Renal

Question 1

LUT adenoCa

Answer 1

urachal remnant, bladder exstrophy (LUT is normally transitional epithelium)

Question 2

LUT SCC

Answer 2

metaplasia –> dysplasia sequence (LUT normally transitional epithelium)
chronic cystitis, schisotoma (middle eastern male!), nephrolithiasis

Question 3

urothelial carcinoma

Answer 3

most common LUT cancer
smoking!
multifocal, recurrent (field defect)

Question 4

Wilms

Answer 4

malignant tumor of blastema (renal progenitor tissue)
can produce primitive glomeruli, tubules, stromal cells
HTN from renin
WT1 mutx
WAGR syndrome: Wilms, Aniridia, Genital abnormalities, mental and motor Retardation

Question 5

RCC

Answer 5

tubular epithelial cell tumor
rarely presents as left-sided varicocele (involves renal vein)
yellow mass (Gross)
clear cell (most common micro)
-pathogenesis: loss of VHL (tumor supressor) → inc IGF-1 and incr HIF → VEGF, PDGF
-sporadic: smoking. single tumor in upper pole
-hereditary: multiple, bilateral, younger
-paraneoplastic: renin, EPO, PTHrP
assoc: VHL syndrome. hemangioblastoma of cerebellum

Question 6

chronic pyelo

Answer 6

interstitial fibrosis from repeated bouts of acute pyelo.
Most commonly in kids with VUR
cortical scarring (characteristically upper and lower poles) and blunted calyces
atrophic tubules with eosinophilic proteinacious material (looks like thyroid colloid) = “thyroidization”

Question 7

Alport

Answer 7

inherited defect in type IV collagen
X linked
isolated hematuria from damaging of GBM
sensory hearing/vision loss

Question 8

IgA nephropathy

Answer 8

Childhood. Episodic gross/micro hematuria, following mucosal infections
IF: granular deposition of IgA in mesangium
may slowly progress to renal failure

Question 9

RPGN

Answer 9

nephritic syndrome → renal failure in weeks/month
Path: crescent in bowman space (composed of fibrin and MPhages–not collagen)
-linear IF = anti-GBM Ab = goodpasture’s
-Granular IF = immune complex = PSGN (sub-epi) or diffuse proliferative GN i.e. SLE (sub-endo)
-negative IF = pauci-immune. c-ANCA = GPA. p-ANCA = microscopic polyangiitis vs churg-strauss (granulomatous inflammation, eos, asthma)

Question 10

nephritic syndrome path

Answer 10

hypercellular, inflamed glomerulus
immune complex → complement → C5a → PMN attraction → damage
IF: immune complexes (duh)

Question 11

amyloidosis

Answer 11

mesangium deposition → nephrotic

apple-green birefringence under polarized light

Question 12

DM kidney

Answer 12

non-enzymatic glycosylation of GBM resulting in hyaline arterolosclerosis. Efferent > afferent –> high filtration pressure
early: hyperfiltration → microalbuminuria
late: sclerosis of mesangium (K-W nodules) → nephrotic syndrome
ACE inhibitors slow progression of hyperfiltration injury by relieving pressure on efferent arteriole!

Question 13

membranoproliferative GN

Answer 13

Nephritic, nephrotic, or both
LM: thick capillary membranes, “tram-track”
appearance
IF: immune complex (“membranous”)
EM: intra-GBM and/or subendo (two locations not seen in membranous nephropathy)
Type I = sub-endo. HBV/HCV
Type II = intra-GBM. C3 nephritic factor Ab. stabilizes C3 convertase

Question 14

SLE kidney

Answer 14

nephritic: diffuse proliferative
nephrotic: membranous

Question 15

membranous nephropathy

Answer 15

nephrotic dz, white people
assoc: HBV, HCV, solid tumors SLE*, drugs (NSAIDs, penicillamine)
Thick GBM on LM
EM: “spike and dome”. subepithelial (podocytes)
IF: immune complex deposition (always true in “membranous” disorders). granular.

Question 16

FSGS

Answer 16

nephrotic dz, hipsanics, AAs
assoc: HIV, heroin, sickle cell dz
light: collagen deposition. focal and segmental (some gloms, parts of each glom)
EM: effacement 
IF: no immune complex
Progress to chronic renal failure

Question 17

minimal change dz

Answer 17

nephrotic dz, kids
assoc: Hodgkin lymphoma, atopy, infection, immunization (cytokine mediated damage to podocytes)
normal light micro
effacement of foot processes on EM
selective proteinuria: no loss of Ig, just albumin
IF: no immune complex
Tx: steroids. excellent response

Question 18

Thiazide vs Loop diuretics side effects

Answer 18

Both cause hypokalemia, alkalosis (due to compensatory aldosterone action)
Thiazides can cause hyponatremia (due to compensatory ADH action – loops can’t because they dissipate corticomedullary concentration gradient)
Thiazides can cause hyperCa and hypocalcuria due to increased proximal and distal Ca reabsorption. Loops can’t. makes thiazides good for osteoporosis, stone formers

Question 19

parts of nephron most sensitive to ischemia

Answer 19

Proximal tubule and thick ascending limb of Henle
located in outer medulla → lower blood supply and
have ATP-dependent active transport

Question 20

Clearance

Answer 20

[U]/[P] * Urine flow

Question 21

inulin and mannitol treatment in glom

Answer 21

filtered, neither reabsorbed or secreted

clearance~GFR**

Question 22

glucose, sodium, urea treatment

Answer 22

net reabsorption

excreted

Question 23

PAH and creatinine

Answer 23

net tubular secretion (PAH&raquo_space; creatinine)
Excreted&raquo_space; filtered
clearance ~ RPF**

Question 24

regulation of K absorption by nephron

Answer 24

principle and alpha-intercalated cells of late distal tubule/collecting duct
100% filtered, 65% absorbed in PT, 30% absorbed in ascending limb so that only 10% remains in distal tubule. even in hyperkalemia
ppl with CKD get hyperkalemic b/c their GFR goes down.

Question 25

Renal Papillary necrosis

Answer 25

hematuria and flank pain
chronic analgesics
DM
Sickle trait/dz
severe acute pyelo

Question 26

chronic pyelo

Answer 26

interstitial fibrosis from repeated bouts of acute pyelo.
Most commonly in kids with VUR
cortical scarring (characteristically upper and lower poles) and blunted calyces
atrophic tubules with eosinophilic proteinacious material (looks like thyroid colloid) = “thyroidization”