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38 Cards in this Set
- Front
- Back
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why is early dx of prerenal AKI critical
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its often reversible
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2 mechanisms of hypoperfusion
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absoloute reduction in ECF volume (hypovolemia)
decrease in effective circulating volume despite normal total ECF volume (CHF) |
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first step to workup a pt with oliguria or aniuria
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put in bladder; can be diagnostic ad therapeutic
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rhabdomyoloysis
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breakdown of muscle, released myoglobin, toxic to kidneys -> ATN
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why are tubular epithelial cells vuunurable to toxic or ischemic injury
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-extensive charged surface
- acive transport system -high metabolic rate -ability to concentrate substances ischemia/toxins -> loss of cell polarity-> abnormal ion transport -> increased distal sodium delivery = vasoconstriction via tubuloglomerular feedback tubular cells start to express cytokines and adhesion molecules that recruit leukoytes which can also contribute to injury injured cels detach -> lumen obstructed -> elevated intratubular pressure -> decreased GFR |
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endothelin
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vasoconstriction; released as a result of decresaed GFR/02 delivery to tubules
ischemia causes vasoconstriction worsening ischemia |
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Ischemic AKI
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skip lesions; straight portion of prox tubule and thick ascnending limb most vulnurable
eosinophilic hyaline casts/pigmented granula casts interstitial edema epithelial regeneration |
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toxic AKI (ATN)
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acute tubular injury is most prominent in the proximal concoluted tubules
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Acute tubular necrosis. Note the tubular vacuolization and dilation. This is from a patient with ethylene glycol poisoning.
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Robbins Pathologic Basis of Disease
Acute Kidney Injury: Note the necrotic tubular epithelial cells. There is evidence of detachment from their basement membranes. |
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know difference between ischemic and toxic AKI
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obstruction causes backpressure which decreases GFR, fluidbackleads into interstitium (edema)
afferent arteriolar construction due to tubuloglomerular feedback -> low blood flow to glomerulus which also causes ischemia to peritubules |
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azotemia vs uremia
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azotemia = lab BUN goes up
uremia = clinical manifestations |
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Uptodate
Urine sediment: This is an epithelial cell cast. The arrow is indicating a free epithelial cell |
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Uptodate
Urine sediment: This shows multiple muddy ,brown granular casts. |
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chronic tubulointerstitial nephritis
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This is characterized by renal insufficiency, non-nephrotic range proteinuria, and tubular damage.
Histologically there is interstitial fibrosis, tubular atrophy, and infiltration predominantly with mononuclear leukocytes. polyuria bc difficulty concentrating urine, nocturia, salt wasting, |
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mcc of infectious tubulointerstitial nephritis
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acute and chronic pyelonephritis and analgesics
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most common agents of pyelonephriis
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e. coli, proteus, klebsiella, enterobacter
immunocompromsied pts susceptible to ciruses like polyomavirus, CMV, adenovirus |
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vesicoureteral reflux
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incomplete ureter compression during micturation; bacterial infections can aggravate reflux
urine gains access to deep renal parenchymal tissue via ducts on tips of papillae; top/bottom pole of kidney |
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acute pyelonephritis
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focal abscesses in upper and lower poles; neutrophils in interstitium/tubules; after awhile can progress to tubular necrosis
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acute pyelonephritis
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focal abscesses in upper and lower poles; neutrophils in interstitium/tubules; after awhile can progress to tubular necrosis
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complications of acute pyelonephritis
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papillary necrosis
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polyoma virus nephropathy
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renal transplant failure in immunosuppressed individuals
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nuclei have glassy inclusion
(viral cytopathic effect); right is EM black = individual viral particles in the nucleus |
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broad depressed areas of cortical fibrosis and atrophy overlying a dilated calyx.
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chroinc glomerulonephritis (chronic pyelonephritis)
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atrophic tubules in some areas and dilated in others (thyroidization) -> casts remain in tubules that look eosinophilic
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chronic pyelonephritis
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yellow nodules in kidney
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xanthogranulomatous pyelonephritis associated with proteus
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messsy asyymetrical gnarled kidneys in chronic pyelonephritis (as opposed to sclerosis)
note thyroidization of kidney the dip indicates fibrosis which contracts down |
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15 days earlier pt was started on penicillin (diuretic, NSAID, sulfomaimde, rifampin); pt w azotemia/acute renal failure
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drug induced interstitial nephritis
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acetaminophen + asprin
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acetominophen depltes glutathione, no ROS protection
asprin inhibits PGE2 = vasoconstriction -> ischemia |
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acute uric acid nephropathy
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leukemia/lymphoma -> acidic pH potentiates the precipitation of uric acid = obstruction/ARF
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chronic urate nephropathy
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chronic hyperuricemia -> gout
monosodium urate crystals deposit in the acidic environment |
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Individual with hypercalcemia (hyperpaathyroidism, mm, vitamin D intoication, metastati cancer)
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deposition of calcium in kidney -> tubulointerstiial dz/renal insufficiency/calcifiedc ellular disease can obstruct lumen
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multiple myeloma
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bens jones protein (free light chains directly toxic to tubules) -> cast nephropathy
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amyloidosis
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light chain dz
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in pt w multiple myeloma
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Robbins Pathologic Basis of Disease
Light –chain cast nephropathy. Note the angulated tubular casts bence-jones cast are pink/blue amorphous masses w can have fracutred or angulated borders |
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child/elderly pt who had diarrhea and influenza followed by GI bleeding, oliguria and hematuria. Blood smear shows shistocytes
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HUS (E. coli 0157:H7)
platelet activation leads to reduction in NO = constricted capillaries to facilitate thrombosis |
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kid w oliguria, hematuria and ablood smear w shistocytes
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microangiopathic hemolytic anemia (schistocytes), thrombocytopenia, neuro Δ’s HTN
platelet activation leads to reduction in NO = constricted capillaries to facilitate thrombosis |
