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71 Cards in this Set

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Which kidney is taken during living donor tranplant
Left kidney- longer renal vein!
Ureters pass UNDER
uterine artery and ductus deferens
water under the bridge
Plasma volume measured by
radiolabeled albumin
Extracellular volume measured by
inulin
Glomerular filtration barrier
composed of fenestrated cap endothelium- size barier, fused bm with heparan sulfate- neg charge barrier, and epi layer with podocyte foot processes
Nephrotic syndrome
charge barrier lost
resulting in albuminuria, hypoproteinemia, gen edema, hyperlipidemia
Inulin
freely filtered, not secreted or reabsorbed
can be used to calc GFR
Normal GFR
100 mL/min
Creatinine clearance
approx measure of GFR
slight overestimate bc Cr is moderately secreted by renal tubules
Effective renal plasma flow (ERPF)
can be estimated using PAH clearance because it is filtered and actively secreted- all PAH entering kidney is excreted
ERPF underestimates true RPF by
10%
RBF=
RPF/(1-Hct)
Filtered fraction (FF)=
GFR/RPF
nml=20%
FIltered load=
GFR x plasma concentration
Excretion rate
V times Ux
Glcuosuria begins at
plasma glucose 160-200 mg/dL
below that, gluc is completely reabsorbed
all transporters are fully saturate at 350 mg/dL
Amino acid clearance in renal nephron
Na dep transporters in prox tubule reabsorb AA by at least 3 distinct carriers with comp inhibition within each group
Hartnup dse
def of neutral AA (tryptophan) transporter, results in pellagra- diarrhea, dementia, dermatitis
PTH action on nephron
inhibits Na/phosphate cotransport in PCT, causes phosphate excretion
inc Ca/Na exchange in DCT, causes Ca reabsorption
AT II on PCT
stimulates Na/H exchange, inc Na and H2O reabsorption, permitting contraction alkalosis
Cl vs Na reabsorption
Cl reabsorbed at a slower rate than Na in prox 1/3 of PCt, then matches the rate of Na reabsorption distally
relative conc inc before it plateaus
TF/P of Na
=1
Na reabsorption drives H2O reabsorption, so it nearly matches osm
AT II
affects baroreceptor function to limit reflex brachycardia which would normally accompany its pressor effects
ANP
from atria in response to inc volume, relaxes vasc smooth muscle via cGMP
causes inc GFR, dec renin
ADH
primarily reg osmolarity but also responds to low blood volume- takes precedence
Aldosterone
primarily reg blood volume
JG cells
modified smooth muscle of afferent arteriole
secrete renin in response to low renal bp, low na delivery to DCT, inc beta 1 sympathetic tone
Macula densa
Na sensor, part of DCT
part of JGA
Proximal tubule cells convert
25 OH vit D to 1,25 OH2 vit D by 1 alpha hydroxylase, PTH stimulates this, inc intestinal absorption of ca and phos
NSAIDs
can cause acute renal failure by inhib renal prod of prostaglandins, ex PGE2- which vasodilate afferent arterioles to inc GFR
What shifts K into cells- causing hypokalemia
Insulin, beta agonists, alkalosis, hypo osmolarity
What shift K out of cells- causing hyperkalemia
insulin def, beta blocker, acidosis, severe exercise, hyperosmolarity, digitalis, cell lysis
Winter's formula
resp comp for met acidosis
Pco2=1.5HCO3 + 8 +/- 2

Pco2 inc by 0.7 for every 1 inc in HCO3
Causes of Inc anion gap met acidosis
MUDPILES
methanol (formic acid), uremia, dka, paraldehyde or phenformin, iron tablets or INH, lctic acidosis, ethylene glycol (oxalic acid), salicylates
Normal anion gap met acidosis (8-12 mEq/L)
diarrhea, glue sniffing, renal tubular acidosis, hyperchloremia
Causes of met alkalosis
diuretic use, vomitnig, antacid use, hyperaldosteronism
Renal tubular acidosis
type 1- defect in CD's ability to excrete H+, ass with hypokalemia and risk for ca stones
type 2- defect in PCT bicarb reabsorption, ass with hypokalemia and hypophosphatemic rickets
type 4- hypoaldosteronism, hyperkalemia, dec urine pH due to dec buffering capacity
RBC casts
glomerulonephritis, ischemia, malignant htn
WBC casts
tubulointerstitial inflammation, acute pyelonephritis, transplant rejection
Granular casts
muddy brown
acute tubular necrosis
Waxy casts
advanced renal dse/ chronic renal failure
Acute cystitis
pyuria, no casts
Bladder cancer and kidney stones have
hematuria, no casts
Nephritic syndrome
Inflammatory process
when it involves glomeruli, leads to hematuria, RBC casts
ass with azotemia, oliguria, htn, proteinuria
MC cause of adult nephrotic syndrome
FSGS- focal segmental glomerulosclerosis
MC glomerular dse in HIV pts
Diffuse proliferative GN
due to SLE or MPGN
wire looping of capillaries
subendothelial and sometimes intramembranous IgG based IC with C3 deposition
MCC death in SLE
SLE's nephrotic presentation
membranous glomerulonephritis
diffuse cap and GBM thickening
spika and dome appearance on EM with subepi deposits
Minimal change dse
lipoid nephrosis
nephrotic syndrome
foot process effacement, selective loss of albumin due to GBM polyanion loss
trigger by recent infxn, MC in children, responds to corticosteroids
Type I membrano-proliferative GN
tram track appearance due to GBM splitting by mesangial ingrowth
subendo ICs with granular IF
ass with HBV, HCV
Type II membrano-proliferative GN
dense deposits on EM
subendo ICs with granular IF
ass with C3 nephritic factor
Diabetic glomerulonephropathy
nonenzymatic glycosylation of GBM, efferent arterioles
GBM thickining, eosinophilic nodular glomerulosclerosis- Kimmelstiel Wilson lesion
Uric acid stones
only kidney stone that is radiolUcent
Calcium stones
can be caused by hypercalcemia- cancer, inc PTH
ca oxalate crystals can result form ethylene glycol or vit C abuse
Staghorn calculi
from struvite stones- ammonium mg phos
caused by infxn with urease positive bugs- Proteus, Staph, Klebsiella
worsened by alkaluria
RCC
originates in renal tubular cells- polygonal clear cells filled with lipids and carbs
hematuria, palp mass, 2ndary polycythemia
invades IVC, spreads hematogenously
ass with VHL, chrom 3p deletion
can secrete ectopic EPO, ACTH, PTHrP, prolactin
WAGR complex
Wilms tumor- nephroblastoma, caused by deletion of tumor suppressor gene WT1 on chrom 11p, Aniridia, Genitourinary malformation, mental Retardation
Painless hematuria with no casts
Bladder cancer
Transitional cell ca MC tumor or urinary tract system
ass with Phenacetin, smoking, aniline dyes and cyclophosphamide
WBC casts are classic for
acute pyelonephritis
affects cortex, spares glomeruli/vessels
fever, CVA tenderness, NV
Thyroidization of kidney
eosinophilic casts in tubules
chronic pyelonephritis!
lymphocytes and fibrosis
VUR required for development
ATN
MCC of acute renal failure in hospital
granular muddy brown casts
inciting event, maintenance phase- oliguric, 1-3 wks, hyperkalemia, recovery phase- polyruric, hypokalemia
death occurs during initial oliguric phase
Renal papillary necrosis
ass with dm, acute pyelonephritis, chronic phenacetin use, sickle cell anemia and trait
In normal nephron, BUN
is reabsorbed for countercurrent multiplication
creatinine is not
Prerenal azotemia
dec RBF ex hypotension, dec GFR, na/h20 and urea retained to conserve volume
INC BUN/Cr ratio
Intrinsic renal injury
ex ATN, patchy necrosis leads to debris obstructing tubule and fluid backflow across necrotic tubule, dec GFR
BUN reabsorption impaired so DEC BUN/Cr ratio
Renal osteodystrophy
failure of vit D hydroxylation, Ca wasting and phos retention, causes 2ndary hyperparathyroidism, dec intestinal Ca absorption
causes subperiosteal thinning of bones
Medullary cystic disease
medullary cysts can lead to fibrosis, inability to conc urine, small kidney, 70% develop stones, poor prog
Furosemide
sulfonamide loop diuretic, inhib Na K Cl pump of thick asc limp of LOH, stim PGE- vasodilate afferent arteriole, inhibited by NSAIDS, Loops Lose Ca
tox ototox, hypokalemia, dehydration, sulfa allergy, interstitial nephritis, gout
Diuresis in pts with sulfa allergies
Ethacrynic acid- same action as furosemide, can cause hyperuricemia- NEVER use in gout!!!
HCTZ
inhib NaCl reabsorption in early distal tubule
tx htn, chf, hypercalciuria, nephrogenic diabetes insipidus
tox hypokalemic met alk, hyponatremia, hyperGLUC- glycemia, lipidemia, uricemia, calcemia, sulfa allergy
Triamterene and amiloride
K sparing diuretics, block Na channels in CCT
ACE inhib
-pril, red levels of ATII, prevent inactivation of bradykinin, renin release inc due to loss of neg feedback
tx htn, chf, diabetic renal dse
tox cough, angioedema, proteinuria, taste changes, hypotension, fetal renal damage, rash, inc renin, low AT II, hyperkalemia
avoid with bilat renal artery stenosis!!