Algorithmic approach to the renal biopsy fellow
Upcoming SlideShare
Loading in...5
×
 

Algorithmic approach to the renal biopsy fellow

on

  • 1,519 views

 

Statistics

Views

Total Views
1,519
Views on SlideShare
1,519
Embed Views
0

Actions

Likes
0
Downloads
105
Comments
0

0 Embeds 0

No embeds

Accessibility

Upload Details

Uploaded via as Adobe PDF

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment

Algorithmic approach to the renal biopsy fellow Algorithmic approach to the renal biopsy fellow Presentation Transcript

  • Algorithmic Approach to theInterpretation of Renal Biopsy
  • Basic stains required for LMH&E PAS• Glomerular: exudative lesions • Glomerular: GBM thickening, capillary• Tubular: tubular epithelial damage wall collapse, Bowman’s capsule,• Interstitial: edema, inflammation hyalinosis, sclerosis, mesangial cellularity and matrix increase,• Vascular: inflammation mesangiolysis, endo/extracapillary proliferation • Tubular: tubular protein droplets, TBM thickening, tubulitis • Vascular: hyaline arteriolosclerosisMethanamine-silver (Jones stain) Masson trichrome• Glomerular: GBM spikes, double • Glomerular: immune deposits, thrombi, contours, breaks in GBM/Bowman’s fibrin, platelets capsule • Tubular: tubular atrophy• Tubular: tubulitis • Interstitial: fibrosis• Interstitial: Fibrosis • Vascular: thrombi• Vascular: internal elastic lamina
  • Routine antibody panel for IF• IgG immune complex disease, Anti-GBM disease• IgA IgA nephropathy, HSP, Liver disease, SLE• IgM Waldenstrom’s macroglobulinemia, mixed cryoglobulinemia• C1q C1q nephropathy, SLE• C3 Dense deposit disease, C3 mesangial GN, resolving PIGN• Fibrinogen Necrotizing lesion, thrombotic microangiopathy, crescents• Kappa & Lambda Monoclonal Ig deposition disease, amyloidosis• C4d (transplant) Humoral rejection
  • Descriptive terms and patterns of glomerular injuryRelated to distributionFocal Involving less than 50% of glomeruli by LMDiffuse Involving 50% or more of glomeruli by LMSegmental Involving a portion of the glomerular tuftGlobal Involving the entire glomerular tuft
  • Descriptive terms and patterns of glomerular injuryRelated to StructureObsolescence Total loss of normal glomerular architecture due to replacement by sclerosisSclerosis Increased collagenous extracellular matrix expanding the mesangium, occluding capillary lumina or forming adhesions to Bowman’s capsuleFibrinoid necrosis Disruption of structure, with degeneration of local cells, extracellular matrix and the basement membrane, often associated with fibrin depositionLobular Hypersegmentation of the normal lobular architecture of the normal glomerular capillary tuft due to intracapillary hypercellularity or significant mesangial expansionsMesangiolysis Dissolution or attenuation of mesangial matrix and degeneration of mesangial cells, often associated with glomerular capillary aneurysmsMesangial interposition Extension of mesangial cells in the peripheral glomerular capillary walls in the space located between endothelial cells and GMB (subendothelial zone)
  • Descriptive terms and patterns of glomerular injuryRelated to StructureHyalinosis Accumulation of glassy, refractile acellular material/plasmatic insudation (PAS positive, methenamine-silver negative) which contains serum proteins, other glycoproteins and lipidsGlomerular capillary collapse Retraction of glomerular tuft with closure of capillary lumina and wrinkling and thickening of glomerular capillary wallsGlomerular capillary aneurysm Capillary lumen balloons out and appears ectatic due to degeneration of mesangial cells and matrix (mesangiolysis)Wire-loops Thickened glomerular capillary walls with a rigid appearance (wire-loop-like) due to the presence of large and confluent subendothelial immune depositsTram-tracking/GBM reduplication Double contoured appearance of glomerular capillary walls on PAS/silver stains due to the presence of deposits and mesangial interposition between the endothelium and the original GBM with creation of a new inner (subendothelial side) basement-membrane-like material
  • Descriptive terms and patterns of glomerular injuryRelated to Cell proliferationMesangial hypercellularity Presence of 3 or more mesangial and/or inflammatory cells per mesangial area away from the vascular pole in a section that is 2-3 micron in thickness (WHO definition)Endocapillary hypercellularity Increased cellularity within the confines of GMB composed of endothelial cells, mesangial cells and /or inflammatory cells, resulting in luminal narrowing or occlusionIntracapillary hypercellularity Hypercellularity present in both mesangium and endocapillariesCrescent The build-up of more than 2 layers of cells within Bowman’s space caused by the proliferation of parietal cells, podocytes and inflammatory cells, often with fibrin and collagen deposition.Adhesion/synechia Localized narrow bridges of connective tissue between glomerular tufts and Bowman’s capsuleMembranoproliferative Glomerular capillary wall thickening due to mesangial interposition and duplication of GMB
  • Descriptive terms and patterns of glomerular injuryRelated to DepositsIntramembranous Within the GBMMesangial Within the mesangial matrixSubendothelial Between the GBM and the endotheliumSubepithelial/epimembranous Between the GBM and podocytesHumps Subepithelial electron-dense immune-type deposits with a cigar-or dome-like appearance
  • Descriptive terms and patterns of tubulointerstitial and vascular injuryTubulesTubulitis Lymphocytes or other inflammatory cells infiltrating tubular epitheliumTubular atrophy Tubular involution/obsolescence due to ischemia, obstruction, toxic or inflammatory injury with different LM appearances including classic atrophy, endocrine and thyroidization changesTubular casts Various coagulated proteins and other elements in tubular lumens usually but not exclusively seen in distal nephronHydropic degeneration/ Fine regular cytoplasmic vacuolization of the proximal tubulesOsmotic nephrosis
  • Descriptive terms and patterns of tubulointerstitial and vascular injuryTubulesHyaline droplet PAS/silver-positive protein reabsorption droplets because of increased protein loss by glomeruliFatty change Finely vacuolated cytoplasm with clear vacuoles in the cytoplasm of tubular epithelium in which the lipid has been dissolved out during preparation of paraffin sectionsHypokalemic change Large irregular sized coarse clear vacuoles in the cytoplasm of tubular epithelial cells, especially the distal tubular cellsIntranuclear inclusions Seen in nuclei with various morphology depending on etiology, often associated with viral infections (CMV, BK polyomavirus and adenovirus), can be observed in tubular epithelial cell regeneration and lead nephropathy
  • Descriptive terms and patterns of tubulointerstitial and vascular injuryInterstitiumEdema Increased extracellular fluid in the interstitium resulting in increased spacing between tubulesInterstitial foam cells Macrophages with cytoplasm lipid-containing vacuolesInflammation Infiltration of lymphocytes, plasma cells, and often eosinophils and neutrophils with associated tubular injuryFibrosis Interstitial expansion by collagenGranuloma Collection of epithelioid histiocytes with/with out surrounding multinucleated giant cells and lymphocytes
  • Descriptive terms and patterns of tubulointerstitial and vascular injuryVesselsIntimal thickening Fibrous thickening of the intimal layer, usually in a concentric configuration and associated with varying degrees of luminal stenosisHyaline sclerosis Accumulation of PAS-positive/silver-negative material in the intima and /or media resulting in a characteristic “glassy” acellular refractile change in small arteries and arteriolesEndothelialitis/endarteritis Infiltration of mononuclear cells under arterial and arteriolar endotheliumArteritis Necrosis, fibrinoid degeneration and inflammation of arteries with leukocytoclasia and disruption of internal elastic laminaVasculitis Necrosis, fibrinoid degeneration and leukocytoclastic inflammation of arteries, arterioles and veins
  • Components of Native Kidney Biopsy Pathology ReportLight microscopy• Presence and relative proportion of renal capsule, cortex, medulla, pelvic urothelial lining and others (i.e., skeletal muscle, liver, intestine)• Total number of glomeruli and the number/percentage of globally sclerotic glomeruli if any• Description of diagnostic morphology lesions/changes/patterns in glomeruli, tubules, interstitium and vessels• Description of important or relevant negative findings
  • Components of Native Kidney Biopsy Pathology ReportImmunofluorescence microscopy• Total number of glomeruli and the number of globally sclerotic glomeruli if present• Description of positive or negative results for each Ig and complement components in glomeruli• Description of the location, stain pattern and intensity of the deposits in glomeruli• Description of immunoreactants in tubulointerstitial compartment and vessels if present
  • Components of Native Kidney Biopsy Pathology ReportElectron microscopy• Total number of glomeruli and the number of globally sclerotic glomeruli if present• Description of glomerular abnormalities/changes• Description of the location, number, size, appearance/substructure of electron dense deposits if present• Description of degree of foot process effacement• Description of relative changes in tubulointerstitial and vascular component
  • Components of Native Kidney Biopsy Pathology ReportDiagnosis• Including morphologic pattern plus a particular pathogenic or clinicopathologic category of the diseaseComment• Clinicopathologic correlation• List of differential diagnoses if necessary• Pertinent histologic prognostic indicators• Activity/chronicity indices of lupus nephritis
  • Components of Renal Transplant Biopsy Pathology ReportLight microscopy• Glomeruli: glomerulitis, fibrin thrombosis, double contours, and other glomerular lesions• Tubules: tubular injury, inflammation (tubulitis), nuclear atypia/inclusions• Interstitium: nature and degree of cellular infiltrate (i.e., edema, activated mononuclear cell, malignant cells, leukocytes in peritubular capillaries)• Vessels: endarteritis, myocyte necrosis, thrombi, nodular hyaline, intimal elastosis
  • Components of Renal Transplant Biopsy Pathology ReportImmunofluorescence microscopy• C4d staining in peritubular capillaries
  • Components of Renal Transplant Biopsy Pathology ReportElectron microscopy• Glomerular abnormalities• Viral particles• Peritubular capillary basement membrane multilayering
  • Components of Renal Transplant Biopsy Pathology ReportDiagnosis• Including a particular patholonic or clinicopathologic category of the disease (Banff Classification for Renal Transplant Pathology)Comment• Clinicopathologic correlation• List of differential diagnoses if necessary• Pertinent histologic prognostic indicators