Tubulointerstitial Disease Flashcards
osmotic nephrosis
reversible renal tubular injury seen after admin of agents used to induce osmotic diuresis
what is this?
osmotic nephrosis
what is this? what does it indicate?
hyaline droplet change = protein resorption droplets in proximal tubular epithelium (results from increased glomerular loss of filtered proteins)
seen in severe proteinuria or nephrotic syndrome
clinical definition of acute renal failure
- acute drop in GFR
- oliguria/anuria
- elevated BUN and creatinine
pathologic appearance of ischemic AKI
which area is most susceptible?
swollen kidney w/ pale cortex and congested medulla
patchy and multifocal
most susceptible: prox tubule and TAL
which cells are most susceptible to toxic AKI
tubular epithelial cells
- tubular reabsorption
- active transport
- concentrationg function
clinical course of AKI/ATN
- initiating phase - 1-2 days w/ mild decrease in urine output
- maintenance phase: less urine, salt and H20 overload, increased BUN and K, metabolic alkalosis
- recovery phase
2 types of tubulointerstitial disease
- pyelonephritis
- tubulointerstitial nephritis
which type of bacteria usually causes pyelonephritis
gram neg
pathogenetic sequence for ascending pyelonephritis
- colonixation of distal urethra and introitis
- introduction into bladder
- incompetence of vesico-ureteral orifice –> reflux
type of infection
ascending pyelonephritis - linear/streaking pattern
type of infection
hematogenous pyelonephritis - miliary pattern of microabcesses throughout kidney
complications of acute pyelonephritis
- papillary necrosis
- pyonephrosis
- perinephric abcess
- scarring: broad-basses and u-shaped
what is chronic pyelonephritis?
name 2 types
pelvi-calyceal damage
- obstructive
- non-obstructive (reflux)
sx of drug/toxin-induced tubulointerstitial nephritis
average onset ~15 days after exposure
fever, eosinophilia, skin rash (25%)
ARF w/ oliguria (~50% cases)
pathogenetic sequence of drug-induced interstitial nephritis
- drug acts as a hapten secreted by the tubule
- drug binds to tubular cell component –> becomes immunogenic
- IgE and cell-mediated immune reaction to tubular cells or their BMs
what is this?
interstitial nephritis
patchy infiltrate w/ no polys (differentiates this from infection)
what is this?
tubulointersitial nephritis - inflammatory infiltrate w/ eosinophils
analgesic abuse nephropathy - causes
phenacetin, aspirin, caffeine, acetaminophen, codeine
additive dosing
pathogenesis of analgesic abuse nephropathy
acetaminophen: covalent binding and oxidative damage
aspirin: inhibits prostaglandin, predisposing papilla to ischemia
pathology of analgesic tubulointersitial nephritis
chronic tubulointerstitial nephritis and fibrosis
papillary necrosis
urothelial carcinoma (predisposed)
3 types of urate nephropathy
- acute uric acid nephropathy
- chronic urate nephropathy
- nephrolithiasis (in gout)
what is this?
myeloma kidney:
brittle casts w/ inflammation
multi-nucleated giant cells
