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Algorithmic approach to the renal biopsy fellow
 

Algorithmic approach to the renal biopsy fellow

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

    • Algorithmic Approach to the Interpretation of Renal Biopsy
    • Basic stains required for LM
      • H&E
      • Glomerular: exudative lesions
      • Tubular: tubular epithelial damage
      • Interstitial: edema, inflammation
      • Vascular: inflammation
      • Methanamine-silver (Jones stain)
      • Glomerular: GBM spikes, double contours, breaks in GBM/Bowman’s capsule
      • Tubular: tubulitis
      • Interstitial: Fibrosis
      • Vascular: internal elastic lamina
      • PAS
      • Glomerular: GBM thickening, capillary wall collapse, Bowman’s capsule, hyalinosis, sclerosis, mesangial cellularity and matrix increase, mesangiolysis, endo/extracapillary proliferation
      • Tubular: tubular protein droplets, TBM thickening, tubulitis
      • Vascular: hyaline arteriolosclerosis
      • Masson trichrome
      • Glomerular: immune deposits, thrombi, fibrin, platelets
      • Tubular: tubular atrophy
      • Interstitial: fibrosis
      • Vascular: thrombi
    • 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 injury
      • Related to distribution
      • Focal Involving less than 50% of glomeruli by LM
      • Diffuse Involving 50% or more of glomeruli by LM
      • Segmental Involving a portion of the glomerular tuft
      • Global Involving the entire glomerular tuft
    • Descriptive terms and patterns of glomerular injury
      • Related to Structure
      • Obsolescence Total loss of normal glomerular architecture due to replacement by
      • sclerosis
      • Sclerosis Increased collagenous extracellular matrix expanding the mesangium,
      • occluding capillary lumina or forming adhesions to Bowman’s capsule
      • Fibrinoid necrosis Disruption of structure, with degeneration of local cells, extracellular matrix
      • and the basement membrane, often associated with fibrin deposition
      • Lobular Hypersegmentation of the normal lobular architecture of the normal
      • glomerular capillary tuft due to intracapillary hypercellularity or significant
      • mesangial expansions
      • Mesangiolysis Dissolution or attenuation of mesangial matrix and degeneration of
      • mesangial cells, often associated with glomerular capillary aneurysms
      • Mesangial 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 injury
      • Related to Structure
      • Hyalinosis Accumulation of glassy, refractile acellular material/plasmatic insudation
      • (PAS positive, methenamine-silver negative) which contains serum
      • proteins, other glycoproteins and lipids
      • Glomerular capillary collapse Retraction of glomerular tuft with closure of capillary lumina and
      • wrinkling and thickening of glomerular capillary walls
      • Glomerular 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 deposits
      • Tram-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 injury
      • Related to Cell proliferation
      • Mesangial 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 occlusion
      • Intracapillary hypercellularity Hypercellularity present in both mesangium and endocapillaries
      • Crescent 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 capsule
      • Membranoproliferative Glomerular capillary wall thickening due to mesangial
      • interposition and duplication of GMB
    • Descriptive terms and patterns of glomerular injury
      • Related to Deposits
      • Intramembranous Within the GBM
      • Mesangial Within the mesangial matrix
      • Subendothelial Between the GBM and the endothelium
      • Subepithelial/epimembranous Between the GBM and podocytes
      • Humps Subepithelial electron-dense immune-type deposits with
      • a cigar-or dome-like appearance
    • Descriptive terms and patterns of tubulointerstitial and vascular injury
      • Tubules
      • Tubulitis Lymphocytes or other inflammatory cells infiltrating tubular epithelium
      • Tubular atrophy Tubular involution/obsolescence due to ischemia, obstruction, toxic or
      • inflammatory injury with different LM appearances including classic
      • atrophy, endocrine and thyroidization changes
      • Tubular casts Various coagulated proteins and other elements in tubular lumens usually
      • but not exclusively seen in distal nephron
      • Hydropic degeneration/ Fine regular cytoplasmic vacuolization of the proximal tubules
      • Osmotic nephrosis
    • Descriptive terms and patterns of tubulointerstitial and vascular injury
      • Tubules
      • Hyaline droplet PAS/silver-positive protein reabsorption droplets because of increased
      • protein loss by glomeruli
      • Fatty 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 sections
      • Hypokalemic change Large irregular sized coarse clear vacuoles in the cytoplasm of tubular epithelial cells, especially the distal tubular cells
      • Intranuclear 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 injury
      • Interstitium
      • Edema Increased extracellular fluid in the interstitium resulting in increased spacing
      • between tubules
      • Interstitial foam cells Macrophages with cytoplasm lipid-containing vacuoles
      • Inflammation Infiltration of lymphocytes, plasma cells, and often eosinophils and
      • neutrophils with associated tubular injury
      • Fibrosis Interstitial expansion by collagen
      • Granuloma Collection of epithelioid histiocytes with/with out surrounding multinucleated
      • giant cells and lymphocytes
    • Descriptive terms and patterns of tubulointerstitial and vascular injury
      • Vessels
      • Intimal thickening Fibrous thickening of the intimal layer, usually in a concentric configuration
      • and associated with varying degrees of luminal stenosis
      • Hyaline 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 arterioles
      • Endothelialitis/endarteritis Infiltration of mononuclear cells under arterial and arteriolar
      • endothelium
      • Arteritis Necrosis, fibrinoid degeneration and inflammation of arteries with
      • leukocytoclasia and disruption of internal elastic lamina
      • Vasculitis Necrosis, fibrinoid degeneration and leukocytoclastic inflammation of
      • arteries, arterioles and veins
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    • Components of Native Kidney Biopsy Pathology Report
      • Light 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 Report
      • Immunofluorescence 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 Report
      • Electron 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 Report
      • Diagnosis
      • Including morphologic pattern plus a particular pathogenic or clinicopathologic category of the disease
      • Comment
      • Clinicopathologic correlation
      • List of differential diagnoses if necessary
      • Pertinent histologic prognostic indicators
      • Activity/chronicity indices of lupus nephritis
    • Components of Renal Transplant Biopsy Pathology Report
      • Light 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 Report
      • Immunofluorescence microscopy
      • C4d staining in peritubular capillaries
    • Components of Renal Transplant Biopsy Pathology Report
      • Electron microscopy
      • Glomerular abnormalities
      • Viral particles
      • Peritubular capillary basement membrane multilayering
    • Components of Renal Transplant Biopsy Pathology Report
      • Diagnosis
      • 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