Nephritic/Nephrotic

Question 1

PSGN

Answer 1

• 2-4 weeks after strep infection (pharyngitis or skin e.g. impetigo; stem might not mention it though b/c people forget) regardless of penicillin use
• Resolve in children; risk of chronic renal insufficiency in adults
• Edema (periorbital) + cola-colored urine
• Glomeruli hypercellular and enlarged; subepithelial deposits (type III HSR)
• Granular IF d/t IgG, IgM, C3 deposits (serum C3 consumptively decr.)

Question 2

Rapidly Progressive (“crescentic”) Glomerulonephritis

Answer 2

This describes a pattern, caused by several diseases:
- Linear IF: Goodpasture’s (type II HSR, but UWorld says “deposits” of IgG, C3)
- Pauci-immune (negative) IF: the ANCA vasculitides (GPA, EGPA, microscopic polyangiitis)
- Granular IF: PSGN, DPGN (e.g. SLE), IgA nephropathy and Henoch-Schonlein purpura
NB: crescents are made of fibrin and C3, even though C3 isn’t decr. for pauci-immune

Question 3

Diffuse Proliferative Glomerulonephritis

Answer 3

“Diffuse-us wire Lupus” (associated w/ SLE; wire looping of capillaries):

• Most. Common. Renal. Disease. In. SLE.
• Nephritic + nephrotic concurrently (like MPGN)
• IF is granular: subendothelial, sometimes subepithelial or intramembranous deposits (IgG, C3, “DNA and anti-DNA”)
• “May complicate acute endocarditis”

Question 4

IgA nephropathy

Answer 4

• Renal pathology of HSP but doesn’t require triad
• Often occurs (hematuria) with URI, GI illness (but not necessary)
• Mesangial proliferation/IgA deposits in mesangium
• Doesn’t alter complement (contrast w/ other nephritic/nephrotic syndromes)

Question 5

Alport syndrome

Answer 5

“Can’t pee, can’t see, can’t hear a bee”

• Can’t pee is really just glomerulonephritis
• Mutation in type IV (BM) collagen leads to thinning and splitting of basement membrane
• “Basket-weave” appearance d/t thickening of GBM
• X-linked dominant

Question 6

Membrano-Proliferative Glomerulonephritis

Answer 6

• Nephritic + nephrotic concurrently (like DPGN)
• Type I: hep B, C, or idiopathic; subendothelial deposits
• Type II: assocaited with C3 nephritic factor (autoantibody that stabilizes C3 convertase leading to persistent complement activation and decr. C3); intramembranous deposits
• Both: GBM splitting leads to “tram track” appearance

Question 7

Minimal Change Disease

Answer 7

• Most common cause of nephrotic syndrome in children
• 4 I’s: Idiopathic, Infection, Immunization, Immune stimulus (this can even be NSAIDs, or atopy)
• Normal glomeruli on LM (just a loss of charge barrier leading to selective proteinuria)
• Podocyte effacement on EM

Question 8

FSGS

Answer 8

• Most common nephrotic syndrome in AA and hispanics
• If not idiopathic, secondary to HIV, heroin, Sickle Cell, obesity
• LM - focal/segmental sclerosis; EM - podocyte effacement (like MCD); IF variable (don’t worry about it)

Question 9

Membranous nephropathy (= membranous glomerulonephritis)

Answer 9

• Most common nephrotic syndrome in caucasian adults
• Still 1o antibodies to PLA2 receptor
• Still 2o drugs (NSAIDs, penicillamine, gold), HBC, HCV, SLE, solid tumors
• But also: GBM thickening; IC deposits (granular IF) = “spike and dome” one

Question 10

Amyloidosis

Answer 10

• Kidney is most commonly involve organ in amyloidosis

- Deposits in mesangium (still apple green birefringence)

Question 11

Diabetic Glomerulonephropathy

Answer 11

Non-enzymatic glycosylation of basement membrane in glomeruli causes hyaline arteriolosclerosis, leading to hyperfiltration, and ultimately mesangial sclerosis (Kimmelsteil-Wilson nodules)