Renal Flashcards
Yang Lectures 5,6
cardiac output value
6000 mL/min
where does most reabsorption occur?
PCT
renal blood flow
1100 mL/min
filtration fraction
110 mL/min
10%
urine output
1mL/min
minimum fluid output to remove waste
30 mL/h or 700 mL/day
where does resorption of large molecules occur?
PCT
where is Na+ reabsorbed?
pretty much everywhere in the nephron
H2O permeability
decreases as you move through the nephron
where is creatinine removed?
glomerulus
increase in SCr
BAD
Blood Urea Nitrogen (BUN)
waste from breakdown of amino acids
what happens to kidney function as you age?
decline in mass sees a decline in function
intact nephron hypothesis
when the loss of nephron mass leads to hypertrophy of the remaining nephrons
hyperfilitration hypothesis
intact nephrons after kidney injury are damaged by increased plasma flow
main causes of renal failure in the US
60% is due to HTN and diabetes
acute kidney failure indications
increase in SCr greater or equal to 0.3 mg/dL within 48 hours
increase in SCr greater than 50% that occurred within prior 7 days
reduction in kidney failure
relationship between GFR and SCr
inverse
GFR increases, SCr decreases
prerenal casues of AKI
hypovolemia
decreased circulating volume
NSAIDs, ACE-I, and cyclosporine
intrinsic causes of AKI
nephrotoxins
ischemia
sepsis
postrenal causes of AKI
obstruction of urine output
NSAIDs effect
increases Afferent resistance
reducing glomerular pressure
ACE-I effect
decreases Efferent resistance
reducing glomerular pressure
chronic kidney disease timeline
over 3 months
calcification
arises as a result of hypocalcemia and impaired excretion
protein uria
due to increased glomerular pressure causing endothelial injury
1,25 dihydroxyvitamin D3
active form of vitamin D
CKD decreases the production
uremia
accumulation of waste
nephritic syndrome
caused by inflammation disrupting the glomerular basement membrane
abrupt onset
some edema
raised blood and jugular vein pressure
some proteinuria and hematuria
RBC casts
normal serum albumin
nephrotic syndrome
caused by podocyte damage disrupting glomerular barrier
insidious onset
very high edema
normal blood and jugular vein pressure
very high proteinuria
no RBC casts
low serum albumin
podocyte detachment
caused by antibodies being the mediators of immune glomerular injury
pyelonephritis
inflammation of kidney tissue caused by bacteria
characterized by WBC in the urine
interstitial nephritis
caused by an autoimmune response
associated with penicillins, NSAIDs, and anticonvuslants (azepines)
cystic renal disease
most commonly seen as simple cysts
autosomal dominant PKD
caused by inherited mutations in the PKD1 or PKD2 genes
PKHD1
gene where mutation occurs leading to autosomal recessive PKD that quickly kills children
nephrolithiasis
kidney stones
contrast-induced nephropahthy
caused by an increase of SCr from contrast media within 72 hours
