AKIN Classification for Acute Kidney Injury (AKI)

AKIN Classification for AKI

Serum Creatinine Criteria

Urine Output Criteria

AKIN Stage: 0

No AKI

Does not meet AKIN criteria for acute kidney injury.

Classifies severity of acute kidney injury, similar to RIFLE Criteria .

Why Use

It is important to recognize when a change in creatinine is clinically significant so that the underlying cause can be identified and further damage prevented.

When to Use

Acute kidney injury (AKI) should be suspected if a patient’s serum creatinine rises above their baseline chronic value.

Formula

To be diagnosed with acute kidney injury by the AKIN definition, patient must have at least one of the following within the past 48 hours: Absolute increase in serum creatinine ≥0.3 mg/dL (≥26.4 μmol/L). Increase in serum creatinine ≥1.5x above baseline. Oliguria (urine output <0.5 mL/kg per hour) for >6 hours. Then, select the appropriate criterion leading to the highest possible stage, e.g. if serum creatinine is normal but urine output is <0.5 mL/kg/hour for >12 hours, AKIN Stage is 2. AKIN Classification Serum creatinine Urine output Not AKI according to AKIN Normal creatinine or <1.5x from baseline ≥0.5 mL/kg per hour for >6 hours Stage 1 Absolute increase ≥0.3 mg/dL (≥26.4 μmol/L) or ≥1.5-2x from baseline <0.5 mL/kg per hour for >6 hours Stage 2 Increase to >2-3x from baseline <0.5 mL/kg per hour for >12 hours Stage 3 Increase to >3x from baseline or ≥4.0 mg/dL (≥354 μmol/L) with acute increase ≥0.5 mg/dL (≥44 μmol/L) <0.3 mL/kg per hour for ≥24 hours or anuria for 12 hours

Pearls / Pitfalls

It is important to remember that creatinine is a product of normal muscle cell turnover and serves only as a marker of kidney function. When an elevation in creatinine is observed, the injury that caused it may still be ongoing, but started 24 to 48 hours prior to the increase. The relationship between serum creatinine and eGFR (amount of kidney function) is curvilinear, not linear. Therefore, the same absolute increase in creatinine may represent different severities of AKI depending on the presence or absence of baseline kidney dysfunction.

Management

The management of AKI is both supportive and focused on etiology. While a kidney biopsy is frequently not needed to determine the cause of AKI, it can provide essential information, particularly if a glomerulopathy is suspected as the cause.

Critical Actions

Management should focus on identifying the cause of kidney injury, determining the need for a kidney biopsy, and reversing all contributing factors to prevent further loss of kidney function. Clinical actions may include correcting volume depletion or hypotension and avoiding medications that can contribute to further kidney injury.

Advice

Causes of elevations in creatinine can be grouped into three categories: Prerenal: Not all elevations in creatinine represent actual injury to cells within the kidneys. Volume depletion (or effective arterial volume depletion) results in a need to retain sodium and other solutes at the level of the tubule to help support blood pressure. This can be marked by the presence of a low fractional excretion of sodium and can be effectively treated with volume expansion. While this is often called AKI, it is technically a physiologic response to decreased renal perfusion. Intrarenal : Intrarenal causes of acute kidney injury include damage to the glomeruli (glomerulopathies) or tubules (acute tubular necrosis or allergic interstitial nephritis). Next steps should include examining the urine to try to determine the location of the injury within the nephron. Postrenal : Postrenal causes are generally due to obstruction to urine flow at the level of the ureters, bladder, or urethra.