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
pathogeneiss if ascending pylo
colonization of urethra–>bladder–>incompetence of vescio-ureteral orifice–>reflux–>infectious agent colonizes pailla
microscopically with ascending puelo
streaking distribution
complications of acute pyelonephritis (4)
papillary necrosis
pyonephrosis
perinephric abscess
scarring
papillary necrosis is common in
ascending PN in DM, outflow obstruction
*usually bilateral
pyeonephrosis
accumulation of pus in kidney to the point where it becomse a big abscess
peripnephric abscess
when the pyonephrotic kidney bursts, releasing contents into periphery
scarring
broad shaped or ushaped, more common in upper or lower poles
chronic pyeloneprhitis cannot___because___
be diagnozed with LM of bx alone because we need to see deformity
MC of chornic pyelo
reflux, but obstructive exists too
most frequent cause of toxic tubulointerstital nephritis
synthetic penicillins/antibiotics (rifampin)
diuretics (thiazides)
Nsaids (phenylbutazone)
cimetidine
50% of drug tin dvelope
acute renal failure
pathogenesis of drug TIN
delayed
Ige hypersens to lypmphovytes
Macrophages
EOSINOPHILS
pathology drug induced TIN
lymphocytes in pathces but key is eosinophils
anaglesic abuse nephropathy is caused by
mass intake of phenacetin, aspirin, caffeine, acetaminophin, codeine
how does acetominophin hurt cells
covalent binding and oxidation
how does aspirin hurt cells
blocks PGE–>VC–>ischemia
what kind of pathology with analgesic abuse nephro
papillary necrosis
three types of urate nephropathy
acute uric acid
chronic urate
nephrolithiasis
acute uric acid nephro
ppy of urate crystasls in CD–>obstruction
**common in chemo
chronic uratenephropathy
patients with hyperuricemia
trophus formation- needle like crystals surrounded by giant cells
nephrolithiasis is seen with
gout patietns
patho in myeloma kidney
brittle (fractured) cast formation–>obstruction +/- granulomas
