Renal Pathology Flashcards
Compare 2 patterns of pathogenesis of glomerular injuries (HSR type, Model, IF pathology, examples)
Pathogenesis: type III; type II
Reflect by: Heymann model; Masugi model
IF: granular; linear
Diseases: most GN; Goodpasture syndrome
Aetiology of glomerulonephritis (2+3+3+1)
Primary:
- nephrotic: minimal change disease, membranous nephropathy
- nephritic: IgA nephropathy, post-Streptococcal GN, Rapidly progressive / Crescentic GN
Secondary:
- Diabetic nephropathy, Lupus nephritis, Amyloidosis
Hereditary: Alport syndrome
MC nephrotic syndrome in children
Minimal change disease
Which GN presents with selective proteinuria?
Minimal change disease
GN pathology: diffuse effacement of podocyte foot processes
Minimal change disease
Treatment for minimal change disease
Steroid
MC nephrotic syndrome in adults
Membranous nephropathy
Which autoAbs (2) are associated with membranous nephropathy?
autoAb against PLA2R, THSD7A
Secondary causes for membranous nephropathy (5)
Infection (e.g. HBV, HCV, syphilis, malaria)
Malignancy
Autoimmune
Drugs (e.g. ACEI, penicillamine)
Heavy metals
Pathology of membranous nephropathy (4)
LM: diffuse GBM thickening
IF: granular pattern
EM: subepithelial deposits, spike and dome pattern
MC detected immunoglobulin and complement in IF for GN
IgG, C3
Compare nephrotic and nephritic syndrome (pathogenesis, presentations (6 vs 5))
Pathogenesis: ↑ permeability to glomeruli to plasma protein v.s. inflammation of glomeruli –> capillary wall injury –> decrease GFR
Presentations
- Nephrotic: proteinuria (>3.5g/day), hypoalbuminaemia, generalised oedema, hyperlipidaemia, hypercaogulability, hypertension
- Nephritic: proteinuria (0.15~3.5g/day), haematuria, oliuria / azotaemia, hypertenion, oedma
Prognosis of membranous nephropathy
1/3 resolve, 1/3 persist, 1/3 progress
Timing of GN: post-streptococcal GN vs IgA nephropathy
Post-streptococcal GN: 1~4 weeks
IgA nephropathy: 1~2 days
Pathology of post-streptococcal GN (4)
LM: diffuse capillary proliferation, leukocytic infiltration
IF: granular pattern
EM: subepithelial “humps”
Prognosis of post-streptococcal GN
95% spontaneous recovery
MC nephritic syndrome
IgA nephropathy
Pathogenesis of IgA nephropathy
production of mutated GD-IgA, which is not degraded, after mucosal infection –> recognised as foreign antigens & autoAb form –> IC form & deposit in mesangium
What is Henoch-Schonlein Purpura (HSP)?
systemic syndrome involving IgA nephropathy, purpuric rash…
Pathology of IgA nephropathy
mesangial deposition of IgA
3 types of crescentic GN
- Anti-GBM Ab-mediated
- IC-mediated
- Pauci-immune type (associated with ANCA)
Presentations of Goodpasture disease
haemoptysis, acute renal failure
Antibodies in Goodpasture disease
anti-a3(IV)NC1
(Ag found in basement membrane of alveoli & glomeruli)
Management of Goodpasture disease (2)
plasma exchange
immunosuppression
Vasculitis associated with crescentic GN (2)
microscopic polyangiitis
granulomatosis with polyangiitis
Pathology of crescentic GN (2)
crescents (extracapillary proliferation)
ruptures in GBM
MC glomerulonephropathy
diabetic nephropathy
Pathogenesis of diabetic nephropathy
hyperglycaemia –> glycation of protein at efferent arterioles (hyaline arteriosclerosis) –> ↑ pressure of glomeruli –> GBM thickening, mesangial expansion –> losing anionic charge & podocyte damage –> albuminuria
Pathology of diabetic nephropathy (4)
- Diffuse GBM thickening
- Diffuse mesangial expansion
- Nodular mesangial sclerosis (Kimmelstiel-Wilson lesion)
- mesangiolysis
Pathogenesis of lupus nephritis
cell damage –> ↑ anti-nuclear Ab –> IC formation & deposition
Most severe form (also MC) of lupus nephritis
diffuse proliferative
Causes of diffuse proliferative GN (2)
lupus nephritis, post-streptococcal GN
Pathology of lupus nephritis
“full house” IC by IF
MC genetic mutation for Alport syndrome (hereditary pattern)
COL4α5 (X-linked)
Presentations of Alport syndrome (4)
- nephritis
- sensorineural deafness
- lens dislocation, cataract
Pathology findings in urine for nephrotic syndrome
fatty casts
GN pathology: GBM thickening (2)
membranous nephropathy, diabetic nephropathy
GN pathology: subepitheial deposits (2)
membranous nephropathy, post-streptococcal GN (subepithelial “humps”)
GN pathology: spike and dome pattern
membranous nephropathy
GN pathology: mesangial abnormalities
- IgA nephropathy (mesangial deposits)
- Diabetic nephropathy
GN pathology: rupture in GBM
crescentic GN
GN pathology: “basketweave”/ “bread crumb” appearance
Alport syndrome
GN pathology: splitting of lamina densa
Alport syndrome
Aetiology of tubulo-interstitial nephritis (1+2+2+3)
- Acute tubular necrosis
- Acute pyelonephritis, Kidney tuberculosis
- Drug-induced TIN, analgesic nephropathy
- Obstructive nephropathy, radiation nephropathy, renal transplant rejection
Pathology of acute tubular necrosis (1+3)
Gross: pale enlarged kidney
Histology:
- granular casts
- interstitial oedema
- necrosis
Pathology of acute pyelonephritis (2)
- enlarged kiney, with yellow abscesses on kidney surface
- neutrophil infiltrate in tubules and interstitium
Pathology of kidney TB (2)
- multiple cavities with yellow necrotic materials
- extensive caseous necrosis, granulomas
Examples of drugs inducing GN
penicillin, septrin, NSAIDs, thiazides, cimetidine…
Pathology of drug-induced GN (3)
- mononuclear cell infiltrate
- Type I HSR: eosinophils
- Type IV HSR: non-necrotizing granuloma