +
  • Normal
 -
Focal Segmental Glomerulosclerosis[43][44][45] - + - + +/- + - + -
Membranous Glomerulonephritis[46][47] - + - + +/- + - + Immune complex deposition Immune complex GN, granular deposite
Diabetic Nephropathy[48][49][50][51][52][53][54][55][56][57] 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[58]
  • 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[59][60][61][62] - + - + +/- + - + -
  • 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[63] - +/- + +/- +/- +/- + +/- +/- -
  • 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[64][65][66] - + - + +/- + - + -
  • 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[67][68][69][70][71][72]
  • 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[73][74] - - + -/+ - -/+ - -/+ - - - Diffuse thinning of the glomerular basement membranes (GBM) -
Nail-Patella Syndrome[75][76]
  • 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[77] 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[78]
  • 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[79]
  • 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[80] 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 [81][82][83] + +/- + +/- +/- +/- - - -
  • 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.

References

  1. ↑ McAdoo SP, Pusey CD (July 2017). "Anti-Glomerular Basement Membrane Disease". Clin J Am Soc Nephrol. 12 (7): 1162–1172. doi:10.2215/CJN.01380217. PMID 28515156.
  2. ↑ Kubaisi B, Abu Samra K, Foster CS (2016). "Granulomatosis with polyangiitis (Wegener's disease): An updated review of ocular disease manifestations". Intractable Rare Dis Res. 5 (2): 61–9. doi:10.5582/irdr.2016.01014. PMC 4869584. PMID 27195187.
  3. ↑ Ferri C, Mascia MT (January 2006). "Cryoglobulinemic vasculitis". Curr Opin Rheumatol. 18 (1): 54–63. PMID 16344620.
  4. ↑ Guo QY, Wu M, Wang YW, Sun GD (2017). "Hepatitis C virus-associated cryoglobulinemia with membrano-proliferative glomerulonephritis treated with prednisolone and interferon: A case report". Exp Ther Med. 14 (2): 1395–1398. doi:10.3892/etm.2017.4671. PMC 5525644. PMID 28810602.
  5. ↑ Sise MJ (February 2014). "Acute mesenteric ischemia". Surg. Clin. North Am. 94 (1): 165–81. doi:10.1016/j.suc.2013.10.012. PMID 24267504.
  6. ↑ McDonald JR (2009). "Acute infective endocarditis". Infect Dis Clin North Am. 23 (3): 643–64. doi:10.1016/j.idc.2009.04.013. PMC 2726828. PMID 19665088.
  7. ↑ Molina JR, Yang P, Cassivi SD, Schild SE, Adjei AA (2008). "Non-small cell lung cancer: epidemiology, risk factors, treatment, and survivorship". Mayo Clin Proc. 83 (5): 584–94. doi:10.4065/83.5.584. PMC 2718421. PMID 18452692.
  8. ↑ Jackman DM, Johnson BE (2005). "Small-cell lung cancer". Lancet. 366 (9494): 1385–96. doi:10.1016/S0140-6736(05)67569-1. PMID 16226617.
  9. ↑ Corrigan JJ, Boineau FG (November 2001). "Hemolytic-uremic syndrome". Pediatr Rev. 22 (11): 365–9. PMID 11691946.
  10. ↑ Byrd JC, Stilgenbauer S, Flinn IW (2004). "Chronic lymphocytic leukemia". Hematology Am Soc Hematol Educ Program: 163–83. doi:10.1182/asheducation-2004.1.163. PMID 15561682.
  11. ↑ Klion A (2009). "Hypereosinophilic syndrome: current approach to diagnosis and treatment". Annu. Rev. Med. 60: 293–306. doi:10.1146/annurev.med.60.062107.090340. PMID 19630574.
  12. ↑ Shankland KR, Armitage JO, Hancock BW (September 2012). "Non-Hodgkin lymphoma". Lancet. 380 (9844): 848–57. doi:10.1016/S0140-6736(12)60605-9. PMID 22835603.
  13. ↑ Lin RY (January 1986). "Serum sickness syndrome". Am Fam Physician. 33 (1): 157–62. PMID 2867672.
  14. ↑ Venugopal A (2014). "Disseminated intravascular coagulation". Indian J Anaesth. 58 (5): 603–8. doi:10.4103/0019-5049.144666. PMC 4260307. PMID 25535423.
  15. ↑ Nomura S (2016). "Advances in Diagnosis and Treatments for Immune Thrombocytopenia". Clin Med Insights Blood Disord. 9: 15–22. doi:10.4137/CMBD.S39643. PMC 4948655. PMID 27441004.
  16. ↑ Chiarchiaro J, Chen BB, Gibson KF (2016). "New molecular targets for the treatment of sarcoidosis". Curr Opin Pulm Med. 22 (5): 515–21. doi:10.1097/MCP.0000000000000304. PMC 5152532. PMID 27454074.
  17. ↑ Murdoch DR (January 2003). "Diagnosis of Legionella infection". Clin. Infect. Dis. 36 (1): 64–9. doi:10.1086/345529. PMID 12491204.
  18. ↑ Tsokos, George C. (2011). "Systemic Lupus Erythematosus". New England Journal of Medicine. 365 (22): 2110–2121. doi:10.1056/NEJMra1100359. ISSN 0028-4793.
  19. ↑ Emmungil H, Aydın SZ (2015). "Relapsing polychondritis". Eur J Rheumatol. 2 (4): 155–159. doi:10.5152/eurjrheum.2015.0036. PMC 5047229. PMID 27708954.
  20. ↑ GERMUTH FG (1953). "A comparative histologic and immunologic study in rabbits of induced hypersensitivity of the serum sickness type". J Exp Med. 97 (2): 257–82. PMC 2136196. PMID 13022878.
  21. ↑ Germuth FG, Senterfit LB, Dreesman GR (1972). "Immune complex disease. V. The nature of the circulating complexes associated with glomerular alterations in the chronic BSA-rabbit system". Johns Hopkins Med J. 130 (6): 344–57. PMID 5031005.
  22. ↑ Radhakrishnan J, Cattran DC (2012). "The KDIGO practice guideline on glomerulonephritis: reading between the (guide)lines--application to the individual patient". Kidney Int. 82 (8): 840–56. doi:10.1038/ki.2012.280. PMID 22895519.
  23. ↑ Neugarten J, Baldwin DS (August 1984). "Glomerulonephritis in bacterial endocarditis". Am. J. Med. 77 (2): 297–304. PMID 6380288.
  24. ↑ Arze RS, Rashid H, Morley R, Ward MK, Kerr DN (January 1983). "Shunt nephritis: report of two cases and review of the literature". Clin. Nephrol. 19 (1): 48–53. PMID 6831779.
  25. ↑ 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 (February 2004). "The classification of glomerulonephritis in systemic lupus erythematosus revisited". Kidney Int. 65 (2): 521–30. doi:10.1111/j.1523-1755.2004.00443.x. PMID 14717922.
  26. ↑ Bolton WK (November 1996). "Goodpasture's syndrome". Kidney Int. 50 (5): 1753–66. PMID 8914046.
  27. ↑ Mathew TH, Hobbs JB, Kalowski S, Sutherland PW, Kincaid-Smith P (February 1975). "Goodpasture's syndrome: normal renal diagnostic findings". Ann. Intern. Med. 82 (2): 215–8. PMID 1090223.
  28. ↑ Suzuki H, Kiryluk K, Novak J, Moldoveanu Z, Herr AB, Renfrow MB, Wyatt RJ, Scolari F, Mestecky J, Gharavi AG, Julian BA (October 2011). "The pathophysiology of IgA nephropathy". J. Am. Soc. Nephrol. 22 (10): 1795–803. doi:10.1681/ASN.2011050464. PMC 3892742. PMID 21949093.
  29. ↑ Wyatt RJ, Julian BA (June 2013). "IgA nephropathy". N. Engl. J. Med. 368 (25): 2402–14. doi:10.1056/NEJMra1206793. PMID 23782179.
  30. ↑ Higgins RM, Goldsmith DJ, Connolly J, Scoble JE, Hendry BM, Ackrill P, Venning MC (January 1996). "Vasculitis and rapidly progressive glomerulonephritis in the elderly". Postgrad Med J. 72 (843): 41–4. PMC 2398323. PMID 8746284.
  31. ↑ Jennette JC (March 2003). "Rapidly progressive crescentic glomerulonephritis". Kidney Int. 63 (3): 1164–77. doi:10.1046/j.1523-1755.2003.00843.x. PMID 12631105.
  32. ↑ Renaudineau Y, Le Meur Y (October 2008). "Renal involvement in Wegener's granulomatosis". Clin Rev Allergy Immunol. 35 (1–2): 22–9. doi:10.1007/s12016-007-8066-6. PMID 18172777.
  33. ↑ Weiss MA, Crissman JD (October 1984). "Renal biopsy findings in Wegener's granulomatosis: segmental necrotizing glomerulonephritis with glomerular thrombosis". Hum. Pathol. 15 (10): 943–56. PMID 6384024.
  34. ↑ Pagnoux C (March 2008). "[Wegener's granulomatosis and microscopic polyangiitis]". Rev Prat (in French). 58 (5): 522–32. PMID 18524109.
  35. ↑ Chung SA, Seo P (August 2010). "Microscopic polyangiitis". Rheum. Dis. Clin. North Am. 36 (3): 545–58. doi:10.1016/j.rdc.2010.04.003. PMC 2917831. PMID 20688249.
  36. ↑ 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 (May 2006). "Renal involvement in Churg-Strauss syndrome". Am. J. Kidney Dis. 47 (5): 770–9. doi:10.1053/j.ajkd.2006.01.026. PMID 16632015.
  37. ↑ Alchi B, Jayne D (August 2010). "Membranoproliferative glomerulonephritis". Pediatr. Nephrol. 25 (8): 1409–18. doi:10.1007/s00467-009-1322-7. PMC 2887509. PMID 19908070.
  38. ↑ Davis AE, Schneeberger EE, Grupe WE, McCluskey RT (May 1978). "Membranoproliferative glomerulonephritis (MPGN type I) and dense deposit disease (DDD) in children". Clin. Nephrol. 9 (5): 184–93. PMID 657595.
  39. ↑ Jennette JC, Falk RJ (July 1994). "The pathology of vasculitis involving the kidney". Am. J. Kidney Dis. 24 (1): 130–41. PMID 8023818.
  40. ↑ Fogo AB, Lusco MA, Najafian B, Alpers CE (February 2016). "AJKD Atlas of Renal Pathology: Cryoglobulinemic Glomerulonephritis". Am. J. Kidney Dis. 67 (2): e5–7. doi:10.1053/j.ajkd.2015.12.007. PMID 26802335.
  41. ↑ Saha TC, Singh H (November 2006). "Minimal change disease: a review". South. Med. J. 99 (11): 1264–70. doi:10.1097/01.smj.0000243183.87381.c2. PMID 17195422.
  42. ↑ Saleem MA, Kobayashi Y (2016). "Cell biology and genetics of minimal change disease". F1000Res. 5. doi:10.12688/f1000research.7300.1. PMC 4821284. PMID 27092244.
  43. ↑ Rosenberg AZ, Kopp JB (March 2017). "Focal Segmental Glomerulosclerosis". Clin J Am Soc Nephrol. 12 (3): 502–517. doi:10.2215/CJN.05960616. PMC 5338705. PMID 28242845.
  44. ↑ Jefferson JA, Shankland SJ (September 2014). "The pathogenesis of focal segmental glomerulosclerosis". Adv Chronic Kidney Dis. 21 (5): 408–16. doi:10.1053/j.ackd.2014.05.009. PMC 4149756. PMID 25168829.
  45. ↑ Gephardt GN, Tubbs RR, Popowniak KL, McMahon JT (October 1986). "Focal and segmental glomerulosclerosis. Immunohistologic study of 20 renal biopsy specimens". Arch. Pathol. Lab. Med. 110 (10): 902–5. PMID 2429634.
  46. ↑ Lai WL, Yeh TH, Chen PM, Chan CK, Chiang WC, Chen YM, Wu KD, Tsai TJ (February 2015). "Membranous nephropathy: a review on the pathogenesis, diagnosis, and treatment". J. Formos. Med. Assoc. 114 (2): 102–11. doi:10.1016/j.jfma.2014.11.002. PMID 25558821.
  47. ↑ Wasserstein AG (April 1997). "Membranous glomerulonephritis". J. Am. Soc. Nephrol. 8 (4): 664–74. PMID 10495797.
  48. ↑ Drummond K, Mauer M, International Diabetic Nephropathy Study Group (2002). "The early natural history of nephropathy in type 1 diabetes: II. Early renal structural changes in type 1 diabetes". Diabetes. 51 (5): 1580–7. PMID 11978659.
  49. ↑ Hørlyck A, Gundersen HJ, Osterby R (1986). "The cortical distribution pattern of diabetic glomerulopathy". Diabetologia. 29 (3): 146–50. PMID 3699305.
  50. ↑ Alpers CE, Hudkins KL (2011). "Mouse models of diabetic nephropathy". Curr Opin Nephrol Hypertens. 20 (3): 278–84. doi:10.1097/MNH.0b013e3283451901. PMC 3658822. PMID 21422926.
  51. ↑ Kimmelstiel P, Wilson C (1936). "Intercapillary Lesions in the Glomeruli of the Kidney". Am J Pathol. 12 (1): 83–98.7. PMC 1911022. PMID 19970254.
  52. ↑ Alpers CE, Biava CG (1989). "Idiopathic lobular glomerulonephritis (nodular mesangial sclerosis): a distinct diagnostic entity". Clin Nephrol. 32 (2): 68–74. PMID 2766585.
  53. ↑ Toyoda M, Najafian B, Kim Y, Caramori ML, Mauer M (2007). "Podocyte detachment and reduced glomerular capillary endothelial fenestration in human type 1 diabetic nephropathy". Diabetes. 56 (8): 2155–60. doi:10.2337/db07-0019. PMID 17536064.
  54. ↑ Najafian B, Crosson JT, Kim Y, Mauer M (2006). "Glomerulotubular junction abnormalities are associated with proteinuria in type 1 diabetes". J Am Soc Nephrol. 17 (4 Suppl 2): S53–60. doi:10.1681/ASN.2005121342. PMID 16565248.
  55. ↑ Najafian B, Kim Y, Crosson JT, Mauer M (2003). "Atubular glomeruli and glomerulotubular junction abnormalities in diabetic nephropathy". J Am Soc Nephrol. 14 (4): 908–17. PMID 12660325.
  56. ↑ Najafian B, Alpers CE, Fogo AB (2011). "Pathology of human diabetic nephropathy". Contrib Nephrol. 170: 36–47. doi:10.1159/000324942. PMID 21659756.
  57. ↑ Najafian B, Alpers CE, Fogo AB (2011). "Pathology of human diabetic nephropathy". Contrib Nephrol. 170: 36–47. doi:10.1159/000324942. PMID 21659756.
  58. ↑ Hutchison CA, Cockwell P, Stringer S, Bradwell A, Cook M, Gertz MA, Dispenzieri A, Winters JL, Kumar S, Rajkumar SV, Kyle RA, Leung N (June 2011). "Early reduction of serum-free light chains associates with renal recovery in myeloma kidney". J. Am. Soc. Nephrol. 22 (6): 1129–36. doi:10.1681/ASN.2010080857. PMC 3103732. PMID 21511832.
  59. ↑ Baker KR, Rice L (2012). "The amyloidoses: clinical features, diagnosis and treatment". Methodist Debakey Cardiovasc J. 8 (3): 3–7. PMC 3487569. PMID 23227278.
  60. ↑ Gillmore JD, Hawkins PN (October 2013). "Pathophysiology and treatment of systemic amyloidosis". Nat Rev Nephrol. 9 (10): 574–86. doi:10.1038/nrneph.2013.171. PMID 23979488.
  61. ↑ Jerzykowska S, Cymerys M, Gil LA, Balcerzak A, Pupek-Musialik D, Komarnicki MA (2014). "Primary systemic amyloidosis as a real diagnostic challenge - case study". Cent Eur J Immunol. 39 (1): 61–6. doi:10.5114/ceji.2014.42126. PMC 4439975. PMID 26155101.
  62. ↑ Pepys MB (2006). "Amyloidosis". Annu. Rev. Med. 57: 223–41. doi:10.1146/annurev.med.57.121304.131243. PMID 16409147.
  63. ↑ Korbet SM, Schwartz MM, Lewis EJ (March 1991). "Immunotactoid glomerulopathy". Am. J. Kidney Dis. 17 (3): 247–57. PMID 1996564.
  64. ↑ Alroy J, Sabnis S, Kopp JB (June 2002). "Renal pathology in Fabry disease". J. Am. Soc. Nephrol. 13 Suppl 2: S134–8. PMID 12068025.
  65. ↑ Meikle PJ, Hopwood JJ, Clague AE, Carey WF (1999). "Prevalence of lysosomal storage disorders". JAMA : the Journal of the American Medical Association. 281 (3): 249–54. PMID 9918480. Unknown parameter |month= ignored (help)
  66. ↑ Branton MH, Schiffmann R, Sabnis SG; et al. (2002). "Natural history of Fabry renal disease: influence of alpha-galactosidase A activity and genetic mutations on clinical course". Medicine. 81 (2): 122–38. PMID 11889412. Unknown parameter |month= ignored (help)
  67. ↑ McCarthy PA, Maino DM (2000). "Alport syndrome: a review". Clin Eye Vis Care. 12 (3–4): 139–150. PMID 11137428.
  68. ↑ Chugh KS, Sakhuja V, Agarwal A, Jha V, Joshi K, Datta BN; et al. (1993). "Hereditary nephritis (Alport's syndrome)--clinical profile and inheritance in 28 kindreds". Nephrol Dial Transplant. 8 (8): 690–5. PMID 8414153.
  69. ↑ Chugh KS, Sakhuja V, Agarwal A, Jha V, Joshi K, Datta BN; et al. (1993). "Hereditary nephritis (Alport's syndrome)--clinical profile and inheritance in 28 kindreds". Nephrol Dial Transplant. 8 (8): 690–5. PMID 8414153.
  70. ↑ McCarthy PA, Maino DM (2000). "Alport syndrome: a review". Clin Eye Vis Care. 12 (3–4): 139–150. PMID 11137428.
  71. ↑ Amari F, Segawa K, Ando F (1994). "Lens coloboma and Alport-like glomerulonephritis". Eur J Ophthalmol. 4 (3): 181–3. PMID 7819734.
  72. ↑ Govan JA (1983). "Ocular manifestations of Alport's syndrome: a hereditary disorder of basement membranes?". Br J Ophthalmol. 67 (8): 493–503. PMC 1040106. PMID 6871140.
  73. ↑ Savige J, Rana K, Tonna S, Buzza M, Dagher H, Wang YY (2003). "Thin basement membrane nephropathy". Kidney Int. 64 (4): 1169–78. doi:10.1046/j.1523-1755.2003.00234.x. PMID 12969134. Unknown parameter |month= ignored (help)
  74. ↑ Hou P, Chen Y, Ding J, Li G, Zhang H (2007). "A novel mutation of COL4A3 presents a different contribution to Alport syndrome and thin basement membrane nephropathy". Am. J. Nephrol. 27 (5): 538–44. doi:10.1159/000107666. PMID 17726307.
  75. ↑ Najafian B, Smith K, Lusco MA, Alpers CE, Fogo AB (October 2017). "AJKD Atlas of Renal Pathology: Nail-Patella Syndrome-Associated Nephropathy". Am. J. Kidney Dis. 70 (4): e19–e20. doi:10.1053/j.ajkd.2017.08.001. PMID 28941488.
  76. ↑ Guidera KJ, Satterwhite Y, Ogden JA, Pugh L, Ganey T (1991). "Nail patella syndrome: a review of 44 orthopaedic patients". J Pediatr Orthop. 11 (6): 737–42. PMID 1960197.
  77. ↑ Hughson MD, Puelles VG, Hoy WE, Douglas-Denton RN, Mott SA, Bertram JF (July 2014). "Hypertension, glomerular hypertrophy and nephrosclerosis: the effect of race". Nephrol. Dial. Transplant. 29 (7): 1399–409. doi:10.1093/ndt/gft480. PMC 4071048. PMID 24327566.
  78. ↑ Lusco MA, Najafian B, Alpers CE, Fogo AB (April 2016). "AJKD Atlas of Renal Pathology: Cholesterol Emboli". Am. J. Kidney Dis. 67 (4): e23–4. doi:10.1053/j.ajkd.2016.02.034. PMID 27012950.
  79. ↑ Wesson DE (June 2002). "The initiation and progression of sickle cell nephropathy". Kidney Int. 61 (6): 2277–86. doi:10.1046/j.1523-1755.2002.00363.x. PMID 12028473.
  80. ↑ Lusco MA, Fogo AB, Najafian B, Alpers CE (December 2016). "AJKD Atlas of Renal Pathology: Thrombotic Microangiopathy". Am. J. Kidney Dis. 68 (6): e33–e34. doi:10.1053/j.ajkd.2016.10.006. PMID 27884283.
  81. ↑ Jayakody Arachchillage D, Greaves M (2014). "The chequered history of the antiphospholipid syndrome". Br J Haematol. 165 (5): 609–17. doi:10.1111/bjh.12848. PMID 24684307.
  82. ↑ Jayakody Arachchillage D, Greaves M (2014). "The chequered history of the antiphospholipid syndrome". Br J Haematol. 165 (5): 609–17. doi:10.1111/bjh.12848. PMID 24684307.
  83. ↑ Popa A, Voinea L, Pop M, Stana D, Dascalu AM, Alexandrescu C; et al. (2008). "[Primary antiphospholipid syndrome]". Oftalmologia. 52 (1): 13–7. PMID 18714484.

Template:WH Template:WS

Retrieved from "https://www.wikidoc.org/index.php?title=Goodpasture_syndrome_differential_diagnosis&oldid=1638667"