acute kidney injury (W3) Flashcards
ischemic injury
- related to volume depletion and decreased perfusion
- toxic injury from chemicals
- sepsis
injury initiates
inflammatory response, vascular response, cell death
3 classes for AKI
- pre-renal
- intra-renal
- post-renal
pre-renal
before the kidneys!
most common cause is inadequate perfusion
hypotension, hypovolemia, sepsis, inadequate CO, renal vasoconstriction, renal artery stenosis
decreased GFR due to low glomerular filtration pressure
failure to restore blood volume, blood pressure, and oxygen delivery can cause ischemic cell injury and necrosis
intra-renal
most common cause is acute tubular necrosis (ATN)
related to pre-renal AKI, nephrotoxic agents, acute glomerulonephritis, vascular disease
pre-renal AKI can become intra-renal AKI
hypotension and hypovolemia cause ischemia and inflammatory response in kidney
cause of nephrotoxic acute tubular necrosis: antibiotics, exposure to heavy metals, contrast dye, rhabdomyolysis
post-renal
rare, usually occurs with urinary tract obstruction
causes: bladder outlet obstruction, prostatic hyperplasia, bilateral urethral obstruction, tumor, neurogenic bladder
acute kidney injury
sudden decline in function and rapidly progressive
decreased GFR (< 90 ml/min)
decreased UOP (> 30 ml/min)
increased BUN (10-20 mg/dl)
increased creatinine (0.5-1.2 mg/dl)
*normal in parenthesis
may be reversible
clinical manifestations of AKI
oliguria, < 400 ml/24 hours
begins 1 day after hypotensive event and lasts 1-3 weeks
AKI pharm treatment
goal to stabilize the patient until kidney function is returned
correct electrolyte imbalance
1. lasix to push kidneys to function and removed potassium
2. dectrose and insulin to help move potassium back into cells
3. binders- sodium potassium sulfonate, patriomer, sodiumzicanium cyclosilicate
correct acid-base imbalance (metabolic acidosis) with sodium bicarbonate
manage BP
avoid nephrotoxic drugs