RENAL PATHOLOGY

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The Medical Renal Biopsy Dr Kelvin St.Pierre-Robson


The Medical Renal Biopsy •

Diagnosis

• •

treatment and management

Degree of chronic damage

may guide prognosis beyond primary diagnosis



Systematic examination of different compartments

glomerulus

tubules

interstitium

blood vessels


Renal biopsy panel •

H&E x 2

Silver stain

PAS

Trichrome

Congo Red


Is this enough?

clinical features - do they correlate?

immunofluorescence or immunohistochemistry

electron microscopic findings


Renal biopsy IHC/IMF •

IgG

IgA

IgM

C9

C3

+/-C1q

Kappa

Lambda


Specific challenges

limited responses to injury

size of biopsy

identifying the primary lesion

• •

does the pathology effect more than one compartment

disease progression to end stage features


Renal disease may have similar clinical presentations

microalbuminuria

subnephrotic proteinuria

nephrotic proteinuria

asymptomatic haematuria

microhaematuria

hypertension

rapidly progressive GN

acute kidney injury

chronic renal faliure


Microalbuminuria

• •

20-200mg/l (spot check) or 30 -300mg/24hrs

Nephrotic syndrome

protein in the urine, low blood albumin, high blood lipids, and significant swelling

>3.5g per 1.73m2 per day

hypoalbuminaemia 2.5g/dl


Frequency of various diagnoses Nephrotic syndrome

FSGS

Membranous GN

Minimal change

Diabetic GN

Membranoproliferative GN type 1

Amyloidosis

C1q

Fibrillary GN


Frequency of various diagnoses •

Haematuria

Lupus nephritis

IgA nephropathy

Pauci immune GN

Post infectious GN

Thin basement membrane disease

Anti GBM disease


Frequency of various diagnoses •

Other GN that cause acute renal failure

Thrombotic microangiopathy

Acute TIN

Light chain cast nephropathy

That manifest as chronic renal failure

Arterionephrosclerosis


Definitions •

Focal

Diffuse

• •

involving all glomeruli

Segmental

• •

involving some glomeruli

involving part of a glomerular tuft

Global

involving total glomerular tuft





Definitions •

Crescent

• •

Spikes

proliferation of parietal epithelial cells (layer of 2 cells or more that partially or completely fill Bowman’s space)

Projections of glomerular basement membrane between subepithelial immune deposits

Endocapillary proliferation

Proliferation of mesangial and/or endothelial cells and infiltrating inflammatory cells filling up and distending capillary lumens






Definitions •

Tram track

• •

double contour of glomerular basement membrane due to deposits

Wire loop

thick, rigid appearance of capillary loop due to massive subendothelial deposits




Definitions •

Activity

• •

treatment sensitive lesions i.e. crescents, cellular infiltrate, necrosis, proliferation

Chronicity

probable irreversible lesions i.e. extent of tubular atrophy, interstitial fibrosis, fibrous crescents, sclerosis


Renal biopsy assessment •

Develop a structure to differential diagnosis

based on clinical presentation

• •

what might you be expecting

based on pattern of response

does this correlate with the clinical information


Report Structure

Useful to have headings (or not as you prefer)


Micro

Glomeruli

Tubules and Interstitium

Vessels

Immunohistochemistry/fluorescence

Electron microscopy

Comment

Conclusion


Case 1 •

66 yr old male

CKD, persistent haematuria

Reduced complement

?GN


Case 1



Case 1 •

IHC/IMF negative

What would you do next?

Why?


Case 1




Case 1

Diagnosis?

Normal biopsy, no pathology


Case 2 •

27 yr old female

Persistent proteinuria

ACR 124




IgG


Case 2 •

IgM, C9 and C3C similar

IgA also positive but less intense

Diagnosis?

What will you see on EM?


Case 2


Case 2

Diagnosis

Lupus nephropathy Class V



Case 3 •

48 yr old male

Nephrotic range proteinuria

Urinary ACR 450

Haematuria

CR 112

Nephrotic syndrome


Case 3





Case 3 diagnosis = Membranous GN •

Membranous nephropathy

Primary – Idiopathic (most common)

Secondary – Drugs, Infections and malignancy

Commonest presentation

Nephrotic syndrome

Haematuria +/-


Membranous • • • • • • • •

4 Stages Stage I - Normal light nicroscopy DIF – fine granular capillary wall IgG EM – Small subepithelial electron dense deposits and foot process effacement Stage II Diffuse thickening of the capillary wall Silver stains – spikes on the capillary wall (extensions of basement membrane in between the deposits)


Membranous • • • • • • • • •

DIF coarse granular IgG and C3 (most cases) EM Many subepithelial deposits Stage III Severe thickening of the basement membrane Silver staining lucent areas( holes in the basement membrane) EM- Subepithelial deposits covered by a new layer of basement membrane Stage IV Severe thickening of the basement membrane associated with segmental or global glomerulosclerosis. Intramembranous deposits some of which are electron lucent due to resorption.


Case 4 •

44 yr old male

AKI

Blood and protein in urine

Hypertension

Nephrotic range proteinuria





Case 4

What might your differential diagnosis be?


IgA






Case 4 •

What is your diagnosis?

Why?

Features favour a fibrillary GN.


Case 4 •

Fibrillary GN

Typically MPGN on light microscopy

Congo red negative

Smudgy IgG and C3

Randomly arranged fibrils on EM


Differential diagnosis of fibrils •

Fibrillary GN

• •

Immunotactoid GN

• •

Organised, parallel, microtubular (>30nm)

Amyloid

• •

Fibrils random, 12-24 nm (mostly 18-20nm)

Random, 8-15nm (mostly 10-12 nm)

Cryoglobulinamia

Microtubular or vague, short fibrillary




Case 5 •

64 yr old female

eGFR 20

Nephrotic range proteinuria

Rapid decline in renal function

ACR 600 +

ANA and ANCA negative




Case 5

What could be a differential diagnosis?

How would you resolve ?


Diagnoses to consider with a nodular pattern •

Amyloid

Light chain deposition disease

MPGN type 1 (and its diseases)

Diabetic nephropathy

Dense deposit disease

Fibrillary GN






Case 5 diagnosis = Amyloid •

• • • • • • •

Amyloid - important cause of nephrotic range proteinuria in the elderly group. May be the main presenting symptom Kidney – nodular glomerulosclerosis Frequently involves the blood vessels and interstitium. Glomerulus replaced by amorphous pink material Silver negative and PAS negative Sirius red and Congo red positive Early biopsy may be subtle and EM may be necessary for the diagnosis EM shows non branching fibrils


Case 6 •

54 yr old male

Raised BP

CR 174

ACR 581

ANA and ANCA -ve


Case 6





Case 6 diagnosis =Diabetic Glomerulosclerosis

Diabetic nephropathy almost always associated with retinopathy Presents commonly with nephrotic range proteinuria Characterstic lesions in kidney Diffuse and nodular glomerulosclerosis PAS positive, silver positive and congo red negative KW lesions, Capsular drop and Fibrin caps Afferent and Efferent arteriolar hyalinosis DIF – pseudolinear IgG EM – Thickened basement membranes




Case 7 •

60 yr old male

Renal impairment of unknown cause

Cr 168 eGFR 37

Gout on allopurinol

Urine dip 1+ protein and 4+ blood










Case 7 •

Diagnosis?

IgA nephropathy

May use Oxford Classification if your clinicians require


IgA disease Commonest glomerulonephritis Commonest presentation haematuria but variable Nephrotic range proteinuria to acute renal failure Variable histology from normal to crescentic glomerulonephritis DIF – Mesangial IgA and in most cases C3 EM – Mesangial, paramesangial and sometimes sub endothelial deposits


Haematuria • Common causes of isolated haematuria • IgA nephropathy • Thin membrane nephropathy • Common causes of nephritic syndrome • IgA nephropathy • Post infectious glomerulonephritis • Mesangiocapillary glomerulonephritis


Case 8 •

30 yr old female

Episode of frank haematuria

Rising creatinine now 167

Urine dip 3+ blood and 4+ protein

ACR 651

Negative ANA and ANCA




Case 8





Case 8

Diagnosis = Vasculitic IgA nephropathy


Crescents in GN •

Pauci immune GN

Anti GBM disease

FSGS

IgA/HSP

Lupus GN

Fibrillary GN


Case 9 •

72 yr old

Nephrotic range proteinuria

eGFR 27

ANCA positive

MPO and PR3 negative












Case 9

Diagnosis?

MPGN type 1


MPGN •

Diagnosis?

Or pattern?

What disease present with MPGN patterns?


MPGN Pattern Disease •

Primary MPGN type 1

Lupus

Fibrillary

Amyloid

Monoclonal immunoglobulin deposition disease

Dense deposit disease

Cryoglobulinaemia


Case 10 •

21 yr old male

AKI

Blood 3+

Protein 2+

Glucose 3+


Case 10






Case 10

Diagnosis = severe acute tubular interstitial nephritis


Acute Tubulointerstitial Nephritis

Renal failure

Drugs – NSAIDS, antibiotics and PPI Inhibitors

Presence of tubulitis

Interstitial Inflammation

Lymphocytes, Plasma cells and Eosinophils

TINU – TIN and Bilateral Uveitis

Sarcodosis – Granulomatous inflammation (case 27)


Case 11 •

78 yr old male

AKI

Cr 88-736

Urine dip 3+ blood, 1+ protein

PCR 93



Case 11

Diagnosis?

Granulomatous interstitial nephritis


Case 12 •

56 yr old male

Hypertension

CKD Cr 150

1month history NSAID and PPI

Cr now 390


Case 12


Case 12


Case 12


Case 12


Case 12

What clinical information are you going to seek?


Case 12

Diagnosis = Cast nephropathy


Cast Nephropathy •

Most common cause of Acute renal failure in Multiple Myeloma Patients.

Casts are rigid and fractured

Surrounded by desquamated epithelial cells

Can be associated with a foreign body giant cell reaction

Casts can be IgA positive


Classifications to be aware of

Lupus GN

Oxford classification of IgA


Lupus nephritis


Type I

Normal Lm few EM mesangial deposits

Type II

Mesangial proliferative nephritis

DIF- full house pattern in mesangium

EM – numerous mesangial deposits few sub endothelial deposits


Type III

Focal lupus nephritis (Less than 50% glomeruli)

Active/inactive, global/ segmental

Acute/chronic

IIIA,IIIA/C and IIIC

DIF - capillary wall and mesangium

EM – Few sub endothelial deposits


TypeIV

Diffuse lupus nephritis

(more than 50% of all glomeruli)

• • •

TypeIVS more than 50% of involved glomeruli segmental lesions TypeIVG more than 50% of involved glomeruli global lesions Segmental – less than half the glomerular tuft


Various combinations

TYPEIVS/A

TYPEIVG/A

TYPEIVS(A/C)

TYPEIV(S/C)

TYPEIVG(C)


DIF full house subendothelial and mostly mesangial

EM Large numbers of subendthelial deposits

Wire loop lesions and hyaline thrombi often seen

Type V

Membranous may be associated with different types


Lupus type II


Lupus typeII


Lupus typeIVS(A)


Lupus typeIVS(A)


Lupus typeIVS(A)


Lupus typeIVG(A)


Lupus typeIVG(A)


Lupus typeIVG(A)


Lupus typeIVG(A)


Lupus typeV


Lupus typeV


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