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Flashcards in Renal Deck (26):
1

LUT adenoCa

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

2

LUT SCC

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

3

urothelial carcinoma

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

4

Wilms

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

5

RCC


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

6

chronic pyelo


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”

7

Alport

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

8

IgA nephropathy

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

9

RPGN

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)

10

nephritic syndrome path

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

11

amyloidosis

mesangium deposition → nephrotic
apple-green birefringence under polarized light

12

DM kidney

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!

13

membranoproliferative GN

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

14

SLE kidney

nephritic: diffuse proliferative
nephrotic: membranous

15

membranous nephropathy

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.

16

FSGS


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

17

minimal change dz


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

18


Thiazide vs Loop diuretics side effects

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

19

parts of nephron most sensitive to ischemia

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

20


Clearance


[U]/[P] * Urine flow

21


inulin and mannitol treatment in glom

filtered, neither reabsorbed or secreted
clearance~GFR**

22


glucose, sodium, urea treatment


net reabsorption
excreted

23

PAH and creatinine

net tubular secretion (PAH >> creatinine)
Excreted >> filtered
clearance ~ RPF**

24

regulation of K absorption by nephron

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.

25

Renal Papillary necrosis

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

26

chronic pyelo

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”