Renal Tubular and Interstitial Diseases Flashcards
Definition of AKI
Loss of renal function over hours or days
Clinically as retention of nitrogenous waste products (rising creatinine and urea)
Causes of AKI in hospital setting
ATN
ATN
Most common cause of AKI in hospitalized
Ischemia or exposure to substance directly toxic to tubular epithelial cells
Types of nephrotoxic injury
Ischemic injury
Aminoglycosides
IV contrast media…other random medicines..also .ethylene glycol
Endogenous - myoglobin from rhabdomyolysis
Ischemic - spetic, burns, homrrhage, prolonged dehydration, CHF
Most susceptible areas of injury of the PCT
S3 segment and TALH (thick ascending loop of Henle)
High tubular energy requirement (ATP)
Decreased O2 supply
Minimal glycolytic machinery
Pathology of ATN…early
Loss of apical brush borders
Blebbing of atypical cytoplams into lumen with eventual loss
Vacuoolization of cytoplasm
Pathology of ATN
Luminal ectasia
Epithelial simplification from loss of cytoplasm
Granular casts (of cellular debris and Tamm-Horsfall prtoein)
With renal tubular epithelial casts
ATN regnerative phase
Mitotic figures
increased N/C ratio
Prominent nucleoli
U/A of ATN
Tubular epithelial cells
Tubular epithelial casts
Granular casts “muddy brown”
Multiple granular casts
GFR and ATN
DECREASED because
Vasoconstriction - AA via increased NaCl and flow to the macula densa
Tubular obstruction - casts and cell debris
Denuded tubular epithelium - back leak of filtrate to the interstitium
Direct toxocity to glomerular vasculature
FENa
Frctional excretion of Na
Urinary (Na)/plasma (Na) *GFR
U(na)P(cr)/(PnaUcr)
When conserving Na, would be below 1%…in ATN, over 1-2%
ATN clincal
Sustained decrease in urine output
some do NOT have oliguria
Sodium and H2O overload - hypervolemia
Elevated BUN, creatinine, K+
Acidosis
ATN management
Prevention is key**
Na, H2O, and K restriction
Diuretics will not alter the outcome but will assist in management
Close assement of dosing
ATN recovery phase
Steady increase in urine volume…solute diuresis, eliminating the accumulated Na and water…decreased ability of kindye to concentrate (loss of medullary osmolarity and ADH)
Hypokalemia
BUN and cr return to normal
More infections
Atn outcome
Prognosis depends on clinical setting