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Biopsy findings12 December 2012
18:33
1: Immune deposits in glomeruli can be seen on LM,
as they are large and are widespread.
On LM, the deposits have a glassy, hyper eosinophilic,
on H &E.
With special stains :
STAIN DEPOSIT MESANGIUM
& BM
Tichrome Red
(fuchsinophilic)
Blue
Jones
methenamine
silver
Pink Black
Methenamine
silver + Masson
Ponceau stain
Red Black
Jones methenamine silver
Sites of immune deposits:1. Mesangium common: all classes2. Subendothelial : class 3 & 4 Wire loops: deposits large enough to
completely involve the peripheral
circumference of the glomerular capillary-
produce a rigid, refractile thickening of the
glomerular capillary wall in hematoxylin-eosin
stained sections
Lupus nephritis class IV. Glomerular capillary walls are
segmentally thickened by wire-loop deposits. An
intraluminal deposit forms a hyaline thrombus in one
capillary, and there is global endocapillary
proliferation.
Lupus nephritis class IV. PAS stain highlights the
thickening of the glomerular capillary walls by
numerous subendothelial deposits.
3. regularly distributedsub epithelial deposits arethe defining feature of membranous lupus
nephritis class V
4. Intracapillary: hyaline thrombi. Class 3 & 4.misnomer, as they are not fibrin thrombi.
Composition similar to subendothelial immune
deposit. actually in continuity with large
subendothelial deposits in a deeper plane of
section. Common in class 4, particularly with
extensive wire loops. Also have exuberant
endocap proliferation.
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Differentiating from fibrin:
a. special stains for fibrin: modified Fraser Lendrum stain -- more sensitive
and specific phosphotungstic acid hematoxylin [PTAH] stain--
less sensitiveb. On H&E:
Fibrin Darkly eosinophilicfibrillar appearance
Hyaline
thrombi
Lightly eosinophilic, homogenous
glassy smooth structure.
Significance of hyaline thrombi:
a: severe disease
b: associated APLA syndrome.
Jones methenamine stain
Massons trichrome stain
2: Mesangial & endocapillary proliferation:
Response to immunedeposits in above areas.
Poor correlation between size & extent of mesangial
immune deposit and degree of mesangial
proliferation.
Endocapillary proliferation:
proliferation of endothelial cells & mesangialcells together with infiltrating PMN-->
narrows/occludes glomerular capillary lumen.
Focal and segmental or diffuse and global. LM identifies only PMN. IHC & EM identifies
other cells also. Good correlation between extent of immune
deposit, complement activation and
proliferative response. No direct correlation between proliferative
response and renal function. On the other hand, the number of macrophages
(as well as tubular macrophages) in a second
renal biopsy taken 6 months following therapy
has been found to correlate well with outcome
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3: Necroses:
Feature of class 3 and 4 LN only. Focus of smudgy fibrinoid obliteration of the
glomerular tuft, which is often associated with
any or all of the following:
deposition of intracapillary fibrin, glomerular basement membrane rupture
or gap formation, and
apoptosis of infiltrating neutrophilsforming pyknotic or karyorrhectic nuclear
debris
Usually segmental, but >1 glomerular lobulemay be involved.
Cellular crescents frequently directly overlie theaffected lobule.
Correlates with low serum CH50 levels, andmore severe proteinuria.
Jones methenamine silver stain of BM:
segmental rupture of BM.
4: Hematoxylin bodies:
Common in necrotising lesions the only truly pathognomonic lesion in lupus
nephritis Extremely uncommon, 2% biopsy specimen
from lupus patients. rounded, smudgy, lilac-staining structures that
are generally smaller than normal nuclei
Isolated or clustered., with indistinct borders. Hematoxylin bodies are the tissue equivalent of
the LE body and consist of naked nuclei whose
chromatin has been altered by binding to ANA,
probably after exposure of the nuclei to theambient circulation in the course of individual
cell death in necrotizing lesions. Owing to their
nuclear origin, they are Feulgen positive. Difference from pyknosis:
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Hematoxylin body Indistinct border Iliac hyaline coloration
Pyknosis Smaller , darkly basophilic
5: Cellular crescents
In class 3 & 4 active LN only.
Definition: aggregates comprising two or morelayers of proliferating visceral and parietal
epithelial cells with infiltrating mononuclearcells lining one fourth or more of the interior
circumference of Bowman's capsule.
TUBULES & INTERSTITIUM:
Changes common in class 4, followed by 3
Less common in class 5.
Least in class 1 &2.
Lesions can be acute or chronic. Due to inflammatory
process or edema.
a: pts with nephrotic range proteinuria : In PCT:
intracytoplasmic lipid resorptiondroplets, appearing as clear
vacuoles in H&E.
Protein resorption droplets :eosinophilic & strongly PAS positive
& trichrome red. Referred to as hyaline
degeneration. Interstitial foam cells in few cases.
Active tubulointerstitial lesions : in class 4 & 3. infiltrate of mononuclear leucocytes, L,M,
plasma cells present along with edema.
Neutrophils and eosinophils are rare. Sometimes, lymphocytic infiltration of
tubules (= tubulitis +) and tubular
epithelial degenerative and regenerative
changes +. Rarely, hematoxylin bodies ingested by
neutrophils are identified in tubular
lumens
Casts of neutrophils, erythrocytes, andshed tubular epithelial cells are readilyidentified in active class III or IV lupus
nephritis Intratubular oval fat bodies consisting of
lipid-laden desquamated epithelial cells
are most common in cases with severe
nephrotic proteinuria Immune deposits : seen in
Tubular basement membrane, any part. Interstitial capillary BM : specific Interstitial collagen.
VASCULAR LESION IN LUPUS NEPHRITIS:
Arteriosclerosis and arteriolosclerosis Uncomplicated vascular immune deposits Noninflammatory necrotizing vasculopathy (so-
called lupus vasculopathy) Thrombotic microangiopathy
o Associated with HUS/TTP syndromeo Associated with antiphospholipid
antibodieso Associated with scleroderma/mixed
connective tissue disease Necrotizing vasculitis (PAN type)
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associated with a higher rate of progression to renal
failure.
Uncomplicated Vascular Immune Deposits :
most common renal vascular lesion immune complex deposition in the walls of
small arteries and arterioles The affected vessels usually appear normal by
light microscopy Diagnosis requires the demonstration of
granular deposits of immunoglobulin (IgG, IgM,
and IgA in various combinations), often
associated with C1q or C3
most common in the more active proliferativeclasses
usually clinically silent, and they have not beenfound to confer a higher risk of hypertension or
progressive renal disease.Noninflammatory necrotizing vasculopathy: Less common. affects predominantly preglomerular arterioles ,
interlobular arteries (less common). Vessels narrowed, sometimes occluded by
abundant intimal and luminal deposits of glassy
eosinophilic material that may extend into the
media
This mterial is red on trichrome stain; showsfocal reactivity for fibrin on lendrum and PTAH
stain. Endothelium is swollen/denuded Degeneration and loss od myocytes, no
inflammatory infiltration of the vessel wall. IF: variable deposition of Ig, complements,
antigens combined processes of vascular immune
deposition and intravascular coagulation
contribute to their morphogenesis.
Severe HTN common in these pts, acceleratesthe vascuolopathy; carries ominous prognosis
H&E stain and lendrum stain of lupus
vasculopathy.