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Kidney (Part 1)
Kidney (Part 1)
Kidney (Part 1)
NEPHRITIC SYNDROME
• A clinical entity caused by glomerular dse.
• Acute onset of either grossly visible hematuria or microscopic
hematuria w/ dysmorphic red cells and red casts on U/A
Ø Diminished GFR; mild to moderate proteinuria, HTN
NEPHOROTIC SYNDROME
• d/t glomerular dse
• Characterized by heavy proteinuria (3.5gm/day);
hypoalbuminemia, severe edema, hyperlipidemia, lipiduria
TUMORS
• Anatomic location & nature of the lesion
NEPHROLITHIASIS
• Manifested by spasms of severe pain (renal colic) & hematuria
GLOMERULUS
Filtering membrane:
✓ In b/w the capillaries there is a thin ✓ Capillary loops cannot be appreciated well
HYALINOSIS
• Accumulation of material that is homogenous and eosinophilic
by light microscopy
• A consequence of endothelial or capillary wall injury & typically
the result of various forms of glomerular damage
Hyalinosis
Normal Glomerulus Affected Glomerulus
SCLEROSIS
• Deposition of extracellular collagenous matrix confined either in
the mesangial areas or involve the capillary loops or both
• Sclerosis process may result to obliteration of some or all of the
capillary lumens in the affected glomeruli
Sclerosis
Normal Glomerulus Affected Glomerulus
DISEASES CAUSED BY IN SITU Immune complexes are formed locally by antibodies that react w/
FORMATION OF IMMUNE intrinsic tissue antigen or w/ extrinsic antigens “planted” in the
COMPLEXES glomerulus from the circulation
• The deposited circulating immune complex in the glomerulus
initiate complement or Fc receptor mediate leukocyte activation
à glomerular injury
HEYMANN NEPHRITIS
• Experimental membranous nephropathy in rats
• Localized immune rxn is induced by immunizing rats w/ an
antigen w/c is now known as megalin present in the epithelial
cell foot processes
• In humans, the known antigen is M-type phospholipase α2
receptor
• Rxn of Ab w/ Ag produce immune complex deposits along the
subepithelial aspects of the BM
Immunofluorescence microscopy:
• Pattern of immune deposits: Granular (reflective of the very
localized Ab-Ab interaction)
ANTIBODIES AGAINST PLANTED Ab’s can react in situ w/ Ag’s that are not normally present in the
ANTIGEN glomerulus but are “planted” there
• Planted Ag can be cationic molecules binding to anionic
molecules of the glomerulus
• DNA bacterial products w/c are deposited in the mesangium b/c
of their large size
Ø Ex. Infants fed w/ cow’s milk
DISEASES CAUSED BY Ab Ab bind to intrinsic Ag homogenously distributed along the entire length
DIRECTED AGAINST NOMRAL of the GBM
COMPONENTS OF THE GBM
GOODPASTURES SYNDROME
• Anti-GBM Ab are produced in response to a normal component
of the GBM w/c is a non-collagenous domain of a3 chain of
collagen type IV
MECHANISMS OF GLOMERULAR Immune complexes elicit a local inflammatory rxn that produces injury
INJURY FOLLOWING IMMUNE (1) Binding of complement
COMPLEX FORMATION (2) Engagement of Fc receptors (WBC, mesangial cells) as
mediators
Proof of GN in humans
• Lacking
sometimes detachment of epithelial cells and protein leakage through defective glomerular
basement membrane and filtration slits.
MECHANISMS OF PROGRESSION Once any renal disease, glomerular, or otherwise, destroys fxning
IN GLOMERUAL DISEASES nephrons & reduces the GFR to about 30-50% of normal, progression to
ESRF proceeds at a steady rate, independent of the original stimulus or
activity of the underlying disease
TUBULOINTERSTITIAL FIBROSIS
• Tubulointerstitial injury, manifested by tubular damage and
intersitial inflammation, is a component of many acute & chronic
glomerulonephritides
Poststreptococcal GN
• A prototypical glomerual disease of immune complex etiology
Morphology
• Glomeruli: enlarged, hypercellular
Laboratory Findings
• Increased antistreptococcal antibody titers
• Decreased serum C3
MEMBRANOUS NEUROPATHY
• Characterized by diffuse thickening of the glomerual capillary
wall d/t the accumulation of deposists containing Ig along the
subepithelial side of the BM
FOCAL SEGMENTAL
GLOMERULOSCLEROSIS
• Hypercellular – d/t E
• GBM thickening – double
contour track appearance
d/t duplication or splitting
of BM
• Lobular architecture
TYPE I
• Subendothelial deposists
TYPE II
• Intramembranous deposits
HEREDITARY NEPHRITIS
A group of heterogenous familial renal diseases assocaited w/ mutations
in collagen genes that manifest primarily w/ glomerual injury
• X-linked inheritance
• Autosomal inheritance
CHRONIC GLOMERULONEPHRITIS
End-stage glomerular disease that may result from specific types of GN
or may develop w/o antecedent history of any of the well recognized
forms of acute GN
Microscopic findings