Acute Kidney Injury in Adults

Background

• Acute kidney injury (AKI) is a rapid reduction in kidney function (within 48 hours) as measured by an increase in serum creatinine, decrease in urine output, and/or need for renal replacement therapy.
• It is characterized by either direct injury to the kidney or acute impairment of function or both.
• AKI may result from various conditions, including:
  • decreased renal perfusion leading to prerenal azotemia (often associated with elevated blood urea nitrogen:creatinine ratio > 20:1 and low fractional excretion of sodium)
  • postrenal obstruction (due to either extrarenal obstruction of urinary flow, or intrarenal obstruction due to crystals, clots, stones, or tumors)
  • tubular disorders including acute tubular necrosis (which can be toxic or ischemic) or acute interstitial nephritis
  • causes of glomerulonephritis (such as systemic lupus erythematosus [SLE], IgA nephropathy, membranous glomerulonephritis, focal segmental glomerulosclerosis [FSGS], antineutrophil cytoplasmic antibodies [ANCA] associated vasculitis, antiglomerular basement membrane [anti-GBM] disease, and thrombotic microangiopathy)
  • vascular diseases including renal atheroembolic disease and malignant hypertension

Evaluation

• Mild-to-moderate acute kidney injury (AKI) can have no symptoms at all, while symptoms in severe cases may include confusion, malaise, swelling, nausea, weight gain, poor appetite, shortness of breath, and lethargy.
• Diagnose AKI in patients with any of the following:
  • increase in serum creatinine by ≥ 0.3 mg/dL (≥ 26.5 mcmol/L) within 48 hours
  • increase in serum creatinine to ≥ 1.5 times baseline, which is known or presumed to have occurred within prior 7 days
  • urine volume < 0.5 mL/kg/hour for 6 hours
• Use findings from history and physical exam to help identify prerenal, intrinsic, or postrenal causes of AKI.
• Initial blood tests should include blood urea nitrogen (BUN), creatinine, serum electrolytes, and complete blood count. BUN:creatinine ratio and fractional excretion of sodium may help distinguish between prerenal and intrinsic causes of AKI.
  • Compare measured BUN and creatinine levels to baseline levels, if they are known, to rule out presence of chronic kidney disease.
  • If baseline creatinine is not known and there is no evidence for chronic kidney disease, assume a previously normal glomerular filtration rate.
  • Perform further blood tests (such as for hemolysis or antibodies) based on clinical suspicion as to the cause of AKI.
• Perform imaging with renal ultrasound to evaluate renal size and to rule out an obstruction (Strong recommendation); noncontrast computed tomography may be considered if there is suspicion of a stone.
• Initial urine studies should include:
  • volume
  • osmolality
  • creatinine and sodium (to calculate fractional excretion)
  • dipstick testing, including urinary protein
  • microscopy
• Consider a kidney biopsy when conditions such as glomerulonephritis, vasculitis, or interstitial nephritis are suspected and prerenal and postrenal causes have been excluded (Weak recommendation).

Management

• Consider hospitalization for patients requiring advanced diagnostic evaluation, with complications, critical illness, or in those not responsive to initial management.
• Monitor and adjust fluid and electrolyte balance to address volume depletion or overload, and electrolyte abnormalities.
• Stop exposure to nephrotoxic agents if possible, or consider dose adjustments to medications as appropriate.
• Utilize procedures such as placement of nephrostomy tube or urinary catheter in patients with urinary obstruction.
• Identify and treat any infectious cause.
• Nutritional support:
  • Consider total energy intake of 20-30 kcal/kg/day in patients with any stage of AKI (Weak recommendation);
  • Consider avoiding protein restriction as means of preventing or delaying initiation of renal replacement therapy (RRT) (Weak recommendation);
  • Consider nutrition via enteral route as preferred option (Weak recommendation).
• Diuretics are not recommended for the routine treatment of AKI (Strong recommendation); reserve diuretics for patients with volume overload. .
• The following medications are not typically recommended for treatment of AKI due to increased risk for hypotension and low-quality of evidence for benefit:
  • low-dose dopamine (1-3 mg/kg/minute) (Strong recommendation );
  • fenoldopam (Weak recommendation);
  • atrial natriuretic peptide (ANP) (Weak recommendation ).
• Consider consultation with a nephrologist.
• Renal replacement therapy (RRT):
  • Start RRT emergently when life-threatening changes in fluid, electrolyte, and acid-base balance occur (Strong recommendation).
  • Take into account the entire clinical scenario, presence of factors that can be modified with RRT, and trends in laboratory tests when deciding whether to start RRT instead of relying on blood urea nitrogen (BUN) and creatinine thresholds alone (Strong recommendation).
• Timely follow-up is important for all patients with AKI, and may include referral to a nephrologist or urologist if appropriate.