Renal Flashcards

1
Q

horseshoe kidney

A

normal ascension will be blocked

kidney will be located abnormally low - stuck on root of IMA

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2
Q

oligohydramnios due to?
complications?
what “sequence” occurs? due to oligohydramnios

A

bilateral agenesis
lung hypoplasia
flat face w/ low set ears, extremity defects (Potter sequence)

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3
Q

dysplastic kidney
what’s the risk of developing the same in a subsequent pregnancy?
unilateral/bilateral?

A

noninherited malformation of parenchyma characterized by abnormal tissue (cartilage)
on exams: BILATERAL (b/c then must distinguish btw inherited PKD)

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4
Q

PKD

A

inherited
bilateral enlarged kidneys
cysts in cortex/medulla

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5
Q

ADPKD (assoc w?)

ARPKD (assoc w?)

A

ADPKD: young adults, HTN, hematuria, renal failure, APKD1/APKD2, inc renin
berry aneurysm, hepatic cysts, MVP

ARPKD: infants, renal failure and HTN, Potter sequence
hepatic fibrosis/hepatic cysts (will see portal HTN)

*INFANT w portal HTN –> think ARPKD

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6
Q

medullary cystic kidney disease

A

inherited dominant
cysts are in medullary CDs
fibrosis –> shrunken kidneys

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7
Q

hallmark of acute renal failure?

A

azotemia w/oliguria

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8
Q

prerenal injury

A

BUN/Cr >15 (bc RAAS activated and BUN reabs inc)

FENa 500

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9
Q

postrenal injury

early v late phase

A

BUN/Cr >15 (bc RAAS activated and BUN reabs inc)
FENa 500

late: BUN/Cr 2%, osm <500

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10
Q

ATN

what do you see on histo?

A

dirty brown, granular casts
necrotic cells plug tubules, dec GFR
cells lose nuclei and detach from BM
BUN/Cr 2%, osm <500

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11
Q

ischemic ATN

which tubules are particularly susceptible?

A

PT and medullary segment of TAL

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12
Q

causes of toxic ATN
*HAREM U
what else will you see?

A
heavy metals
aminoglycosides
radiocontrast
ethylene glycol
myoglobinuria
urate (tumor lysis)

hyperkalemia with AGMA

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13
Q

when ATN reversed, oliguria continues for?

A

2-3 weeks

PT cells are stable cells (need time to regenerate)

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14
Q
AIN
what agents can cause this?
what on histo?
presentation?
may progress to?
A
drug-induced HSR resulting in ARF
NSAIDS/PEN/diuretics
inflammatory infiltrate in interstitium
tubules look normal
oliguria, fever, rash, EOS in urine, resolves after stopping drug
renal papillary necrosis
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15
Q

renal papillary necrosis
presentation?
causative agents? (4)

A

gross hematuria and flank pain
long term phenacetin/aspirin use
diabetes, sickle cell, acute pyelonephritis

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16
Q

nephrotic syndrome

A
>3.5g protein
hypoalbuminemia
hypogammaglobulinemia
hypercoagulable state (AT3)
hyperlipidemia/cholesterolemia
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17
Q

MCD
what causes damage?
findings?

A
most common cause of Nephrotic in children, usually idiopathic
can be assoc w Hodgkin's lymphoma
cytokines --> podocytes
normal glomeruli on H&E
EM: effacement of foot processes
No immune complex deposits
Negative IF
responsive to steroids
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18
Q

FSGS

most common in whom? (2)

A
hispanics/af-am's
idiopathic, *HIV*, heroin, sickle cell
no immune complxs, negative IF
effacement of foot processes
poor response to steroids
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19
Q

HIV/sickle cell pt who develops nephrotic syndrome?

A

FSGS

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20
Q

membranous nephropathy
most common in whom?
see what?

A
caucasian adults
HEP B/C, tumors, SLE, drugs
thick BM on H&E
immune deposition (granular IF)
sub epithelial "spike & dome" on EM
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21
Q

SLE pt develops which nephrotic syndrome?

A

membranous nephropathy

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22
Q

MPGN
type 1 (cause, assoc?)
type 2
nephritic nephrotic or both?

A

thick capillary membranes on H&E
“tram-track” appearance
immune-complex deposition (granular on IF)

type 1: subendothelial (hep B/C), more often assoc w tram-tracks

type 2: deposition of IC’s in BM, C3 nephritic factor that stabilizes C3 convertase, so more C3 around –> inflammation + damage

all of the above!

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23
Q

diabetes
which vessel affected most?
tx?
hallmark pathognomonic finding?

A

high serum glucose –> NEG of BM –> hyaline arteriolosclerosis –> nephrotic –> sclerosis of mesangium and formation of K-W nodules
efferent more affected than afferent (up GFR

tx: ACEi slow hyperfiltration damage

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24
Q

systemic amyloidosis
most common organ?
amyloid deposits where?

A

kidney most commonly involved
mesangium –> nephrotic
apple-green on polarized

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25
Q

nephritic syndrome

what seen on biopsy?

A

protein s

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26
Q

PSGN
virulence factor?
presentation?
hallmark on EM?

A
GBS in kids
M protein
hematuria (cola-color), oliguria, HTN, periorbital edema
granular on IF
antigen-ab complexes sub-endothelially
hallmark: subepithelial hump on EM
rarely progresses
most common renal disease in SLE
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27
Q

RPGN

what seen on biopsy?

A

seen in adults

on biopsy: crescents composed of FIBRIN and MP’s (not collagen)**

28
Q

3 conditions with negative IF (pauci-immune)

A

Wegener
Microscopic polyangiitis
Churg-Strauss

29
Q

knee-jerk on boards for Goodpasture’s BUT with sinus infections/sinusitis

A

not good pastures but
WEGENERS
linear IF for GP
C-ANCA with Wegener (no IF)

30
Q

P-ANCA

A

either microscopic polyangiitis

or Churg-Strauss

31
Q

3 things to distinguish Churg-Strauss from MP?

A

granulomatous inflammation
eosinophillia
asthma

32
Q

IgA nephropathy

A
mesangial deposition of IgA
following mucosal infections
childhood
RBC casts
slowly progresses to failure after multiple bouts w infections
33
Q

Allport syndrome

what other two sx?

A

type IV collagen
thinning of BM
only hematuria
can have hearing loss and ocular disturbances

34
Q

cystitis
sx?
labs?
gold std?**

A
inflammation of the bladder
dysuria
frequency/urgency/suprapubic pain
no systemic signs
cloudy urine w >10 WBCs/hpf, +LE, nitrites, **>100k colony FU's on culture**
35
Q

UTI etiology

A

E. coli, S. saprophyticus, klebsiella, proteus, E. faecalis

36
Q

sterile pyuria (w negative culture)

A

think urethritis

Chlamydia, Neisseria gonorrhoeae

37
Q
pyelonephritis
risk inc w?
what sx?
UA looks like?
most common bugs?
A

risk w vesicoureteral reflux
fever, flank pain, WBC casts, leudocytosis
E. coli, klebsiella, E. faecalis

38
Q

chronic pyelonephritis

A
could be malformation of ureter
cortical scarring (upper and lower poles, which is char of vesiculouretal reflux) and blunting of calyces
39
Q

atrophic tubules containing eosinophilic proteinacious material
see what in urine?

A

thyroidization of the kidney

waxy casts

40
Q

colicky pain w hematuria and unilateral flank tenderness

A

kidney stone presentation

41
Q

CaOx, CaP
seen w which disease?
tx?

A

exclude hypercalcemia
check for idiopathic hypercalcuria
Crohns
hydrochlorothiazide

42
Q

second most common
results in stag horn caliculus
tx?

A

ammonium Mg P stone
infection w urease bugs (kleb, proteus)
organism and surgical removal

43
Q

3rd most common stone that is radiolucent, not seen on CxR
most common in pts w/ what conditions?
tx?

A

hot arid climates, low urine, acidic pH
gout, hyperuricemia (leukemia/myeloproliferative)
hydration, alkalinization, allopurinol

44
Q

cysteine stones
defect in kids?
tx?

A

can cause nephrolithiasis in kids
staghorn caliculi
cystinuria –> genetic defect results in decreased cysteine reabsorption
hydration/alkalinization

45
Q

staghorn caliculi in adults?

staghorn caliculi in kids?

A

Ammonium Mg P

Cysteine

46
Q

most common causes of ESRD (3)?

A

diabetes
HTN
glomerular disease

47
Q

sx of uremia?

A

nausea, anorexia, pericarditis, plt dysfxn, encephalopathy w asterixis, urea crystals in skin

48
Q

features of ESRD

A

salt/water retention –> HTN
hyperkalemia
NAGMA –> AGMA (cannot excrete organic acids)
anemia
hypocalcemia
renal osteodystrophy (OFC, osteomalacia, osteoporosis)

49
Q

EPO produced by which cells?

A

renal peritubular interstitial cells

50
Q

osteomalacia

A

when blasts lay down osteoid that cannot be calcified due to lack of calcium

51
Q

cysts that develop on shrunken kidneys on dialysis?

A

ESRD pts, not PKD

52
Q

patients on dialysis have an increased risk for what in their shrunken kidneys?

A

renal cell carcinoma

53
Q

angiomyolipoma composed of?

increased frequency with which condition?

A

blood vessels, adipose, smooth muscle

tuberous sclerosis

54
Q

renal cell carcinoma
classic presenting triad?
gross exam reveals?
most common variant?

A

malignant epithelial tumor arising from the kidney tubules
Hematuria, palpable mass, flank pain
also fever, wt loss, paraneoplastic (EPO, renin, PTHrP, ACTH)
yellow mass
clear cell (clear cytoplasm)

55
Q

may present with left -sided varicocele

A

renal cell carcinoma

56
Q

pathogenesis of renal cell carcinoma

what is lost? then increased what?

A

loss of VHL (3p) suppressor gene
increased IGF-1
increased HIF –> VEGF/PDGF

57
Q

sporadic renal cell carcinoma? who?

hereditary renal cell? who?

A

single tumor at upper pole of kidney –> adult smokers

multiple/bilateral tumors
younger pts

58
Q

VHL disease

A

dominant disorder
inactivation of VHL gene
inc risk of hemangioblastoma of cerebellum and RCC

59
Q

T & N of renal tumor staging

A

T: size/involvement of renal vein
N: retroperitoneal nodes

60
Q

Wilms tumor
seen in who?
comprised of?
presentation?

A

WT1 mutation
malignant, common in kids (~3)
blastema, primitive glomeruli/tubules/stromal cells
large unilateral flank mass w/ hematuria and HTN (renin)

61
Q

WAGR Syndrome

A

Wilms tumor
Aniridia
Genital abnormalities
Retardation (mental/motor)

62
Q

Beckwith-Wiedemann syndrome

A

Wilms tumor
Neonatal hypoglycemia
Muscular hemihypertrophy
Organomegaly (e.g. tongue)

63
Q

urothelial carcinoma
risk factors?
presentation?

A

malignant via lining of renal
most common type
pelvis, ureter, bladder (most common), urethra

RF: cigarrettes (PAHs), naphtylamine, azo dyes, cyclophosphamide, phenacetin

painless hematuria
two pathways:
flat (high grade –> invades, early p53 mutations), papillary (low grade –> HG –> invades)

64
Q

field defect

A

entire urothelium has been hit with carcinogens, so multiple tumors can develop/recur

65
Q

squamous cell carcinoma

A

malignant
bladder
must first develop squamous metaplasia
RF: chronic cystitis, schistosoma hematobium, long-standing nephrolithiasis

common theme: irritation/inflammation of urothelium –> squamous metaplasia

66
Q

adenocarcinoma

A

malignant
glands/bladder
urachal remnant (fetal bladder to yolk sac; this cancer would be found at the DOME OF THE BLADDER), cystitis gladularis (chronic inflammation –> columnar metaplasia), exstrophy (failure to form lower portion of bladder wall/abdomen, exposing bladder to outside world)