ABSTRACT
BILE DUCT INFLAMMATION/DAMAGE
●● Minority of ducts cuffed by inflammatory cells, mild epithelial reactive changes = 1
●● Majority of ducts cuffed by inflammatory cells, moderate epithelial degenerative changes = 2
●● All the ducts with marked inflammation, degenerative changes, focal luminal disruption = 3
VENOUS ENDOTHELIAL INFLAMMATION
●● Sub-endothelial lymphocytic infiltration involving some of the hepatic/portal veins = 1
●● Sub-endothelial lymphocytic infiltration involving most of the hepatic/portal veins = 2
●● As in sub-endothelial lymphocytic infiltration involving most of the hepatic/portal veins, with moderate to severe perivenular inflammation and perivenular hepatocyte necrosis = 3
1. Normal 2. Antibody-mediated rejection: C4d deposition,
acute antibody mediated, chronic active antibody mediated
3. Borderline changes: “Suspicious” for acute T-cell-mediated rejection
stitial infiltration (>25% of parenchyma affected, i2 or i3) and foci of moderate tubulitis (t2)
●❑ Type IB: Cases with significant interstitial infiltration (>25% of parenchyma affected, i2 or i3) and foci of severe tubulitis (t3)
●❑ Type IIA: Cases with mild to moderate intimal arteritis (v1)
●❑ Type IIB: Cases with severe intimal arteritis comprising >25% of luminal area (v2)
●❑ Type III: Cases with “transmural” arteritis or arterial fibrinoid change and necrosis of medial smooth muscle cells with accompanying lymphocytic inflammation (v3)
Chronic active T-cell-mediated rejection ●❑ “Chronic allograft arteriopathy” (arte-
rial intimal fibrosis with mononuclear cell infiltration in fibrosis, formation of neo-intima)
5. Interstitial fibrosis and tubular atrophy: No evidence of any specific etiology
●● Grade I: Mild interstitial fibrosis and tubular atrophy (<25% of cortical area)
●● Grade II: Moderate interstitial fibrosis and tubular atrophy (26%–50% of cortical area)
●● Grade III: Severe interstitial fibrosis and tubular atrophy/loss (>50% of cortical area)
6. Other: Changes not considered to be due to rejection
Quantitative criteria for mononuclear cell interstitial inflammation
●● ti0: No or trivial interstitial inflammation (<10% of parenchyma)
●● Stage 1: Tumor confined to kidney parenchyma and completely resected. Renal capsule intact and not penetrated by tumor. No
involvement of vessels of renal sinuses. No biopsy before surgery
●● Stage 2: Tumor extends beyond renal parenchyma but is completely resected. Resection margin uninvolved by the tumor. Tumor penetration of the renal capsule into vessels of the renal sinus including renal vein. No biopsy before surgery
●● Stage 3: Residual non-hematogenous tumor confined to abdomen. Tumor in abdominal nodes, tumor spillage invo lving parenchyma, peripheral implants, tumor involvement of resection margins. Includes the cases in which a biopsy of the tumor was done before surgery
●● Stage 4: Hematogenous metastasis or nodal deposits outside abdomen
●● Stage 5: Bilateral renal tumor (substage should be for each side)
●● Components; laser light source, series of prisms and filters for emitted light, computer driven including analytical system software
●● Forward angle light scatter (FALS) relates to cell size (light collected along axis of laser beam)
●● Side scatter (SS) relates to internal cellular characteristics such as nuclear complexity or cytoplasmic granularity (light collected at 90 degree angle to beam axis)
face and cytoplasmic antigens utilized in different combinations to assign cell lineage, detect aberrant antigenic profiles and detect clonality
●● Antibodies are conjugated to different fluorochromes which emit light at different wavelength
●● Several antibodies linked to different dyes utilized to stain cells of interest and study antigens associated with cells of interest fluorochromes
●● CD45 antigen density versus side scatter utilized for initial gating strategy, then cells
interest to diagnose disease process, useful for detection of recurrent/residual neoplastic cell populations including minimal residual disease
●● Beckwith-Wiedemann syndrome: CDKN1C/ NSDI
