Basics of renal pathology - cairopedneph.com
Transcript of Basics of renal pathology - cairopedneph.com
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Basics of renal pathology
Hafez M. Bazaraa
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Juan RosaiItalian American (1940)
Pathology, the parent discipline, started withphysicians doing autopsies [on their patients] during the Renaissance in Italy... to try to understand the reasons for the symptoms and the signs that they had beenmonitoring
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Marcello MalpighiEarliest descriptions of renal microanatomy Based on his observations with the newly developed microscope (1666)Urine formed in kidney, filtration mechanism between blood & tubules
Giovanni Battista Morgagni (1682) Related PM & clinical findings Refused to rely on microscopic examination
REN
AL
PATH
OLO
GY
William Bowman (1816–1892)English physician OphthalmologistDescribed components of the proximal nephron & periglomerular capsule Tubule Schematic representation
of Nephron (Bowman)
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Epithelial Cells
Podocytes
endotheliumB.M.
Filtration barrier
Cells: endothelial, epithelial, mesangial
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Back to 19th Century
Edema (Dropsy) Hypertension Hematuria Oliguria Albuminuria Uremia Well described Underlying processes still not clear
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Friedrich Gustav Jakob Henle(1809–1885) Berlin, Zurich, Heidelbergdissected the microanatomy of the
kidney (and many other organs)discovered the tubular segment
(loop of Henle)the Henle–Koch postulates
Theodor Fahr (1877–1945) Hamburg & Paristhe first modern renal pathologistdocumented pathological changes in
renal tissue relating these to clinical expression
of renal diseasewith the internist Franz Volhard
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1950s
The renal needle biopsy Aspiration first used by Nils Alwall from Sweden
(1944) 13 patients, 1 death, stopped, published 1952 Cutting needle The pathology world was at first hostile to the idea
of a tiny specimen to diagnose
300 yrs after Malpighi
Immunofluorescence microscopy to detect tissue-bound immune deposits (Coons and Kaplan, 1950)
Electron microscopy The first observations of ultrastructural changes in glomerular disease (1957)
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Epithelial and Basement membrane changes require E/M
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Thick BM:-Diabetic nephropathy-Alport (silver irregular) -Chronic TMA (silver splitting)-Deposits*Membranous (subepithelial) *Amyloid*MPGN (subendothelial) *Immunotactoid
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Yet pathology is never alone ….
DISEASE
Small doctors treat findings, Average doctors treat diseases,Great doctors treat patients
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I’m not a pathologist
Clinical condition
Biopsy
Specimen examined
Pathology report
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Clinical conditions
SRNS AKI & RPGN Hematuria & proteinuria Secondary nephropathies CKD Transplantation
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What is adequate?
2 Cores 10 Glomeruli 2 Arteries 3 (1) Glomeruli for IF 1 Glomerulus for EM
+ Clinical data+ timing+ sample handling
Fix in 10% Neutral (buffered) formalin-Cheap & available-Suitable for all stains & IHC (but NOT IF)-Reversible (can transfer to other fixative for E/M)
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Stains
Hx&E PAS B.M. & Mesangial matrix
Masson TrichromeFibrosis
Silver B.M. & Mesangial matrix
Congo redAmyloid
Martius Scarlet Blue(MSB) Fibrin
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Immunofluorescence
Performed on unfixed, frozen sections: IgG, IgM and IgA C3, C1q, and C4 C4d in allograft biopsies Others:
– fibrin– kappa and lambda light chains– collagen IV alpha chains – virus identification– lymphocyte phenotyping in allografts in suspected
PTLD
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In-situ hybridization
Uses labeled cDNA or RNA probes It localizes specific DNA/RNA sequence in
tissue section The commonly used:
– BK virus.– EB virus probes in the diagnosis of PTLD.– Pathogenic cytokines such as platelet-derived
growth factor, epithelial growth factor, etc.
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Electron Microscopy
“Electron microscopy provides essential or helpful information to a substantial fraction (50-60%) of cases, and whether a biopsy will fall into the latter fraction is not apparent from the clinical history”
Haas M, 2007
Reembedding of tissue for E/M possible but not the best thing to do
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Electron Microscopy
Thin GBM nephropathy Alport nephropathy Recurrence of focal segmental sclerosis Staging membranous nephropathy Dense deposit disease (MPG type II) Cryoglobulinemic glomerulopathies Early diabetic changes Fabry´s disease Immunotactoid nephropathy
Most valuable with Hematuria, Familial conditions & also proteinuria with normal KF
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What to look at?
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Glomeruli Glomerular pathology:
– Cellularity– Inflammation– Scarring– Abnormal deposits– GBM changes
Tubules
• Tubular pathology :
– Cellular injury
– Inflammation
– Atrophy
– Casts
Interstitium
• Interstitial pathology:
– Cellular infiltrates
– Edema/fibrosis
Vascular disease
• Vascular pathology:
– Inflammation
– Thrombosis– Hyalinosis
– Sclerosis
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CLINICAL
-Nephrotic syndrome
-Isolated proteinuria
-Recurrent/ persistent Hematuria
-Glomerulonephritis
-RPGN
PATHOLOGICAL•Minimal change•Focal/ diffuse mesangial•Membranous•MPGN•Focal/ diffuse proliferative•Crescenteric•FSGS
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Diffuse proliferative GN
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Crescenteric GN:Proliferating & infl. Cells fill Space
Cellular Fibrocellular Fibrous
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Crescenteric GN:Proliferating & infl. Cells fill Space
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RPGN
•Rapidly-progressive renal failure•GlomerularNOT vascular (TMA, APL, RVT)NOT tubulointerstitialNOT pre or post renal
Type 1
AntiGBM
Linear IF; IgG
-Goodpasture (+ pulm hge)
-AntiGBM nephritis
Type 2
Immune complex
Granular IF-IgAN/HSP-PSGN-MPGN-MembGN-SLE-Cryoglobulinemia
Type 3
Pauci-Immune
No IFANCA +ve-Wagener-Microscopic polyangitis-Churg Straus-Renal limited
Type 4 : double Ab ANCA-ve, idiopathic, type5
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Proliferative GN (cellular lesions)
Diffuse proliferative Crescenteric Focal proliferative Mesangioproliferative Membranoproliferative
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Focal Proliferative
Focal Mesangial
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Mesangial
IgA
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Double contour
Peripheral migration and interposition of mesangium: Mesangial cells and often matrix extend from the central lobular portion of the tuft into the peripheral capillary wall.
Migrating between endothelial cell and basement membrane and causing capillary wall thickening with two layers of extracellular matrix.
This two-layer or double contour appearance may involve a few or all capillaries.
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-ve ?TMA
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DDD (MPGN II)
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Membranous
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Diffuse= affects all/ most glomeruli Focal= affects some (<50%) glomeruli Global= affects all of the involved glomerulus Segmental= affects part of the involved
glomerulus
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FSGS
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Glomerulosclerosis
Scarring glomerular lesion Obliterated capillaries & solidified tuft ↑ Extracellular matrix ± Obliterated space by collagen=Hyalinosis (old imprecise term)Vs Fibrosis (healed necrotizing ; PAS-ve,
lesion)
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FSGS: pattern of injury; Diverse Causes
Idiopathic sporadic Genetic Drugs (CNI, Li, IFNalpha, Pamidronate, Heroin, ..) Viral (HIV, Parvo, ..) Adaptive responses
– ↓renal mass: unilat. Agenesis, dysplasia, reflux nephropathy, progressive CKD
– DM, HTN, obesity, sickle, CCHD Renal scarring pattern: TMA. Focal proliferative,
Membranous, Alport, …
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FSGS: subtypes
NOS Segmental sclerosis Typical
Collapsing Tuft collapse, epithelial hyperplasia
Worse
Cellular Endocapillary proliferation & usu. epithelial hyperplasia
Early
Tip Tuft sclerosis at prox. Tubule pole
Better
Perihilar Tuft sclerosis at vascular pole
May be 2ry
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Obsolescent (globally sclerotic) glomeruli
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Glomeruli Glomerular pathology:
– Cellularity– Inflammation– Scarring– Abnormal deposits– GBM changes
Tubules
• Tubular pathology :
– Cellular injury
– Inflammation
– Atrophy
– Casts
Interstitium
• Interstitial pathology:
– Cellular infiltrates
– Edema/fibrosis
Vascular disease
• Vascular pathology:
– Inflammation
– Thrombosis– Hyalinosis
– Sclerosis
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Vascular
InflammationVasculitis, Rejection HyalinosisAgeing, DM, HTN, CNI (isometric vacuolization) ThrombosisTMA, PSS, Malignant HTN, emboli, … Sclerosis: HTN
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TMA: traditional views
It is a specific disease It is uncommon It is an acute condition It is always associated with HUS or TTP
•IT IS A COMMON PATTERN OF INJURYwith many potential causes/ complement activation patterns•Acute & chronic forms, some very subtle
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Glomeruli Glomerular pathology:
– Cellularity– Inflammation– Scarring– Abnormal deposits– GBM changes
Tubules
• Tubular pathology :
– Cellular injury
– Inflammation
– Atrophy
– Casts
Interstitium
• Interstitial pathology:
– Cellular infiltrates
– Edema/fibrosis
Vascular disease
• Vascular pathology:
– Inflammation
– Thrombosis– Hyalinosis
– Sclerosis
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Tubulointerstitial
ATN/ ATI (ischemic or toxic) Epithelial degeneration/ necrosis NO inflammation vs Interstitial Nephritis
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Acute interstial nephritis
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NPHPCysts arise from CM junction of normal-sized kidneys. N size, ↑echog, ↓CM diff, CM cysts
Histological triad-Tubular (& glom) cysts-Tubular membrane disruption-Tubulointerstitial infl. & fibrosis
Hildebrandt et al.
JASN 2007
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IFTA
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Active and chronic lesions
Vascular sclerosis Glomerular sclerosis Fibrous crescents Tubular atrophy Interstitial fibrosis
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amyloid
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TRANSPLANTATIONHyperacute rejection
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Banff classification
Category 1: Normal biopsy or nonspecific changes
Category 2: Antibody-mediated changes Category 3: Borderline changes Category 4: TCMR Category 5: Interstitial fibrosis and tubular
atrophy Category 6: Other changes not considered to
be caused by acute or chronic rejection
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Borderline & acute TCMRTCMR Tubulitis Interstitial Infl. ArteritisBorderline/ suspicious
Foci t1-3 Minor i0-1 NONEMild t1 i 2-3
Grade Ia Foci t2 i 2-3 in >25% of non-sclerotic cortex
Grade Ib Foci t3
Grade II ± ± Intimal arteritisIIa V1 (mild-mod)IIb V2 (severe >25%
luminal area)Grade III V3 Transmural arteritis and/or arterial fibrinoid
change and necrosis of medial smooth muscle cells with lymphocytic inflammation
Chronic active TCMR
Chronic allograft arteriopathy
Borderline, acute & chronic TCMR
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Cellular rejection
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Intimal arteritis
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Transmural arteritis & C4d
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Acute ABMR
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glomerulitis
Double contours
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Acute/ Active ABMR
Histological evidence of acute tissue injury;any of: arteritis, microvasvular infl. (G &/or ptc), acute TMA, acute tubular injury
Evidence of current/recent antibody interaction with vascular endothelium ;any of: Linear C4d in ptc (2-3 by IF or >0 by IHC), mod microvascular infl (G+ptc= 2+), endothelial injury by ↑ gene transcripts expr. in Bx.
Serologic evidence of DSA (HLA or otherwise)
All 3= ABMR, 1+ 2or3 = suspicious
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C4d staining without evidence of rejection
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Banff classification
Category 1: Normal biopsy or nonspecific changes
Category 2: Antibody-mediated changes Category 3: Borderline changes Category 4: TCMR Category 5: Interstitial fibrosis and tubular
atrophy Category 6: Other changes not considered to
be caused by acute or chronic rejection
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Others; not acute or chronic rejection
BK virus nephropathy Posttransplant lymphoproliferative disorders Calcineurin inhibitor nephrotoxicity Acute tubular injury Recurrent disease De novo glomerulopathy (other than transplant
glomerulopathy) Pyelonephritis Drug-induced interstitial nephritis
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CNI toxicity
Isometric vacuolization of proximal tubular cells Striped pattern of tubular atrophy/interstitial fibrosis Tubular microcalcinosis Arteriopathy with hyalinosis, vacuolization of
smooth muscle cells of arterioles Glomerulosclerosis, ischemic shrinkage of
glomeruli
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Three final words ….
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Fine Needle biopsy
Analysis of immunologically activated cells in grafts TCMR
Less invasive & repeatable Limitations in interpretation
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Urine: the fluid biopsy of the kidney(Prof. Ramzi El Baroudi)
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Yet pathology is never alone ….
•Assess patient carefully
•Need for pathology
•Do it early
•Do it properly
•Do it completely
•Interpret the whole picture
•Do it with care
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Further references
Weening JJ, Jennette JC. Historical milestones in renal pathology. Virchows Arch. 2012;461(1):3-11. doi: 10.1007/s00428-012-1254-7.
Agarwal SK, Sethi S, Dinda AK. Basics of kidney biopsy: A nephrologist's perspective. Indian J Nephrol. 2013;23(4):243-52.
Stephen M.Bonsib. Atlas of medical renal pathology. Springer 2013
Agnes Fogo. Renal pathology. Avner E, Harmon W, Niaudet P, Yoshikawa N (eds). Pediatric nephrology. Springer 2009 (6th ed) 24:565-98
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1. Pathological lesions denoting chronicity include
A cellular crescentsB vasculitis C tubular injuryD interstitial fibrosis
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2. In acute antibody-mediated graft rejection, immunofluorescence shows deposits of
A IgAB C1q C C4dD Collagen type IVa
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3. The picture shows
A Minimal change diseaseB Crescenteric nephritisC Focal segmental glomerulosclerosisD Diffuse mesangial sclerosis