Acute Kidney Injury

Descriptive text is not available for this image BASICS

DESCRIPTION

  • An abrupt loss of kidney function, acute kidney injury (AKI) defined as (1):
    • Increase in serum creatinine (SCr) of ≥0.3 mg/dL within 48 hours
    • ≥50% increase in baseline SCr within 7 days
    • Urine output of <0.5 mL/kg/hr for 6 hours
  • Staging is based on SCr or urine output:

    StageIncrease in Baseline CreatinineIncrease in CreatinineUrine Output
    11.5 times≥0.3 mg/dL<0.5 mL/kg/hr for 6–12 hours
    22.0–2.9 timesN/A<0.5 mL/kg/hr for ≥12 hours
    33.0 times≥4.0 mg/dL<0.3 mL/kg/hr for ≥24 hours

  • The result is retention of nitrogenous waste, electrolyte, acid–base, and volume abnormalities (1).

EPIDEMIOLOGY

Incidence

  • 5% of hospital and 30% of ICU admissions have AKI. 25% of patients develop AKI while hospitalized; 50% of these cases are iatrogenic.
  • Developing AKI as an inpatient is associated with >4-fold increased risk of death (2).

ETIOLOGY AND PATHOPHYSIOLOGY

Three categories: prerenal, intrarenal, and postrenal

  • Prerenal (reduced renal perfusion, typically reversible):
    • Decreased renal perfusion (often due to hypovolemia) leads to a decrease in glomerular filtration rate (GFR)
    • Caused by hypotension, volume depletion (GI losses, excessive sweating, diuretics, hemorrhage); renal artery stenosis/embolism; burns; heart/liver failure; if decreased perfusion is prolonged or severe, can progress to ischemic acute tubular necrosis (ATN)
  • Intrarenal (intrinsic kidney injury, often from prolonged or severe renal hypoperfusion)
    • ATN—from prolonged prerenal azotemia, radiographic contrast material, aminoglycosides, nonsteroidal anti-inflammatory drugs (NSAIDs), or other nephrotoxic substances
    • Glomerulonephritis (GN)
    • Acute interstitial nephritis (AIN; drug induced), arteriolar insults, vasculitis, accelerated hypertension, cholesterol embolization (following an intra-arterial procedure), intrarenal deposition/sludging (uric acid nephropathy and multiple myeloma [Bence Jones proteins])
  • Postrenal (obstruction of the collecting system)
    • Extrinsic compression (e.g., benign prostatic hypertrophy [BPH], carcinoma, pregnancy); intrinsic obstruction (e.g., calculus, tumor, clot, stricture, sloughed papillae); decreased function (e.g., neurogenic bladder), leading to obstruction of the urinary collection system.

Genetics

No known genetic pattern

RISK FACTORS

  • Chronic kidney disease (CKD); comorbid conditions (e.g., diabetes mellitus, hypertension, heart failure, liver failure); advanced age; radiocontrast material exposure (intravascular), female gender, African American
  • Medications that impair autoregulation of GFR (NSAIDs, angiotensin-converting enzyme inhibitors [ACEIs], angiotensin II receptor blockers [ARBs], cyclosporine/tacrolimus)
  • Nephrotoxic medications (e.g., aminoglycoside antibiotics, platinum-based chemotherapy); hypovolemia (e.g., diuretics, hemorrhage, GI losses); sepsis, surgery, rhabdomyolysis, burns; solitary kidney (risk in nephrolithiasis); BPH; malignancy (e.g., multiple myeloma)

GENERAL PREVENTION

  • Maintain adequate renal perfusion with isotonic fluids, vasopressor support if necessary.
  • Avoid nephrotoxic agents.

COMMONLY ASSOCIATED CONDITIONS

Hyperkalemia, hyperphosphatemia, hypercalcemia, hyperuricemia, hydronephrosis, BPH, nephrolithiasis, congestive heart failure (CHF), uremic pericarditis, cirrhosis, CKD, malignant hypertension, vasculitis, drug reactions, sepsis, severe trauma, burns, transfusion reactions, recent chemotherapy, rhabdomyolysis, internal bleeding, dehydration

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