Drug-Induced Kidney Disease- Intrinsic Renal; ATN Flashcards
Number 1 cause of hospital AKI
ATN
Clinical presentation of ATN
Acutely progressive increase in SCr and BUN, with decrease in GFR and urinary output
Metabolic acidosis
Hyperkalemia (depending on the site of injury)
FeNa >1%
Mg-wasting with cisplatin
Clinical presentation of ATN: urinalysis
Proteinuria
Cellular debris, muddy brown color, granular casts (“muddy brown casts”)
Drugs that can cause ATN
Aminoglycosides
Amphotericin B
Contrast media
Antineoplastic agents
Mechanisms that can cause ATN
Direct cellular toxicity
Prolonged ischemia
AGs: ATN risk is highest when aminoglycosides are used with what drugs?
Concomitant nephrotoxic drugs like vanco, amphotericin, contrast media, NSAIDs, etc.
AG nephrotoxicity is related to what?
trough concentrations
Goal trough concentration of gentamicin and tobramycin
<2mg/L
Goal trough concentration of amikacin
<8mg/L
What type of AG dosing interval may reduce risk of nephrotoxicity?
Extended-interval dosing
Goal trough concentrations of AGs in EID
Undetectable at 24 hours!!
ATN is more likely to occur in what formulation of Amphotericin B?
Conventional (compared to liposomal)
IV contrast media-induced ATN (CIN) pathology
combo of pre-renal and intrinsic renal injury, maybe post-renal
CIN risk factors
CKD
GFR <60ml/min/1.73m2
Low effective circulatory volume
Concomitant nephrotoxic agents
LARGE DOSE (volume) IODINATED CONTRAST
HIGH OSMOLAL CONTRAST
IONIC CONTRAST
SHORT TIME INTERVAL BETWEEN 2 CONTRAST ADMINISTRATIONS
CIN prevention: what is the gold standard of treatment?
SALINE HYDRATION
NS 1-1,5ml/kg/hr 12 hours prior to and after procedure