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116 Cards in this Set

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name 6 nephritic syn
Poststrep, RPGN, MPGN, Goodpasteur, IgA, Alport
name 5 nephrotic syn
mem, minimal change, FSGS, DM, Lupus
Potter sequence
bilateral renal agenesis leading to hypoplastic lung, defect in extremities. present oligohydramnios
oligohydramnios: mech?
unable to renally excrete amniotic fluid swallowed by fetus
hyperhydramnios seen with
duo atresia (or tracheo-eso fistula
renal ectopia
MC pelvic kidney
increase incidence UTI
in women bc shorter urethra, and increased in pregnancy
vesicoureteral reflux, role UTI
reflux from bladder into ureter--can cause spread of UTI to kidneys
cystitis characteristics, labs
pyuria, hematuria, but no urinary WBC
difference UTI and acute pyelonephritis
acute pyelo=acute infxn of renal parenchyma, has pathognomoninc white cell casts with F, incr WBC, and flank pain
(UTI-freq, dysuria, pyuria**, bacteriuria, +/-hematuria)
def bacteruria
>10^5 org per mm urine
key causes AIN
penicillin derv (methicillin), NSAIDs, diuretics
natural course AIN
should resolve on cessation of Rx
def renal papillary necrosis, what 3 assoc?
ischemic necrosis of tips of renal papillae
MC DM (infxn w vascular dz), abuse phenacetin w ASA and analgesics, rarely acute pyelo
ATN natural course
reversible, should resolve within 2 wks (necrotic tubular cells replaced)
initial phase ATN, beware of
oliguric phase, increasing K (beware of arrhyth, pts most likely to die in this stage)--must make sure its not prerenal oliguria
oliguria
-initial phase ATN
-prerenal
-postrenal obstruct
ATN pathophysio/mech, assoc w 3 conditions
ppt by renal ischaemia, ie hypotension, shock
assoc w gram neg sepsis, trauma, hemorrhage
ATN main causes 3
renal ischaemia (shock), myoglobinuria, toxins
toxicities cause ATN
direct injury to prox tub:
mercuric Cl, gentamicin, ethylene glycol
results ethylene glycol ingestion
ATN, renal oxalosis w intratubular oxalate deposits
fanconi syndrome, def/problem
hereditary or acquired impaired resorption glu, aa, phosphate, HCO3
MC acute renal failure
ATN
fanconi syndrome-clinical presentation
glycosuia, hyperphosphaturia, hypophosphatemia, aminoaciduria, systemic acidosis
hartnup dz-problem and manifestations
genetically impaired reabsorption of Tryp, causes pellagra (B3 defic)
how diagnose chronic pyelo
histology-coarse, asymm corticomed scarring and deformity renal pelvis and calices
histol of chronic pyelo
coarse, asymm corticomed scarring and deformity renal pelvis and calices, interstitial fibrosis, tubular atrophy which can contain eosinophillic proteinaceous casts (thyroidization of kidney)
acute pyelo is damage where (cortex? glom? tubules?)
cortex, sparing glomeruli/vessels
cause chronic pyelo, progression dz
usu chronic UT obstruction and repeated acute inflamm
leads to renal HTN, ESRD
diffuse cortical necrosis, def
acute, generalized infarction of both cortices sparing the medulla
diffuse cortical necrosis-mech
vasospasm and DIC
diffuse cortical necrosis-assoc w
obstretric cxns (abruptio placentae, preeclampsia), septic shock
nephrocalcinosis, def, assoc
diffuse dep of Ca due to hyperCa: hyperPTH, milk alkali, hyperphosphate 2/2 RF
Note: this can be both a cause and effect of RF
urolithiasis: main types general character
1. Ca (80%)
2. Al/Mg/P (struvite)-urease + infxn, radioopaque
3. uric acid-radiolucent
4. cystine-radiolucent
types Ca kidney stones, assoc dz
Caoxalate or CaP or both.
causes hyperCa: hyperPTH, cancer, inc vitD, milk-alkali synd
T/F: Ca kidney stones tend to recur
T
Struvite stone charac
2nd MC, radioopaque, staghorn calculi
complication struvite stone
staghorn calculi can become nidus for UTI
struvite assoc w which infxns
urease positive (Proteus, Staph)
struvite grow in urine of what pH
alkaline
uric kidney stones assoc
hyperuricemia, incl gout, high cell turnover in leuk/MPD
T/F Cystine stones almost always assoc cystinuria
T (or genetically determined aminoaciduria)
cxns assoc w APKD, or problems assov w APKD
-berry aneury
-secondary polycythemia (hi renin,HTN)
-cysts in liver and other organs
-MVP (?)
clinical presentation APKD
HTN, hematuria, palpable renal masses
describe genetics APKD, when present
AD 90% mutat in APKD1 on chrom 16, MC genetic disorder of kidney presents age 15-30 although defect present from birth
where are cysts in APKD? bilateral?
bilateral in renal parenchyma
IPKD, (infantile polycys kid dz) genetics, present
AR, cysts are evident at birth, dies shortly after
acquired cystic dz assoc w
long-term dialysis, increased chance RCC
path of aquired cystic dz
multiple cysts w glomerular and tubular atrophy and scarring
lab characteristics uremia
acidosis (from accum sulfates, phosphates)
hyperK, hypoCa, anemia, HTN (very hi renin)
how does kidney fxn progress in uremia (early and late)
initially unable to concentrate urine, later unable to dilute
clinical present uremia
anorexia, N/V, neuro (AMS to convulsion/coma), bleeding, accum of urochrome in skin, fibrinous pericarditis
nonrenal causes azotemia (2 general)
pre-renal, post-renal obstruct (must be bilateral)
how does gram - sepsis result in pre-renal azotemia
marked vasodilation leads to peripheral pooling blood, less RBF
key lab characteristics pre-renal cause ARF
hi urine osmo (>500), relatively low urine Na (<10) FENa<1%, BUN/Cr>20
lab characteristics post-renal cause ARF
very hi urine Na (>40) with urine osmo <350, FENa >4%, (BUN/Cr >15)
lab character intrinsic renal cause ARF
key-epithelial/granular casts
labs: urine osm<350, urineNa>20, FENa>2%, BUN/Cr<15
def ARF
abrupt decline renal fxn with incr Cr and BUN (over span several days)
kidney retains ___ in pre-renal ARF
both Na and H2O
main causes chronic renal failure
HTN, DM
consequences RF (8)
(think hormone, metabolic, and systemic)
anemia (no EPO), renal osteodystrophy (no vitD), metab acidosis (decr acid sxn and decr gen HCO3), hyperK, uremic encephalolpathy, Na/H2O overload (leads to CHF, pul edema), chronic pyelonephritis, HTN
T/F chronic pyelonephritis is a cxn of RF
T
T/F pul edema can be seen with RF
T (H2O and Na overload causes CHF, pul edema)
hormonal related problems due to RF
anemia (no EPO), and renal osteodystrophy (no activ vitD)
"classic" triad presentation RCC, "commonly"
flank pain, palpable mass, hematuria
commonly: fever
clinical present RCC other than renal
polycythemia (incr EPO)
hyperCa (para neo PTH), also ACTH, prolactin
RCC originates
renal tubules, starting in poles (often superior)
risk factors RCC
smoking, long-term dialysis (via acquired cystic kidney dz)
RCC spread
hematogenous (often early), via IVC
histol RCC cells
polygonal clear cells
RCC assoc with what genetic? which chromo?
VHL, deletion chrom 3
Wilms tumor, genetics, age present
WT1 deletion short arm chrom 11 (tumor suppressor), present 2-4 (MC renal cancer of childhood)
WAGR syndrome
Wilms' tumor, Aniridia, GU malform, Retardation
how wilms tumor present
huge palpable flank mass, hemihypertrophy
Beckwith Wiedermann, descrip, genetics
macroglossia, oragnomegaly, neonatal hypogly, embryonal tumors, deletion WT2
**genomic imprinting, abnl alleles always from mom
risk factors TCC
PeeSAC: phenacetin, smoking, aniline (or benzidine), cyclophosphamide
T/F EtOH a risk factor for TCC
F
natural process TCC: mech spread, tx
local extension, removed but tends to recur
SCC UT malignancy seen with
Schisto or chronic bac infxn
compensation in metab alkalosis
for every incr 1 HCO3, incr 0.7PCO2
compensat in acute respir acidosis for incr 10PCO2
incr 1 HCO3 for every incr 10 PCO2
(chronic it's 3.5 for every 10)
respir alkalsos compensat for decrease 10PCO2
for every decr 10PCO2:
acute= decr 2 HCO3
chronic=decr 5 HCO3
clinical Nephrotic
proteinuria, hypoalbuminemia->edema, hyperlipid
histol min change dz
LM: normal
IF: none
EM: fusion epithelial foot processes
min change-in who? when? tx?
usu young children, responds well to steroids
FSGS histol
LM: segmental sclerosis and hyalinosis of capially tufts of deep juxtameduallry glom
FSGS similar to,
worse in pts
similar to minimal change but older pts
worse in HIV
membranous GN epidemio
one of main primary causes of nephrotic seen in teens, young adults.
clinical present mem GN
nephrotic syn with azotemia
histol mem GN
LM: thickened capillary
IF: subepithelial IC (granular IF)
EM: spike and dome
assoc/cxns of mem GN
-10% of SLE have this
-cause renal vein thrombosis
DM kidney damage
nephrotic
EM/LM: incr GM thickness (earliest change EM)
increased mesangial in either diffuse or nodular way
Kimmelstiel-Wilson nodules
seen in nodular DM nephropathy
renal dz assoc with RA, plasmoid dzs
renal amyloidosis-subendo and mesangial amyloid deposits
renal amyloidosis causes what type kidney damage
nephrotic syndrome
histol of 5 stages of SLE kidney damage
1-nothing observable
2=mesangial, little protein and little hematuria, not very clin significant
3=focal prolifer, involves <1/2 glom
4=diff prolifer, most severe
5=membranous (exactly same as mem)
describe Diffuse Prolifer SLE kidney dz and histol
both nephrotic and nephritic presentation, involves almost all glomeruli
LM: wire loop abnormalities from IC deposits
IF: subendo IC
EM: endothelial cell prolifer
clinical charact of nephritic syn
oliguria, azotemia, HTN, hematuria (some red cell casts)
causes renal nephritic syn
1) Post strep (usu GAS)
labs on post strep GN
low C3, hi ASO
T/F Post-strep GN is a result of moderate inflamm rxn
F, result of intense inflamm rxn, almost all glom in both kidneys
gross specimen: changes in post-Step GN
punctate hemorr on surface both kidneys,
enlarged, swollen, hyper cellular bloodless glommerli
LM, EM histol post strep GN
IF: lumpy bumpy, subepithelial
RPGN
nephritic
post-strep
nephritic
membranous-type of GN?
nephrotic
histol RPGN and types (3)
all kinds: LM: crescentic
1) 10% Goopasteure: IF: linear (anti glom BM)
2) 50% post strep (IC)
3) pauci immune (no IC, but ANCA+)
nomenclature RPGN types
ANCA-neg forms:
RPGN I=anti G BM
RPGN II=IC

RPGNIII=ANCA +
goodpasteur present, type pts
anti BM Abs (both alveolar and glomerular), hemorrhagic pneumonitis (pneu w hemoptysis), + nephritic syn
seen in med mid 20's
Alport syndrome, descrip and genetics
hereditary nephritis (ESRD by 30) w nerve deafness, lens dislocation and cataracts.
mutat in alpha5 col IV
histol of Alport syn nephritis
irregular G BM thickening with foci of splitting of lamina densa
most common cause adult and child nephrotic
adult=mem GN
child=min change
Berger's dz, descrip
IgA nephropathy, mild dz often post infxs
IgA nephropathy histol
IF/EM: mesangial deposits IgA
slow progression to RF, v fast
slow=MPGN
fast=RPGN/crescentic
main clinical differences nephritic v nephrotic
nephritic=hematuria, HTN,
nephrotic=proteinuria, edema