Postinfectious glomerulonephritis - IPNA Onlineipna-online.org/Media/Junior Classes/2015 - 2nd IPNA...
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Postinfectious glomerulonephritis
Ali Düzova
M.D., Professor of Pediatrics
Division of Pediatric Nephrology
Hacettepe University Faculty of Medicine, Ankara, Turkey
The 2nd IPNA-ESPN Master for Junior Classes,
01-02 September 2015, Leuven
Hacettepe University Ankara
A.Duzova
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Outline
• Definition
• Epidemiology
• Pathogenesis
• Clinical features and pathology
• Management
– Evidence?
• Outcome
A.Duzova
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Definition
• Postinfectious glomerulonephritis (GN) – “…. is an immune mediated glomerular injury that occurs as a result of
host response to an extrarenal infection”1
• Following terms are often, and incorrectly, used interchangeably 2 – Acute post-streptococcal GN (PSGN)
– Acute nephritic syndrome
– Acute glomerulonephritis
Kambham N. Adv Anat Pathol 2012;19:338–347.1
Rodriguez-Iturbe B, Mezzano S. Pediatric Nephrology, 6th edn.2
A.Duzova
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Etiological Agents Associated with Acute Postinfectious Glomerulonephritis
Bacterial Viral Fungal Parasites
Streptococcus group A, C, G Streptococcus viridans Staphylococcus (aureus, albus) Pneumococcus Neisseria meningitidis Mycobacteria Salmonella typhosa Klebsiella pneumoniae Escherchia coli Yersinia enterocolitica Legionella Brucella melitensis Treponema pallidum Corynebacterium bovis Actinobacilli Cat-scratch bacillus
Coxsackievirus Echovirus Cytomegalovirus Epstein-Barr virus Hepatitis B, C HIV Rubella Measles Varicella Vaccinia Parvovirus Infl uenza Adenovirus Rickettsial scrub typhus
Coccidioides immitis Plasmodium malariae Plasmodfalciparum Schistosoma mansoniium Toxoplasma gondii Filariasis Trichinosis Trypanosomes
Tasic V. Acute Postinfectious GN. In: Comprehensive Pediatric Nephrology, 2009
A.Duzova
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Epidemiology
• Sporadic, epidemic
• Poor communities, deficient hygienic conditions
• A decline in industrialized countries in the past three decades – Living conditions
– Fluorination of water
• Streptococcus pyogenes are reduced
– Access to health facilities
• Central Europe – Adult population; alcoholism, diabetes
A.Duzova
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• Decreasing incidence – The Italian Biopsy Registry
• PSGN – Adult, > 60 year: 0.9 patients/million versus 0.4 patients/million – Children <15 year:
» 1987-1992: 2.6-3.7% of primary glomerulopathies » 1992-1994: only 9 cases
– Maracaibo, Venezuela – 1980-1985: 90-110 cases/year – 2001-2005: 15 cases/year
– Guadalajara, Mexico – Memphis, TN
• Communities with low socioeconomic status – Aboriginal communities – Valencia, Venezuela: 70% of admissions in a pediatric nephrology service – India: 73% of acute GNs in elderly
Epidemiology
Rodriguez-Iturbe B, Musser JM. The Current State of Poststreptococcal GN. JASN 2008; 19: 1855–1864.
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0
10
20
30
40
50
60
Hypoxic/ishemic injury Sepsis Acute gastroenteritis Acute glomerulonephritis Malignancy
1980s
2006-07
Acute kidney injury in children in Turkey
Gokalp et al. Ann Trop Paediatr 1991; 11: 119–121 Duzova et al. Pediatr Nephrol 2010; 25: 1453-1461
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Rodriguez-Iturbe B, Musser JM. The Current State of Poststreptococcal GN. JASN 2008; 19: 1855–1864.
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Carapetis JR et al. The global burden of group A streptococcal diseases. Lancet Infect Dis 2005; 5: 685–694.
•95% less developed countries •Mortality rate: 1% •5,000 death/year
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Clinical features
• Age, gender – 4-14 years – Rare: < 2 years and >20 years – M/F : 2/1
• Antecedent infection, latent period – Skin 3-5 weeks – Upper resp. 1-2 weeks
• Clinical course – Subclinical – Acute nephritic syndrome – Nephrotic syndrome – Rapidly progressive (crescentic) GN (RPGN)
A.Duzova
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Course Clinical features Remarks
Subclinical ↓Complement level Microscopic hematuria N, Blood pressure
• 4-5 x more common than symptomatic patients in household members
Acute nephritic syndrome
Typical picture Hematuria (1/3 gross) Hypertension (60-80%) Edema (90%) Moderate proteinuria Oliguria (<%50%)
Macroscopic hematuria: few days Edema and hypertension: 5-10 days
Nephrotic syndrome
2-4% Risk factor for progression to CKD
RPGN
<1% Risk factor for progression to CKD
Clinical features
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Pathogenesis
• Activation of the complement system and of the coagulation cascade
• Immune complexes: in circulation, in situ (cationic antigens, subepithelial)
– Antigen size, load
– Antigen/antibody ratio
– Duration of exposure
– Host’s capacity to remove the deposited complexes
• Location of immune complexes (granular, not linear) – Mesangium (speckled ) appearance
– Glomerular basement membrane (garland appearance)
– Both
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Pathogenesis: nephritogenic antigens
• Specific M proteins were considered first; but they are not – Rheumatogenic species
– Nephritogenic species (Group A strep: GAS) • Pyodermitis GAS M types 47, 49, 55
• Upper respiratory tract GAS M types 1, 2, 4, 12
• Other nephritogenic antigens
– S. zooepidemicus epidemic in Brazil
• SPEB/zSPEB: Streptococcal pyrogenic exotoxin (erythrotoxin) B and its zymogen precursor
• NAP1r : nephritis associated plasmin receptor
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Pathogenesis: nephritogenic antigens
• SPEB/zSPEB: Streptococcal pyrogenic exotoxin (erythrotoxin) B and its zymogen precursor
– Co-localized with complement and Ig deposits
– Localized within dense deposits
– Cationic nature (pk>8.0)
– Increased production of IL-6
• NAP1r : nephritis associated plasmin receptor
– Glyceraldehyde 3-phosphate dehydrogenase (GAPDH)
– Plasmin binding characteristics • Local inflammatory reactivity, penetration of nephritogenic Ag-Ab complexes
A.Duzova
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A.Duzova
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A.Duzova
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Pathogenesis: other factors
• And cellular immunity – Infiltration of lymphocytes and macrophages
– Overexpression of ICAM-1 and LFA
– IL-8
– TGF-beta
– TNF-alpha
• Autoimmune reactivity – Anti –IgG Ab
– Anti-DNA antibodies
– ANCA
• Host factors?
A.Duzova
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Laboratory findings
• Reduction in serum complement level (>90%)
• Activation of complement system
– Alternative (mainly): low C3; normal C1 and C4
– Classic
– Lectin
• IgG, IgM elevated (80%)
• Antistreptococcal antibody titers
– Anti-streptolysin O (ASO)
– Anti-DNase B
– Anti-zSPEB/SPEB
• Positive cultures (20-25%)
A.Duzova
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Indications for renal biopsy Early Stage Recovery Phase
•Short latent period •Severe anuria •Rapid progressive course •Hypertension >2 weeks •Depressed GFR >2 weeks •Normal complement levels •Nonsignificant titres of antistreptococcal antibodies •Extrarenal manifestations
•Depressed GFR >4 weeks •Hypocomplementemia >12 weeks •Persistent proteinuria > 6 month •Persistent microhematuria > 18 months
• Atypical features that prompt a renal biopsy:
– RPGN
– Persistent gross hematuria
– Hypertension or nephrotic syndrome
– Extrarenal manifestations
– Short latency period to renal disease,
– Hypocomplementemia lasting >6 weeks
– Patient <2 years of age
– The threshold for performing a biopsy in an adult is generally lower
Kambham N. Adv Anat Pathol 2012;19:338–347.
Tasic V. Acute Postinfectious GN. In: Comprehensive Pediatric Nephrology, 2009.
•Normal complement level: r/o IgAN? •Low complement level after 1-2 months: r/o SLE, MPGN •Nephrotic range proteinuria •Rising proteinuria, RPGN •Age •Extrarenal manifestations
A.Duzova
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Early Biopsy (<2 wk) Typical Features
Late Biopsy (>4-6 wk)
Clinical features Mild albuminuria and hematuria
Acute nephritic syndrome
Persistent microscopic hematuria and/or proteinuria
Light microscopy
Glomerular endocapillary proliferation may be focal and segmental
Diffuse global proliferation (“exudative” early on; lymphocytes, monocytes along with mesangial and endothelial proliferation predominate later)
Mesangial proliferation
IF microscopy
C3 and IgG; starry sky pattern
C3 and IgG; starry sky or garland pattern*
C3±IgG; mesangial pattern
Electron microscopy
Mesangial, subepithelial (humps), and± subendothelial deposits
Mesangial, subepithelial (humps), and±subendothelial deposits
Mesangial and±rare subepithelial humps in the mesangial “notch”
Kambham N. Adv Anat Pathol 2012;19:338–347. A.Duzova
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By courtesy of Dr. D. Orhan, Hacettepe University.
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By courtesy of Dr. D. Orhan, Hacettepe University.
Endocapillary proliferation and neutrophil infiltration
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By courtesy of Dr. D. Orhan, Hacettepe University.
Crescent formation
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C3
By courtesy of Dr. D. Orhan, Hacettepe University.
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Kambham N. Adv Anat Pathol 2012;19:338–347.
Starry-sky pattern
Garland pattern
A.Duzova
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Subepithelial dense deposit (hump)
By courtesy of Dr. D. Orhan, Hacettepe University.
A.Duzova
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By courtesy of Dr. D. Orhan, Hacettepe University.
Subepithelial dense deposit (hump)
A.Duzova
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Diagnosis, differential dignosis
• Clinical features
• Positive cultures
• Antibodies
– Anti NAP1r, SPEB
– ASO, Anti-DNase B
– Streptozyme test • ASO, Anti-DNase B, streptokinase, hyaluronidase
A.Duzova
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Diagnosis, differential dignosis
• Complement level – Normal complement:
• IgAN, MPGN, HUS, HSP, vasculitis, anti-GBM
– Low
• C4↓↓; C3 N, ↓ cryoglobulinemia
• ↓ C4, C3, C1 SLE
• Nephrotic proteinuria: – r/o: SLE, MPGN, nepritis associated with visceral abscesses
A.Duzova
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Kambham N. Adv Anat Pathol 2012;19:338–347. A.Duzova
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Management • Antibiotic treatment
– Prevention • Skin infection • Throat infection • McIsaac (sensitivity 85 %; specificity 92%)
– Temperature 38°C – No cough, – Tender anterior cervical adenopathy – Tonsillar swelling or exudates – Age
» between 3 and 14 yr. 1 point » 15 to 44 no point » age > 44 yr gets 1 point. -1 point
• Rapid test: sensitivity low
– PSGN patients: treatment – Family members
McIsaac WJ et al. The validity of a sore throat score in family practice. CMAJ 2000; 163: 811–815. Edmonson MB, Farwell KR: Relationship between the clinical likelihood of group A streptococcal
pharyngitis and the sensitivity of a rapid antigen-detection test in a pediatric practice. Pediatrics 2005; 115: 280-285. A.Duzova
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Management
• Edema, hypertension
– Loop diuretics
– Antihypertensives • Nifedipine
• Hydralazine
• ACE-i?
• …..
A.Duzova
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A.Duzova
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A.Duzova
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A.Duzova
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Rodriguez-Iturbe B, Musser JM. The Current State of Poststreptococcal GN. JASN 2008; 19: 1855–1864.
Outcome
A.Duzova
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Rodriguez-Iturbe B, Musser JM. The Current State of Poststreptococcal GN. JASN 2008; 19: 1855–1864.
Outcome
A.Duzova
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Shunt nephritis
• Ventriculoatrial shunts (<2%)
• Ventriculoperitoneal shunts; rare
• S. epidermidis (75%)
• Less frequent
– S. aureus
– Propionibacterium acne, diphtheroids, Pseudomonas and Serratia
• C3 and C4 low
• The renal lesion
– Usually MPGN
– Deposits: complement and IgM; IgG in about two-third
– EM, dense deposits: subendothelial and mesangial
Haffner D, Schinderas F, Aschoff A. Nephrol Dial Transplant 1997;12:1143–1148. Fukada Y et al. Am J Nephrol 1993;13:78–82.
Rodriguez-Iturbe B, Mezzano S. Pediatric Nephrology, 6th edn.
A.Duzova
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Infective endocarditis
• Microembolism (%30)
• Glomerulonephritis (%26)
• Tubulointerstitial nephritis
• Vasculitis
• Microorganisms – S. aureus, S. epidermidis, Streptococcus viridans and pyogenes,
Enterococcus fecalis
– E. coli, Proteus, Bartonella , Candida species.
Majumdar A et al. Renal pathological findings in infective endocarditis. Nephrol Dial Transplant 2000;15:1782–1787.
A.Duzova
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Summary
• Changing epidemiology of PSGN
• Pathogenesis: nephritogenicity
• Biopsy: in specific cases, not pathognomonic
• Diagnosis: clinical, laboratory features
• Limited data for evidence based management
• Treatment and prevention for PSGN
• Prognosis is not always excellent
A.Duzova