Glomerular Pathology

Question 1

Pathology of bowmans capsule

Answer 1

Filter can block -> renal failure, decreased GFR

Filter can leak -> proteinuria, haematuria

• Subepithelial (podocytes damaged)
• within GBM
• subendothelial (lining)
• mesangial and paramesangial

Question 2

Proteinuria/ nephrotic syndrome - site of injury, common primary and secondary causes

Answer 2

Podocyte/ subepithelial damage/ GBM

Primary:

• minimal change glomerulonephritis
• focal segmental glomerulosclerosis
• membranous glomerulonephritis

Secondary:

• diabetes mellitus
• Ct diseases (e.g. systemic lupus Erythematosus)

Question 3

What is minimal change glomerulonephritis? who’s most likely to get it, treatment, cause

Answer 3

causes proteinuria/ nephrotic syndrome

Childhood/ adolescence
Incidence reduces with increasing age

Responds to steroids (turn off immune system) - long term
May recur
Usually no progression to renal failure
Slide 13

Unknown blood circulating factor damaging podocytes, no immune complex deposition

Podocyte pathogenesis ranges from steroid- responsive minimal change disease to devastating focal segmental glomerulosclerosis

Question 4

what is the spectrum of FSGS?

Answer 4

Podocyte pathogenesis ranges from steroid- responsive minimal change disease to devastating focal segmental glomerulosclerosis

Question 5

What is focal segmental glomerulosclerosis? Treatment, cause, who gets it, what Can it lead to?

Answer 5

Nephrotic 
Adults
Less responsive to steroids 
Direct scarring of glomerulus 
Progressive to renal failure 
From minimal change glomerulonephritis 

✅renal transplant, dialysis

Question 6

What’s the commonest cause of primary nephrotic syndrome in adults? Prognosis? Cause? Histopathology, diagnosis

Answer 6

Membranous glomerulonephritis - 1/3 recover completely, 1/3 LT treatment, 1/3 progress renal failure

Immune complex deposits (antibody/ antigen) -> complement activation -> podocytes damage attached by IgG

May be secondary (associated with other diseases e.g. lymphoma)

Thicker capillary loops, spiked podocytes slide 17

Autoimmune- PLA2-R antigen blood test

Question 7

What is diabetic nephropathy? Progression, histopathology

Answer 7

Overt diabetic nephropathy - had diabetes for around 8-15yrs

Hyperinfiltration + increased GFR -> microalbuminuria (special dipstick) -> after 7yrs overt proteinuria + decrease GFR -> often ES Renal disease

Thickening of BM and mesangial expansion, nodule formation (kimmelsteil- Wilson nodules), glomerulosclerosis, hyalinization of arterioles

Secondary cause of nephrotic syndrome

Question 8

Haematuria/ neohrITIC syndrome - site of injury, cause, histopathology

Answer 8

Glomerular capillary loop/ supporting structures - IgA nephropathy - Thin glomerular BM disease/ hereditary nephropathy (Alport)

Or endothelium/ blocks glomerulus, vasculitis, goodpasture syndrome, anti-GBM disease (rare, systemic)

Question 9

What’s the most common cause of glomerulonephritis? Prognosis, treatment

Answer 9

IgA nephropathy

Any age
(Non)Visible haematuria
Relationship with mucosal infections e.g. recent cold
+/- proteinuria
Significant proportion progress Renal failure
No effective treatment

Question 10

What are two hereditary neohropathies?

Answer 10

thin GBM nephropathy:
- benign familial nephropathy, isolated haematuria

alport x-linked, abnormal collagen 4, associated with deafness, abnormal appearing GBM, progresses to renal failure, abnormally split and laminated GBM

Question 11

What is vasculitis?

Answer 11

Group of systemic disorders, no immune complex/ antibody deposition, association with anti neutrophil cytoplasmic antibody, nephritic presentation

BM blown apart form inflammation, segmental necrosis, crescent slide 30

Treatable if caught early (can turn catastrophic v quickly) ✅immunosuppression

Urgent biopsy service