Acute Kidney Injury Flashcards
Sudden impairment of kidney function –> retention of nitrogenous and other waste products normally cleared by the kidneys
Acute Kidney Injury
Common Diagnostic Features of AKI
↑ in BUN concentration
↑ in plasma or serum creatinine concentration
↓ in urine volume
KDIGO 2012 Definition of AKI
↑ in SCr by >0.3 mg/dL (>26.5 mmol/L) w/n 48 hrs
↑ in SCr to >1.5 x the baseline - occured w/n the prior 7 days
urine volume <0.5 mL for 6 hrs
MC form of AKI
prerenal azotemia
Due to inadequate renal plasma flow and intraglomerular hydrostatic pressure to support normal glomerular filtration
prerenal azotemia
-NO parenchymal damage
MC causes of intrinsic AKI
sepsis
ischemia
nephrotoxins (endogenous and exogenous)
Very important cause of AKI in the developing world
sepsis
The site of one of the most hypoxic regions in the body
renal medulla
Intrinsic AKI
tubular damage
glomerular damage
interstitial damage
vascular damage
Small Vessels Damage (Intrinsic AKI)
Glomerulonephritis Vasculitis TTP/HUS DIC Atheroemboli Malignant HTN Calcineurin inhibitors Sepsis
Tubules (Intrinsic AKI)
Toxic ATN Endogenous (rhabdomyolysis,hemolysis) Exogenous (contrast, cisplatin, gentamicin) Ischemic ATN Sepsis
Intratubular (Intrinsic AKI)
Endogenous • Myeloma proteins • Uric acid (tumor lysis syndrome) • Cellular debris
Exogenous
• Acyclovir, methotrexate
MC clinical conditions associated with prerenal azotemia
hypovolemia
↓ cardiac output
medications that interfere with renal autoregulatory responses (NSAID and inhibitors of Angiotensin II)
Risk factors for nephrotoxicity
age
CKD
prerenal azotemia
Clinical course of contrast AKI
↑ in SCr beginning 24–48 h following exposure
peaking within 3–5 days
resolving within 1 week