SM 208: Nephrosis

Question 1

What is renal ablation?

Answer 1

Progressive out of control injury to parenchyma arising from attempts to control injury
Compensation starts accelerating renal failure
Renal loss = increases SNGFR = residual glomerular hypertrophy = decreased renal function = more renal loss

Question 2

Minimal Change Disease

Population, CC, Biopsy, Tx

Answer 2

Pop: young kids after URI
CC: edema
LM/FM: normal
EM: effacement of podocyte foot processes
TX: corticosteroids

Question 3

FSGS

Population, Etiology, Biopsy, Tx

Answer 3

NOT disease, but a PATTERN
shows partial scarring of some gloms
Pop: adults
Etiology: most primary, 2/2 drugs, HIV, other diseases, rarely genetic
LM: FSGS
FM: non-specific due to underlying disease
EM: loss of foot processes + podocyte attachment
TX: most non-responsive to steroids with worse prognosis

Question 4

Membranous Nephropathy

Population, Cause, Biopsy

Answer 4

Pop: Adults with slowly progressive renal failure
Cause: 2/2 lupus, Hep B/C, drugs, idiopathic
LM: diffuse capillary wall thickening (WIRE-LOOP)
FM: variable - granular deposits of C3/IgG
EM: subendothelial deposits along GBM containing IgG imparting “SPIKE-AND-DOME” pattern (dense dark deposits surrounded by lighter normal GBM)

Question 5

Membranoproliferative GN

Biopsy, Cause

Answer 5

LM: hypercellularity with pronounced lobulation; “TRAM TRACKS” on Silver Stain
FM: C3/IgG positive, or C3 positive
EM: variable deposits (usually subendothelial)

Cause: Hep C! or other systemic disease

Question 6

Diabetic Nephropathy

Biopsy

Answer 6

KIMMELSTEIL-WILSON NODULES (pink, hyaline nodules in glom)

Diffuse GBM thickening causing proteinuria (sometimes nephrotic range)

Question 7

Chronic Glomerulonephritis

Population, Cause, Biopsy

Answer 7

Pop: End-stage renal disease patients
Cause: difficult to pinpoint underlying disease
LM: diffuse sclerosis of most gloms, interstitial fibrosis + inflammation (lymphocyte and fibroblasts), tubular atrophy (weak thin walls with dense secretions)

Question 8

Tubulointerstitial Nephritis
(Cause)

Answer 8

Infectious: Acute (UTI/hematogenous spread)
Chronic/Reflux Nephropathy (bladder blackflow increases infectious risk

Non-infectious: drug-induced, ischemic, metabolic derangements, physical damage

Question 9

Pathogenesis of TIN: Analgesis-Induced Nephropathy

Answer 9

Long-term large dose analgesic patients/ppl (acetaminophin, aspirin, caffeine, codeine)
increases risk of tubule damage

Acetaminophin/phenacetin - causes oxidative damage to tubules
Aspirin - inhibits prostaglandin synthesis - less VD - more VC - more ischemia (leads to atrophy, fibrosis, renal failure)