Diagnostics

• Compare current and previous creatinine levels to determine if the process is acute.

• Check diagnostic criteria and perform staging of AKI.

• Determine the most likely mechanism of AKI (i.e., prerenal, intrinsic, or postrenal) based on:

  • A comprehensive chart review, history, and physical examination

  • Supportive diagnostic findings and response to initial interventions

• Consider further testing for specific underlying causes of AKI.

In the absence of previously documented creatinine levels, stable creatinine levels with findings such as chronic anemia and small hyperechoic kidneys on ultrasound suggest CKD rather than AKI.

Clinical presentation, laboratory tests, imaging, response to initial therapy, and, in some cases, histopathology are required to determine the underlying cause of AKI.

• Acute kidney injury is defined as the presence of any of the following criteria: [7]

  • Increase in serum creatinine by ≥ 0.3 mg/dL (26.5 μmol/L) within 48 hours.

  • Increase in serum creatinine to ≥ 1.5 times baseline level within 7 days.

  • Decrease in urine output to < 0.5 mL/kg/hour for ≥ 6 hours.

• The KDIGO stages are widely used and correlate with the risk of death, need for renal replacement therapy, and long-term outcomes (e.g., CKD).

• Other classifications include: [7]

  • RIFLE criteria: A classification system for acute kidney injury

    • The acronym stands for Risk, Injury, Failure, Loss, and End-stage kidney disease.

    • For the first three categories, patients are classified according to the level of kidney injury (i.e., degree of increase in serum creatinine and/or decrease in GFR and urine output) and for the last two categories, according to the duration of complete loss of kidney function.

  • Acute Kidney Injury Network (AKIN) criteria

• Blood study findings

  • Elevated serum creatinine

  • Serum BUN:creatinine ratio ≥ 20:1

• Urine study findings

  • Normal urinalysis

  • Low urinary sodium and urea excretion

    • Low fractional excretion of sodium (FENa < 1%)

    • Low fractional excretion of urea (FEUrea < 35%)

  • High urine osmolality (> 500 mOsm/kg) and specific gravity (> 1.020)

  • Urine sediment: hyaline casts due to concentrated urine in the setting of low renal perfusion

• Clinical findings: rapid improvement in renal function following acute intervention

Patients with prerenal AKI receiving diuretic therapy may have a falsely elevated FENa. Therefore, FEUrea may be more informative in this setting.

• Blood study findings

  • Elevated serum creatinine concentration and rapidly rising serum creatinine level

  • BUN:creatinine ratio ≤ 15:1

• Urine study findings

  • High urinary sodium and urea excretion

    • High urine sodium concentration (> 40 mEq/L)

    • High fractional excretion of sodium (FENa > 2–3%) [8][15]

    • High fractional excretion of urea (FEUrea > 50%) [15]

  • Low urine osmolality (< 350 mOsm/kg)

  • Urine sediment: renal tubular epithelial cells or granular, muddy brown, or pigmented casts

• Biopsy: e.g., in suspected rapidly progressive glomerulonephritis

• Clinical findings: lack of response to acute intervention

A falsely low FENa may be seen in some patients with intrinsic AKI, e.g., due to glomerulonephritis, acute interstitial nephritis, rhabdomyolysis, or contrast-induced nephropathy.

• Blood study findings

  • Elevated serum creatinine concentration in bilateral obstruction

  • BUN:creatinine ratio varies; usually normal (i.e., 10:1–20:1)

• Urine study findings

  • Normal urinalysis: e.g., when due to neurogenic bladder

  • Hematuria: e.g., when due to stones, bladder cancer, clots

  • Urine osmolality varies.

• Imaging (renal ultrasound or noncontrast CT scan)

  • Bladder distention, high postvoid residual volume, bilateral hydronephrosis, and/or obstructing stones

  • See “Imaging modalities” in “Urinary tract obstruction.”

• Clinical findings: rapid improvement in renal function following resolution of the obstruction

Imaging

Imaging of the kidneys and urinary tract is not necessary to establish a diagnosis of AKI but may be needed to determine the etiology.

• Ultrasound

  • Obtain urgently to assess for hydronephrosis in patients with risk factors for urinary tract obstruction.Consider when evaluating renal dysfunction of unclear etiology.

• Noncontrast CT

  • Obtain if ultrasound shows hydronephrosis but does not reveal the cause of the obstruction.

  • Consider when clinical suspicion of obstruction remains high despite the absence of hydronephrosis on ultrasound.

  • See also “Imaging modalities” in “Urinary tract obstruction.”

Obtain an urgent ultrasound to rule out hydronephrosis in patients with risk factors for urinary tract obstruction.

While ultrasound is the initial test of choice to assess for urinary tract obstruction, CT has greater sensitivity for detecting obstructions and stones.

Not routinely indicated

• Consider if:

  • The cause of AKI cannot be identified after a thorough initial evaluation

  • Diagnostic confirmation of the cause (e.g., glomerulonephritis, myeloma nephropathy) is needed prior to initiating disease-specific therapy