7. DISEASES OF GLOMERULI
DISEASES OF TUBULES
DISEASES OF INTERSTITIUM
DISEASES OF BLOOD VESSELS
8. AZOTEMIA –
--- GFR BUN,
UREMIA – Azotemia + Clinical signs and
symptoms + Biochemical abnormalities +
Involvement of
..
G I tract, Peripheral nerves
and heart;
9.
10.
11. DEFINITION
Abnormalites of glomerular funtion can be
caused by damage to the major components of the
glomerulus: Epithelium (podocytes), Basement
membrane, capillary endothelium, mesangium.
Damage manifested by an inflammatory process.
12.
13. a) hypercellularity:
i) cell proliferation of mesangial cells or
endothelial cells
ii) leukocyte infiltration (neutrophils,
monocytes and sometimes lymphocytes)
iii) formation of crescents
- epithelial cell proliferation (from
immune/inflammatory injury)
- fibrin thought to elicit this injury
(TNF, IL-1, IFN- are others)
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14. c) hyalinization (hyalinosis) and sclerosis
-accumulation of material that is
eosinophilic and homogeneous
- obliterates capillary lumen of glomerulus
(sclerotic feature)
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15. a) diffuse (all glomeruli)
b) global (entire glomerulus)
c) focal (portion of glomeruli)
d) segmental (part of each
glomerulus)
e) mesangial (affecting mesangial
region)
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16. Most are of
immunologic origin, and
caused by immune
complexes !
• metabolic
stress: DN
• mechanical
stress:
• hypertension
19. a) 2 forms of Ab-associated injury
i) injury resulting from soluble
Ag-Ab deposits in glomerulus
ii) injury from Ab reacting in-situ
with glomerulus
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20. • In Situ Immune Complex Deposition
a) Ab act directly with intrinsic
tissue Ag “planted” in the
glomerulus from the circulation
b) 2 forms of Ab-mediated
glomerular injury
i) anti-GBM Ab-induced nephritis
- Ab directed against fixed Ag
in
ii) Heymann nephritis
- a form of membranous GN
- Ab bind along GBM in
“granular pattern”
29. Common form of GN in developing countries.
6 to 10yrs of age
1 - 4 weeks after a streptococcal infection of pharynx
or skin (Impetigo)
GroupA β-haemolytic streptococci - types 12, 4, 1
Immunologically mediated disease
Immune Complex mediated
Anti - endostreptosin & other cationic antigens .
Serum – C
30. Glomeruli-
Enlarged , hypercellular glomeruli
- proliferation of endothelial & mesangial
cells,
- crescent formation (severe cases)
- obliteration of capillary lumen
Fibrin deposition in capillary lumen &
mesangium.
Interstitial edema and leucocytic infiltration
Tubules contain red cell casinfiltration by
leukocytes
Diffuse
40. Severe glomerular injury
Does not denote a specific etiologic form
of GN
Clinically - rapid & progressive loss of
renal function & death within weeks to
months
Crescents in most glomeruli – parietal
epithelial cells proliferation;
41. Type - I RPGN ( Anti-GBM antibody
induced disease)
.. Idiopathic,
.. Goodpasture syndrome;
Type - II RPGN (immune Complex)
.. Idiopathic, postinfecious, SLE,
Henoch-Schonlein purpura (IgA), others;
Type - III RPGN ( Pauci-immune )
.. ANCA associated, Idiopathic,
Wagener granulomatosis, PAN;
42. Linear deposits of IgG , C3 in GBM
Cross reaction with pulmonary
alveolar BM
Good - Pasture’s antigen located in
noncollagenous portion of α3
domain of collagen type - IV
43. Immune complex mediated disease
Complication of immune complex
nephritides
- Post infectious GN , SLE , IgA
nephropathy
Granular deposit of immune
complexess of IgG and C3 along
glomerular capillary walls.
IF - lumpy bumpy granular pattern
44. Lack of anti GBM antibody ,
immune complexesby IF ,
EM
ANCA present- defect in humoral
immunity.
Usually a component of systemic
vasculitis - Wegeners Granulomatosis
, Polyarteritis
Idiopathic
45. Gross :
Kidneys enlarged , pale ,smooth
outer surface.
C/S petechial hemorrhages on
cortical surface
46. Crescents
proliferation of parietal cells migration
of monocytes ,macrophages into
Bowmans space
Crescents obliterate Bowman’s
space , compress
glomerular tuft
Fibrin strands are prominent between
cellular layers in the cresents.
47.
48.
49. Crescents Sclerosis
EM : subepithelial deposits
ruptures in GBM
IF : Postinfectious cases -
granular
Good Pastures syndrome -
linear Idiopathic - granular
/ linear
55. Latent GN
(asymptomatic
urinary
abnormalities)
Acute GN RPGN Chronic GN
Macroscopic
hematuria
Proteinuria
Dysmorphic
Glomerular
erythrocytes
Hyperlipidemia
Edema
microscopic or
Proteinuria>3.5g/d
Hematuria
(1-3g/d)
ARF
Edema
•Rapidly
renal function
•Hematuria,
Proteinuria
Hypertension• oliguria or
Red cell castsanuria
Red cell casts
•With or
without
systemic
symptom
•Hematuria
Hypoalbuminemia
Proteinuria deterioration of Proteinuria
•Hypertens
on
•Reduced
GFR
