Renal Pathology

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Renal Pathology

Renal Pathology - How kidney biopsy tissue is processed and how common glomerular and tubulointerstitial patterns are interpreted.

Practical orientation: Integrate LM, IF and EM. No single modality is sufficient for many glomerular diseases.

Use first: clinical summary and algorithm.

Then: differential diagnosis, workup and management tables.

Escalate: use red flags and biopsy/urgent-care sections.

Clinical summary

Light microscopy

Pattern of injury, activity, chronicity and compartment involvement.

Immunofluorescence

Immune deposit type, location, complement, light-chain restriction and C4d.

Electron microscopy

Deposit location/structure, GBM changes, podocyte foot process effacement and ultrastructure.

Method	Tissue / stains	Main use
LM	Formalin-fixed tissue; H&E, PAS, JMS, trichrome.	Morphologic pattern and chronic scarring.
IF	Frozen tissue in transport medium; IgG, IgA, IgM, C3, C1q, fibrinogen, kappa/lambda.	Immune phenotype and deposit pattern.
EM	Glutaraldehyde-fixed tissue.	Ultrastructural confirmation.

Term	Meaning
Focal	<50% of glomeruli involved.
Diffuse	>50% of glomeruli involved.
Segmental	Part of a glomerulus involved.
Global	Whole glomerulus involved.
Mesangial proliferation	Increased mesangial cells/matrix.
Endocapillary proliferation	Capillary lumina occluded by leukocytes or swollen endothelial cells.
Crescent	Extracapillary proliferation, often with severe active injury.

Pattern	LM / IF / EM clues	Differential
Mesangial proliferative GN	Mesangial hypercellularity; mesangial deposits.	IgAN, lupus class II, resolving infection-related GN, C3G.
Endocapillary proliferative GN	Leukocytes/endothelial swelling; subendothelial +/- mesangial deposits.	Infection-related GN, lupus, cryoglobulinemic GN, PGNMID.
MPGN pattern	Hyperlobulated glomeruli, double contours, interposition.	Immune-complex MPGN, C3G, TMA mimics.
Crescentic GN	Cellular/fibrocellular/fibrous crescents; necrosis may be present.	Pauci-immune ANCA, anti-GBM, immune-complex GN.
FSGS	Segmental sclerosis; variants include collapsing, tip, cellular, perihilar and NOS.	Primary podocytopathy or secondary hyperfiltration/adaptive disease.
Membranous nephropathy	Granular capillary wall IgG/C3 with subepithelial deposits and spikes.	Primary PLA2R/THSD7A or secondary autoimmune/infection/malignancy/drugs.
TMA	Thrombi, endotheliosis, mesangiolysis, double contours, onion-skinning.	TTP/HUS, malignant HTN, scleroderma, APS, drugs, complement-mediated.

Disease	Clue
Cryoglobulinemic GN	MPGN/DPGN, intracapillary immune thrombi, annular-tubular deposits.
Immunotactoid GN	Parallel microtubules; often monoclonal IgG.
Fibrillary GN	Random fibrils, Congo red negative, DNAJB9 positive.
Light chain cast nephropathy	Hard fractured casts with light-chain restriction.
Light chain proximal tubulopathy	Proximal tubular crystals, often kappa restricted.
MIDD	Linear staining of renal basement membranes, granular deposits.
AL amyloidosis	Congo red positive fibrils, usually lambda more than kappa.
PGNMID	Monoclonal IgG subclass and light chain with proliferative GN.

Pattern	Clues
ATN	Tubular simplification, loss of brush border, casts, vacuolization.
AIN	Interstitial inflammation/edema and tubulitis; eosinophils suggest drug allergy.
IgG4-related TIN	Plasma cell-rich infiltrate, storiform fibrosis, IgG4-positive plasma cells.
Pyelonephritis	Neutrophilic tubulitis and neutrophil casts.

Pattern	Key concept
T-cell mediated rejection	Tubulitis, interstitial inflammation and/or intimal arteritis.
Antibody-mediated rejection	Tissue injury + antibody-endothelium interaction + donor-specific antibodies.
Chronic active rejection	Chronic tissue injury with ongoing immune activity.