Acute kidney injury: recognition and staging

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

AKI is a clinical syndrome of abrupt loss of kidney function, not a complete diagnosis. NICE uses changes in creatinine and urine output to detect and stage it, but those markers respond on different timescales. A patient may have extensive tubular injury before creatinine has accumulated, and administered fluid may dilute the apparent rise. Conversely, a transient creatinine change can occur without established structural damage. The useful bedside task is therefore to confirm the trend, grade severity, identify complications and find the mechanism in parallel.

Initial assessment should combine ABCDE, haemodynamic and congestion examination, a reliable urine-output record, urinalysis, medication and exposure history, infection assessment and a search for obstruction. Look for the precipitating illness—vomiting, haemorrhage, sepsis, cardiac failure, surgery, urinary symptoms, contrast or a new medicine—and for evidence that the kidneys are themselves inflamed or vascularly injured. Haematuria with significant proteinuria, systemic inflammatory features, thrombocytopenia or a rapidly rising creatinine changes the urgency and differential.

Use adapted specialist pathways for children, pregnancy, kidney transplant recipients and people already receiving dialysis. In adults, align observation frequency, laboratory alerts, renal referral and medicine changes with the treating organisation’s current policies.

Key points

Diagnose AKI in an adult when serum creatinine rises by at least 26 micromol/L within 48 hours, rises to at least 1.5 times a known or presumed baseline within 7 days, or urine output falls below 0.5 mL/kg/hour for more than 6 hours.
Use the worst KDIGO creatinine or urine-output criterion. Stage 1: creatinine 1.5–1.9 times baseline or a rise of at least 26 micromol/L; urine output below 0.5 mL/kg/hour for 6–12 hours. Stage 2: creatinine 2.0–2.9 times baseline; urine output below 0.5 mL/kg/hour for at least 12 hours. Stage 3: creatinine at least 3 times baseline, an increase to at least 354 micromol/L with an acute rise of at least 44 micromol/L, or initiation of renal replacement therapy; urine output below 0.3 mL/kg/hour for at least 24 hours or anuria for at least 12 hours.
Creatinine is a delayed concentration marker influenced by muscle mass, fluid balance and laboratory timing; an apparently normal result cannot exclude evolving injury after shock, sepsis or toxin exposure.
Retrieve previous results and reconstruct the timeline. The same creatinine may represent stable CKD, AKI on CKD, or a major acute fall in filtration in a person with low muscle mass.
Measure and document urine output rather than relying on the phrase ‘passing urine’; non-oliguric AKI can still be severe, while blocked catheters and inaccurate fluid charts can mimic oliguria.
Classify the likely mechanism as impaired perfusion, intrinsic renal injury or urinary obstruction, while recognising that hospital AKI commonly has several concurrent causes.
Review every medicine for haemodynamic effect, direct nephrotoxicity, renal accumulation and the consequences of temporary interruption; create an explicit restart plan rather than allowing important long-term therapy to disappear.
Escalation follows physiology and trajectory, not a creatinine threshold alone: rapidly rising potassium, oxygen requirement, acidosis, altered cognition or worsening oliguria may demand action before stage 3 is reached.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Reduced effective renal perfusion

Hypovolaemia, haemorrhage, sepsis-related vasodilatation, reduced cardiac output and severe systemic congestion can lower renal perfusion; several may coexist, and prolonged haemodynamic stress can progress to structural tubular injury.

Direct parenchymal injury

Ischaemia, sepsis, nephrotoxins, pigments, interstitial hypersensitivity, glomerular inflammation and renal vascular disease can injure tubules, interstitium, glomeruli or vessels and produce distinct urine and systemic patterns.

Urinary tract obstruction

Prostatic or bladder-outflow disease, stones, malignancy, retroperitoneal disease, clots and blocked catheters can raise upstream pressure; bilateral obstruction or obstruction of a solitary functioning kidney causes AKI.

Mixed and iatrogenic triggers

Hospital AKI is commonly multifactorial, with infection, surgery, contrast exposure, haemodynamic medicines, direct nephrotoxins and impaired drainage combining in a susceptible person with CKD, diabetes or frailty.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Abrupt filtration loss
Reduced glomerular capillary pressure or filtration-surface injury lowers GFR, while creatinine accumulates only after a delay and is modified by distribution volume, production and renal secretion.
2
Tubular dysfunction
Injured tubular cells lose polarity and transport function, obstruct the lumen and permit filtrate back-leak; impaired sodium and water handling contributes to oliguria, acidosis and electrolyte disturbance.
3
Inflammation and microvascular injury
Endothelial dysfunction, microcirculatory shunting, leukocyte activation and interstitial oedema can sustain renal injury even after systemic blood pressure or apparent circulating volume has improved.
4
Systemic consequences
Declining excretion and homeostasis cause potassium, acid, salt, water and uraemic-solute accumulation; severity depends on injury rate, residual kidney function, catabolic load and administered fluid or medicines.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Creatinine-defined AKIRed flag

A rise of at least 26 micromol/L within 48 hours or at least 50% above baseline within 7 days meets an adult AKI criterion. Search laboratory records for a credible baseline and state whether the timing is known, estimated or uncertain.

Urine-output-defined AKIRed flag

Output below 0.5 mL/kg/hour for over 6 hours is sufficient even before creatinine rises. Confirm measurement, catheter patency and body weight, and distinguish oliguria from complete anuria because anuria strongly raises obstruction or catastrophic vascular disease.

AKI on chronic kidney disease

A previously reduced eGFR does not prevent an acute diagnosis. Compare current creatinine with stable historical values, examine kidney size and chronic complications, and stage the acute component from the appropriate baseline rather than labelling all impairment as chronic.

Intrinsic renal warning patternRed flag

Blood and protein on urinalysis, red-cell casts if microscopy is available, hypertension, oedema, rash, pulmonary haemorrhage or systemic vasculitic features suggest glomerular or interstitial disease and warrant early nephrology discussion rather than repeated fluid challenges.

Complicated AKIRed flag

ECG change from hyperkalaemia, refractory pulmonary oedema, severe metabolic acidosis, uraemic pericarditic pain or encephalopathy, and a suspected infected obstructed system are time-critical complications whose treatment must begin while staging and cause are refined.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Serial serum creatinine, urea and electrolytesFirst step
Why
Confirm an acute change, stage severity and expose dangerous potassium or bicarbonate disturbance.
Interpretation and limitations
Plot values against dates and a reliable baseline; a rising creatinine despite resuscitation suggests continuing injury, while a falling result may lag behind clinical recovery. Urea is affected by catabolism, gastrointestinal bleeding and hydration and must not stage AKI.
02
Measured urine output and fluid balance
Why
Detect oliguria early and relate renal response to intake, losses and congestion.
Interpretation and limitations
Use hourly output in unstable or catheterised patients and a weight-based rate where possible. Check the drainage system before calling anuria; persistent oliguria despite restored perfusion signals higher risk, but preserved output does not exclude severe AKI.
03
Urinalysis with urine albumin or protein quantification
Why
Separate a bland haemodynamic or tubular picture from glomerular, interstitial, infective or pigment patterns.
Interpretation and limitations
Blood plus substantial protein supports glomerular disease; leukocytes can accompany infection or interstitial nephritis; haem-positive urine with few red cells suggests myoglobin. Quantify unexpected protein and interpret infection markers with symptoms and culture.
04
Full blood count, CRP, venous blood gas and relevant cultures
Why
Assess sepsis, anaemia, thrombocytopenia and acid–base consequences that may reveal the cause or urgency.
Interpretation and limitations
Thrombocytopenia with haemolysis raises thrombotic microangiopathy; severe acidaemia or lactate directs resuscitation; cultures should precede antimicrobials when feasible but must not delay treatment of sepsis.
05
Renal tract ultrasonography
Why
Identify hydronephrosis, bladder distension and structural clues when obstruction is possible or the cause remains unclear.
Interpretation and limitations
NICE recommends urgent imaging when there is no identified cause or obstruction risk, and more immediate imaging when pyonephrosis is suspected. Early obstruction can lack dilatation, so a negative scan does not overrule a compelling clinical picture.
06
ECG and cardiorespiratory assessment
Why
Find hyperkalaemic conduction toxicity and pulmonary oedema before biochemical deterioration becomes catastrophic.
Interpretation and limitations
Peaked T waves, PR prolongation, P-wave loss or QRS widening demand emergency hyperkalaemia treatment; normal ECG does not make a markedly raised or rapidly rising potassium safe. Lung signs, oxygen need and imaging help distinguish congestion from simple dehydration.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Chronic kidney disease

A stable high creatinine, small kidneys, longstanding albuminuria or chronic anaemia and mineral-bone changes suggest CKD; historical results distinguish stable CKD from AKI and reveal acute-on-chronic injury.

Drug-related creatinine rise

Trimethoprim, cobicistat and other transporter inhibitors can raise creatinine by reducing tubular secretion without a matching fall in GFR; timing, clinical stability and an alternative filtration marker may expose this mimic.

Creatinine production or dilution

Muscle injury, creatine intake or assay interference can increase creatinine, whereas low muscle mass and fluid accumulation can conceal injury; interpret the biochemical change with urine output and trajectory.

Apparent oliguria

Incomplete collection, catheter kinking, drainage-bag position or unrecorded voids can mimic oliguria; bladder retention is genuine post-renal risk and must not be dismissed as a charting problem.

Acute kidney disease

Subacute kidney dysfunction persisting for 7 to 90 days may represent acute kidney disease rather than resolved AKI or established CKD; the timeline and repeat values determine the appropriate temporal label.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First hourStabilise and establish severityFirst stepA laboratory alert, new oliguria or clinical suspicion of acute renal dysfunction.

11. Perform ABCDE, obtain observations, assess perfusion and congestion, verify urine output and check the catheter or bladder when relevant.
22. Send urgent creatinine, electrolytes and venous gas, obtain an ECG if potassium may be raised, and begin treatment of any immediate physiological threat.
33. Retrieve baseline results, apply both creatinine and urine-output criteria, record the highest stage and document the direction and speed of change.
44. Review medicines and exposures, treat sepsis or shock promptly, and call renal, critical care or urology early when complications or diagnostic red flags are present.

02Cause searchDifferentiate perfusion, parenchymal injury and obstructionOnce immediate threats are controlled or when the mechanism is not already secure.

11. Reconstruct fluid losses, haemorrhage, infection, peri-operative hypotension, cardiac or hepatic decompensation, new drugs and urinary symptoms on a dated timeline.
22. Examine jugular venous pressure, oedema, lungs, capillary refill, abdomen, bladder and prostate where appropriate; interpret a single blood pressure in its usual clinical context.
33. Use urinalysis and focused blood tests to identify inflammatory, pigment, infectious or microangiopathic patterns, and request ultrasound promptly if obstruction is credible.
44. Reassess after each intervention; a label such as ‘pre-renal’ should be revised if the trajectory, sediment or systemic findings point elsewhere.

03EscalationRespond to severe or non-resolving injuryEscalationStage 3 AKI, rapidly worsening values, persistent oliguria, unclear cause or any dialysis-level complication.

11. Contact nephrology urgently for refractory hyperkalaemia, acidosis, pulmonary oedema, uraemic complications, suspected intrinsic renal disease or possible renal replacement therapy.
22. Contact urology immediately for infected obstruction and urgently for upper-tract obstruction, solitary-kidney obstruction or failure to drain the bladder.
33. Increase observation frequency, stop avoidable kidney insults, adjust all renally cleared medicines and prepare access, transfer or critical-care support according to specialist advice.
44. Communicate stage, suspected cause, baseline, trend, urine output, fluid status, current threats and treatments rather than referring with creatinine alone.

Key medicines and prescribing safety1 treatment · regimens, roles and cautions

Restores circulating volume in genuine hypovolaemia and may reverse haemodynamic kidney dysfunction before tubular damage becomes established.

Balanced isotonic crystalloid

Give a cautious bolus only when clinical assessment supports intravascular depletion, then reassess immediately; use the current local resuscitation protocol rather than a fixed cumulative volume.

Avoid automatic repeated boluses in pulmonary oedema, advanced cardiac failure or venous congestion. Document endpoints such as perfusion, blood pressure, lung findings and urine response; fluid is a treatment, not a diagnostic ritual.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Hyperkalaemia and acidosis

Reduced potassium and acid excretion can cause malignant arrhythmia, muscle weakness and severe acidaemia; trajectory and physiological effects matter more than the creatinine stage alone.

Fluid overload

Salt and water retention, capillary leak and excessive resuscitation can produce pulmonary oedema, impaired oxygenation and difficult drug or nutritional delivery.

Uraemic organ dysfunction

Severe or sustained AKI can cause encephalopathy, pericarditis, bleeding tendency, nausea and nutritional decline, prompting urgent specialist assessment for kidney replacement therapy.

Medicine accumulation

Reduced clearance can expose patients to opioid, antimicrobial, anticoagulant and other toxicity, while indiscriminate medicine cessation can remove essential cardiovascular or endocrine treatment.

Incomplete recovery

AKI can leave persistent kidney dysfunction, increase later CKD and recurrent-AKI risk, prolong admission and raise short- and long-term mortality.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Record creatinine, potassium and bicarbonate at a frequency matched to trajectory and treatment; unstable severe AKI may require several checks within a day rather than a routine next-morning panel.
Measure urine output hourly when clinically necessary, validate catheter function and calculate cumulative balance rather than inferring renal recovery from one void.
Repeat weight, oxygen requirement, lung examination, perfusion and oedema assessment because iatrogenic fluid overload can coexist with poor effective circulation.
Track medicine holds, renal dose adjustments and serum drug levels where applicable, with a named decision point for restarting prognostic therapies.
Document AKI stage, presumed cause, peak creatinine and recovery in the discharge communication, together with the date and owner of follow-up blood tests.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

The baseline can change the diagnosis

A result inside the laboratory reference range may still be a large relative rise for a frail person with low muscle mass. Conversely, a high but stable value may be CKD rather than new AKI. Historical data are therefore part of the diagnostic test.

Fluid balance alters creatinine

Large positive balance expands the distribution volume and can blunt the measured rise, so apparent biochemical stability after resuscitation should be compared with urine output, illness severity and cumulative fluid.

Stage is not the mechanism

Stage describes severity and prognosis. It does not distinguish dehydration from tubular injury, glomerulonephritis or obstruction, and the causal assessment must continue after the alert is acknowledged.

Renal-dose review is dynamic

Estimated GFR equations assume relatively stable creatinine and are unreliable during rapid change. Dose decisions in AKI need the trajectory, clinical toxicity risk, drug levels where available and pharmacy or specialist advice.

Recovery is not discharge from risk

Even when creatinine returns near baseline, an AKI episode predicts later CKD and recurrent AKI. Clear follow-up, medicine reconciliation and prevention advice are components of treatment, not administrative extras.

11Common pitfallsFrequent interpretation and management errors.

01
Calling AKI only when creatinine exceeds the laboratory reference range misses substantial relative rises and delays staging in people with low baseline creatinine.
02
Using the current eGFR as though filtration were in steady state can falsely reassure or lead to unsafe drug dosing during a rapidly changing creatinine.
03
Giving repeated fluid because urine output remains low, without reassessing lungs and venous congestion, can convert renal injury into life-threatening pulmonary oedema.
04
Assuming a patent-looking catheter excludes obstruction overlooks kinking, debris, retention above the balloon or upper-tract disease.
05
Stopping ACE inhibitors, diuretics or diabetes medicines without documenting why, when to review and who will restart them creates avoidable long-term cardiovascular harm.