Renal Flashcards
horseshoe kidney
normal ascension will be blocked
kidney will be located abnormally low - stuck on root of IMA
oligohydramnios due to?
complications?
what “sequence” occurs? due to oligohydramnios
bilateral agenesis
lung hypoplasia
flat face w/ low set ears, extremity defects (Potter sequence)
dysplastic kidney
what’s the risk of developing the same in a subsequent pregnancy?
unilateral/bilateral?
noninherited malformation of parenchyma characterized by abnormal tissue (cartilage)
on exams: BILATERAL (b/c then must distinguish btw inherited PKD)
PKD
inherited
bilateral enlarged kidneys
cysts in cortex/medulla
ADPKD (assoc w?)
ARPKD (assoc w?)
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
medullary cystic kidney disease
inherited dominant
cysts are in medullary CDs
fibrosis –> shrunken kidneys
hallmark of acute renal failure?
azotemia w/oliguria
prerenal injury
BUN/Cr >15 (bc RAAS activated and BUN reabs inc)
FENa 500
postrenal injury
early v late phase
BUN/Cr >15 (bc RAAS activated and BUN reabs inc)
FENa 500
late: BUN/Cr 2%, osm <500
ATN
what do you see on histo?
dirty brown, granular casts
necrotic cells plug tubules, dec GFR
cells lose nuclei and detach from BM
BUN/Cr 2%, osm <500
ischemic ATN
which tubules are particularly susceptible?
PT and medullary segment of TAL
causes of toxic ATN
*HAREM U
what else will you see?
heavy metals aminoglycosides radiocontrast ethylene glycol myoglobinuria urate (tumor lysis)
hyperkalemia with AGMA
when ATN reversed, oliguria continues for?
2-3 weeks
PT cells are stable cells (need time to regenerate)
AIN what agents can cause this? what on histo? presentation? may progress to?
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
renal papillary necrosis
presentation?
causative agents? (4)
gross hematuria and flank pain
long term phenacetin/aspirin use
diabetes, sickle cell, acute pyelonephritis
nephrotic syndrome
>3.5g protein hypoalbuminemia hypogammaglobulinemia hypercoagulable state (AT3) hyperlipidemia/cholesterolemia
MCD
what causes damage?
findings?
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
FSGS
most common in whom? (2)
hispanics/af-am's idiopathic, *HIV*, heroin, sickle cell no immune complxs, negative IF effacement of foot processes poor response to steroids
HIV/sickle cell pt who develops nephrotic syndrome?
FSGS
membranous nephropathy
most common in whom?
see what?
caucasian adults HEP B/C, tumors, SLE, drugs thick BM on H&E immune deposition (granular IF) sub epithelial "spike & dome" on EM
SLE pt develops which nephrotic syndrome?
membranous nephropathy
MPGN
type 1 (cause, assoc?)
type 2
nephritic nephrotic or both?
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!
diabetes
which vessel affected most?
tx?
hallmark pathognomonic finding?
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
systemic amyloidosis
most common organ?
amyloid deposits where?
kidney most commonly involved
mesangium –> nephrotic
apple-green on polarized
nephritic syndrome
what seen on biopsy?
protein s
PSGN
virulence factor?
presentation?
hallmark on EM?
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