• nephritis- inflammatory rxns
• acute tubular necrosis leading to renal failure- ischemic or toxic injury

• histology- destruction of tubular epithelial cells
• clinically- suppression of renal function

• renal ischemia (rarely marked, frequently not seen)
• toxic injury (MORE COMMON)

• think anything that results in decreased renal perfusion (associated with hypovolemia and shock)
  • surgical procedures
  • extensive trauma/burns
  • pancreatitis
  • rhabdomyolysis
  • septicemia
  • marked hemolysis (as seen in hemolytic transfusion rxns)
  • obstetric complications
  • heat stroke

• followed by prolonged period of prerenal azotemia
  • loss of ability to concentrate urine
  • elevated urine sodium
• onset usually symptomatic as oliguria (can be present without it though)

• ischemic damage to tubules causes tubular dysfunction, with backleak of filtered compounds into the tubular interstitium
• epithelial cells may slough into tubular lumen and form casts which increase pressure within Bowman's space, thus decreasing GFR
• intrarenal vasoconstriction may be stimulated, further decreasing glomerular filtration pressure

• elevated serum BUN and creatinine
• urinalysis
  • nonselective proteinuria
  • +/- mild hematuria
  • hyaline and granular casts
• urine chemistry
  • SG>serum SG
  • sodium and FENA are elevated

• enlarged kidneys
• kidneys tense pale
• on section
  • parenchyma appears to bulge out of capsule
  • cortex is pale and medula is dark with exaggeration of corticomedullary junction

necrosis of individual tubular cells, irregular spacing of epithelial cells, dropout of cells from tubules are characteristic of ATN

• minimal glomerular changes
• capillary tufts collapsed and bloodle3ss
• urinary space somewhat expanded
• parietal epithelial cells of Bowman's capsule may become tall and cuboidal (tubularization)
• PCT dilated with flattening of individual epithelial cells and loss of brush border (distalization)
• lumina with eosinophilc debris
• DCT's similar changes to PCT with dilation of lumina and flattening of epithelial cells, with cell casts often present (most hyaline and PAS positive)
• sloughed cells and cell fragments may be present in tubular lumina
• rare peritubular granulomas
• interstitium edematous
  • appears as pale and loose CT between widely spaced tubules
  • inflammatory cells are scant (but present)

• direct toxicity against tubular epithelial cells, with most toxins affecting the proximal portion of the nephron
  • unlike ischemic ATN which is patchier and usually involves tAL

• similar to ischemic ATN
• changes can be more subtle and closely resemble ischemic ATN depending on toxin

• tx- supportive
  • peritoneal dialysis or hemodialysis in severe cases until tubular function returns\
• prognosis- depends on status of other organs and control of complications (ex: infection)
  • renal failure generally lasts 1-2 weeks
  • likelihood of recovery diminishes after 4-6 weeks
  • poor prognostic signs- advanced age, multisystem organ failure, prolonged renal impairment, severe oliguria

• primary
• secondary (glomerular disease, vascular disorders, cystic disorders, metabolic disorders)

• definition- absence of hallmarks of glomerular injury
  • presence of defect in tubular function
• acute
  • interstitial edema
  • leukocyte infiltrate
  • focal tubular necrosis
• chronic
  • infiltration with mononuclear cells
  • prominent interstitial fibrosis
  • widespread tubular atrophy

• affects tubules, interstitium, renal pelvis
• acute
  • bacterial
  • associated with UTI
• chronic
  • bacterial infection and other factors
    • vesico-ureteral reflex
    • obstruction

ascending

hematogenous

• most common cause of pyelonephritis
• bacteria introduced into bladder will multiple in the presence of stasis in case of bladder dysfunction/ obstruction
• incompetence of vesicoureteral valve allow bacteria to ascend to ureter into pelvis
• intrarenal reflux to upper and lower pole of kidney

• ureteral obstruction
• immunosuppressed patient
• causative agents- nonenteric organisms (S. aureus and fungi)

• patchy interstitial suppurative inflammation (focal abscess or coalescent areas)
• early limited to interstitium then involves and destroys tubules producing tubular necrosis
• extends along the involved nephrons and collecting tubules

• papillary necrosis
  • epidemiology: diabetcis with UTI's
  • characteristics
    • usually bilateral
    • distal 2/3 of pyramid gray-white to yeellow
    • microscopy- coagulative infarct necrosis
    • leukocytic response at junction of viable tissue
• pyeonephrosis
  • associated wtih complete obstruction
  • microscopy- suppurative exudate fills pelvic calyceal system
• perinephric abscess
  • suppurative inflammation through renal capsule into perinephric tissue

• mononuclear infiltrate replaces the neutrophilic infiltrate
• scar and interstitial fibrosis
• tubular atrophy

• pain at CV angle- bladder symptoms and systemic evidence of infection
• uncomplicated pyelonephritis resolves with antibiotics
• persistent bacteriuria may lead to repeated episodes
• papillary necrosis may lead to acute renal failure

• definition- chronic tubulointerstitial inflammation and renal scarring with pathologic involvement of the calyces and pelvis
• two forms
  • chronic obstructive pyelonephritis
  • chronic reflux nephropathy
• important cause of end stage renal disease

• irregularly scarred kidneys
• coarse, discrete corticomedullary scar overlying dilated deformed calyx

• mixed tubular atrophy and hypertrophy
• variable interstitial inflammation and fibrosis
• periglomerular fibrosis, ischemic fibrous obliteration

1. gradual onset of renal insufficiency and HTN
2. bacteruria and pyuria
3. radiographically irregularly contracted scarred kidneys
4. proteinuria
5. glomerulosclerosis
6. end stage renal disease

• interstitial immunologic reactions
• acute renal failure
• subtle cummulative injury to tubules

• sulfonamides
• synthetic antibiotics and penicillins
• NSAIDs

• onset 2 weeks after exposure to drug
• symptoms
  • fever
  • eosinophilia
  • rash
  • renal abnormalities- hematuria, proteinuria, leukocyturia
• rising creatinine or acute renal failure
• immune mechanism
• withdrawal of offending drug is followed by recovery

• interstitial edema
• mononuclear infiltrate
• eosinophils and PMN's
• sometimes granulomas
• tubular necrosis and regeneration

• definition- chronic renal disease caused by excessive intake of analgesic mixtures (precipitated by injusting a mixture of at least two of the antipyretic analgesics)
  • phenacetin
  • aspirin
  • caffeine
  • acetaminophen
  • codeine
• symptoms
  • headache
  • anemia
  • GI symptoms
  • HTN
    UTI
  • inability to concentrate urine (early sign)
  • hematuria, renal colic (excreted papillae)

• tubulointerstitial nephritis with renal papillary necrosis
• papillae with various stages of necrosis
• loss and atrophy of tubules secondary to damaged papillae
• interstitial fibrosis and inflammation
• analgesic microangiopathy

• kidneys normal or slightly reduced in size
• cortex display depressed areas and raised areas
• papillae with various stages of necrosis

• clinical consequence: hemodynamically induced acute renal failure
• microscopy
  • acute HS interstitial nephritis
  • acute interstitial neprhitis and lipoid nephrosis
  • membrane glomerulonephritis

• cause- acute precipitation of uric acid crystals
• clinical consequences
  • chronic precipitation of crystals (gouty tophus)
  • neprholithiasis (uric acid stones)