Tubulointerstitial Disease Flashcards
Acute kidney injury comes in two varieties
ischemic
toxic
two reversible diseases that dont require much attention
osmotioc nephrosis (hypertonic solution causes foamy, disteneded PT) hyaline droplet change (increased protein loss causes increased protein resorption)
Acute renal failure decribed as
decreased GFR
oliguria
increased BUN
increased creatinine
mechanisms of acute renal failure
VC of aff arteriole–>decreased perfusion–>decreased GFR
casts obstruct the tubule (increase tubule luminal pressure, decreased glomerular transcap perfusion pressure)
tubular backleak–>accum of protein products in interstitum–>increase interstital oncotic and decrease tubular oncotic–>tubules collapse
what kind of catsts in acute kidney injury
granular
toxic AKI
diffusely hypereosinophilic tubules with necrosis and sloughing of epithelial cells into the lumen
3 phases of AKI
initiating phase (1-2 days) maintenance phase recovery phase (days-weeks)
initiating phase
mild decrease in urine output
maintenance phase
sustained decrease in urine output
water and salt retention
increase in BUN, Cr, K, metabolic acidosis
recovery phase
increase in urine output (>3 l/day) with decrease in BUN, Cr, K
clinical manifestations of tubulointerstital disease
decreased urine concentration (polyuria)
decrease in Na reabsorption (salt wasting)
decrease in acid secretion (metabolic acidosis)
2 major categories of tubulointerestital disease
pyelonephritis: infection
tubulo-interstital: non-infectious
4 types of tubulo-interstital nephritis
drug/toxin induced
analgesic abuse
urate nephropathy
myeloma kidney
common bugs of pyelonephritis
g negative bacili (e cioli, proteus, klebsiella, enterobacter)
strep fecalis, staph, fungi,
pathogenesis if comes from blood (pyelo)
infecting agent enters blood through ALL regions of kidney–>gross miliary distribution of microabsecesses
*lovalized to tubules and interstitum