2 Assessment and Laboratory Findings in Acute Kidney Injury

Learn how to recognize acute kidney injury, apply KDIGO diagnostic and staging criteria, and interpret laboratory and imaging findings when investigating its cause.

Recognizing acute kidney injury

is a sudden decline in kidney function. It may lead to accumulation of waste products and fluid, but early AKI can have few noticeable symptoms. Assessment combines the clinical history and examination with trends in and measured .

Compare results with a known baseline whenever possible: a single creatinine value may not reveal an acute change. Creatinine can rise only after kidney function has already declined, so falling can be an earlier warning. Estimated glomerular filtration rate (eGFR) is less reliable while creatinine is changing rapidly.

Ask about recent illness or surgery, fluid losses, urinary symptoms, relevant medical history, and prescription, over-the-counter, and other drug exposures. Examine for findings that may suggest reduced circulation, infection, or fluid accumulation, such as low blood pressure, tachycardia, edema, or crackles. These findings are not specific to AKI and must be interpreted alongside the history and test results.

Diagnosis and KDIGO staging

AKI is diagnosed when any one of the is met:

rises by at least $0.3\ \mathrm{mg/dL}$ ( $26.5\ \mu\mathrm{mol/L}$ ) within $48$ hours.
rises to at least $1.5$ times baseline within the previous $7$ days.
Urine volume is less than $0.5\ \mathrm{mL/kg/hour}$ for $6$ hours.

is measured over time and interpreted relative to body weight. A brief or unmeasured period of low output is not enough to apply a duration-based criterion.

Assigning a stage

Stage AKI using the most severe serum-creatinine or urine-output criterion met. The criteria can identify different patients, so assess both. can vary by cause, and some people with AKI are not oliguric.

Stage 1: is $1.5$ to $1.9$ times baseline, or increases by at least $0.3\ \mathrm{mg/dL}$ ; alternatively, is less than $0.5\ \mathrm{mL/kg/hour}$ for $6$ to $12$ hours.
Stage 2: is $2.0$ to $2.9$ times baseline; alternatively, is less than $0.5\ \mathrm{mL/kg/hour}$ for at least $12$ hours.
Stage 3: is at least $3$ times baseline, is at least $4.0\ \mathrm{mg/dL}$ ( $353.6\ \mu\mathrm{mol/L}$ ), or renal replacement therapy is initiated; alternatively, is less than $0.3\ \mathrm{mL/kg/hour}$ for at least $24$ hours, or there is no urine (anuria) for at least $12$ hours.

For patients younger than $18$ years, KDIGO also includes a decrease in eGFR to below $35\ \mathrm{mL/min/1.73\ m^2}$ as a Stage 3 criterion. The terms oliguric and nonoliguric describe ; they are not separate KDIGO stages. A patient does not have to pass through every stage in order.

Tests that help identify the cause

Testing helps assess kidney-function changes, identify complications, and investigate possible causes. No single test necessarily establishes the cause.

Blood tests: Serial and blood urea nitrogen (BUN) help assess changing kidney function. Electrolytes and bicarbonate help identify complications, while a complete blood count may help evaluate other causes or consequences.
: Dipstick testing checks for blood, protein, leukocytes, nitrites, and glucose. Granular casts and tubular cells may support tubular injury. Red-cell casts, or blood with protein, may suggest glomerular disease. A bland result does not rule out AKI.
Urine chemistries: Urine sodium, urea, and creatinine, or calculated indices such as , may help distinguish causes in context. Medications and the patient’s clinical state can affect these results, so they should not be interpreted alone.
Bladder assessment and imaging: A bladder scan or postvoid residual can identify urinary retention. Renal or urinary-tract ultrasound is useful when obstruction is suspected or the cause remains unclear; it is not routinely required when the cause is already established.
Targeted testing: Depending on the presentation, clinicians may order tests for infection, muscle injury, immune-mediated disease, or other suspected causes. Kidney biopsy is considered in selected cases when the diagnosis remains uncertain and the result could guide care.

Expected laboratory changes

As kidney filtration and excretion decline, creatinine and BUN commonly rise. Other abnormalities depend on severity, cause, intake, medications, and treatments; they are possible findings, not automatic features of every AKI stage.

Possible associated findings include:

.
Metabolic acidosis, reflected by low bicarbonate.
Phosphate retention and low calcium.
Low serum sodium, particularly when there is excess water relative to sodium.

An electrocardiogram may be checked when is suspected because high potassium can affect cardiac conduction. Trends and clinical findings matter more than any isolated result.

KDIGO stages describe severity using creatinine and urine-output criteria. They do not prescribe a fixed sequence of laboratory abnormalities. Urine-output descriptions such as oliguric and nonoliguric do not determine a separate stage.

Applying the criteria

These examples show how to apply the criteria; when creatinine and urine-output criteria indicate different stages, use the most severe stage met.

A baseline creatinine of $1.0\ \mathrm{mg/dL}$ rising to $1.4\ \mathrm{mg/dL}$ over $36$ hours meets the AKI definition: the increase is $0.4\ \mathrm{mg/dL}$ within $48$ hours. It meets the creatinine-based Stage 1 criterion.
of $0.4\ \mathrm{mL/kg/hour}$ for $8$ hours meets the Stage 1 urine-output criterion. Continue assessing duration and trends; do not infer the cause from alone.
Creatinine at $2.2$ times baseline with below $0.3\ \mathrm{mL/kg/hour}$ for $26$ hours is Stage 3, because the urine-output criterion reaches Stage 3.
To investigate obstruction and intrinsic kidney disease in a patient with rising creatinine, a bladder scan or postvoid residual and, when indicated, urinary-tract ultrasound can assess for obstruction. can provide clues to intrinsic kidney disease.