2. Amyloidosis Kidney
Amyloidosis is extracellular deposition of fibrillar
protein amyloid in different organs
G/A The kidneys may appear normal, enlarged
Terminally contracted due to ischaemic effect of
narrowing of vascular lumina.
The cut surface is pale, waxy and translucent
3. The kidney is small and pale in colour. Sectioned surface shows loss of corticomedullary
distinction (arrow) and pale, waxy translucency.
4.
5. M/E
◦ The amyloid is seen as amorphous, eosinophilic, hyaline
extracellular material. It is deposited mainly in the
glomeruli, initially on the glomerular basement memb-
rane but later extends to produce luminal narrowing and
distortion of the glomerular capillary tuft.
◦ The amyloid deposits in the tubules begin close to the
tubular epithelial basement membrane. Subsequently, the
deposits may produce degenerative changes in the
tubular epithelial cells
6. ◦The walls of small arteries and arterioles in
the interstitium of the kidney are narrowed
due to amyloid deposit.
◦Congo red staining imparts pink or red
colour to the amyloid when seen in
ordinary light but demonstrates green
when viewed under polarising microscopy .
7. Amyloidosis of kidney. The amyloid deposits are seen mainly in the glomerular capillary tuft.
The deposits are also present in peritubular in the interstitium producing luminal narrowing.
8.
9. Kidney infarct ( Coagulative
necrosis)
Coagulative necrosis is the most common type of
necrosis caused by irreversible cessation of blood
supply or ischaemia (infarction).
G/A Renal infarcts are often multiple and may be
bilateral. Characteristically, they are pale or
anaemic and wedge-shaped
10. The wedge-shaped infarct is
slightly depressed on the
surface.
The apex lies internally and
wide base is on the surface.
The central area is pale while
the margin is haemorrhagic.
11. Coagulative necrosis in infarct kidney.
intensely eosinophilic The nuclei show
granular debris.
12. M/E
The hallmark of coagulative necrosis kidney is that
architectural outlines of glomeruli and tubules may
be preserved though all cellular details are lost.
The margin of infarct shows inflammatory reaction,
initially by polymorphonuclear cells but later
macro- phages, lymphocytes and fibrous tissue
predominate