Lucan · Conditions

Acute kidney injury

Australian guidance: CARI Guidelines AKI + Kidney Health Australia

1. Definition and epidemiology

Acute kidney injury (AKI), formerly referred to as acute renal failure, is a complex clinical syndrome defined by an abrupt decline in glomerular filtration rate (GFR), manifesting as a rise in serum creatinine (SCr) or a fall in urine output. AKI is common in hospitalised patients and is independently associated with significant morbidity and mortality. In Australia and New Zealand, the KDIGO criteria as adapted by KHA-CARI form the basis for definition and staging, with landmark fluid management trials conducted specifically in Australian and New Zealand ICU populations.

2. Pathophysiology

AKI is not a single disease but a syndrome arising from multiple aetiologies, broadly classified by the anatomical site of insult. Pre-renal AKI results from reduced renal perfusion pressure due to volume depletion, cardiac failure, or septic shock, impairing GFR without initial tubular cell death; however, evidence from damage biomarker studies suggests this represents the mild end of a continuum of cellular injury rather than a purely reversible functional state. Intrinsic renal AKI involves direct tubular, glomerular, vascular, or interstitial injury; acute tubular necrosis from ischaemia or nephrotoxins is the most common intrinsic cause and produces patchy coagulative necrosis of tubular epithelium with loss of brush border, cast formation, and tubular back-leak, as detailed in Robbins Ch 20. Post-renal AKI arises from obstruction to urine outflow. Regardless of trigger, downstream pathways converge on intrarenal vasoconstriction, tubular obstruction, and inflammatory cell recruitment that sustain GFR depression beyond the initial insult.

3. Clinical presentation and diagnostic criteria

Symptoms are often non-specific: reduced urine output, peripheral oedema, nausea, and, in severe cases, features of uraemia including encephalopathy, pericarditis, or coagulopathy. Clinical assessment should determine whether the AKI is pre-renal, intrinsic, or post-renal, with bladder palpation and bedside ultrasound identifying obstruction early. The KHA-CARI adaptation of KDIGO criteria defines AKI as any of the following: a rise in SCr by 26.5 micromol/L or more within 48 hours; a rise to 1.5 times or more the baseline value known or presumed to have occurred within the prior 7 days; or urine output below 0.5 mL/kg/h for 6 or more hours. When creatinine and urine output criteria map to different stages, the patient is staged at the highest (worst) level. Cause should be identified as early as possible after diagnosis.

4. Investigations and AU-specific cutoffs

The initial investigation sequence prioritises establishing baseline renal function, confirming AKI, and identifying its cause. First-line investigations include serum creatinine and electrolytes (sodium, potassium, bicarbonate), full blood count, urine microscopy and dipstick, spot urine albumin-to-creatinine ratio, and a renal tract ultrasound to exclude obstruction. Staging uses the KDIGO table as adopted by KHA-CARI: Stage 1 is SCr 1.5 to 1.9 times baseline or a rise of 26.5 micromol/L, or urine output below 0.5 mL/kg/h for 6 to 12 hours; Stage 2 is SCr 2.0 to 2.9 times baseline, or urine output below 0.5 mL/kg/h for 12 or more hours; Stage 3 is SCr 3.0 times baseline, or SCr at or above 353.6 micromol/L, or initiation of renal replacement therapy, or in patients under 18 years a fall in eGFR to below 35 mL/min per 1.73 m2, or urine output below 0.3 mL/kg/h for 24 or more hours or anuria for 12 or more hours. When patients have received large volumes of intravenous fluid, serum creatinine should be corrected for fluid balance to avoid misclassification. Baseline creatinine is often unknown; KHA-CARI supports back-calculation using the MDRD formula assuming 75% GFR as a pragmatic approach, while acknowledging this introduces errors, particularly in pre-existing chronic kidney disease. Additional investigations directed at cause include blood cultures (sepsis), autoimmune screen (anti-GBM, ANCA, ANA, complement), protein electrophoresis (myeloma), urine sodium and fractional excretion of sodium, and CT or cystoscopy where indicated.

5. Management

Management is structured by AKI stage and underlying cause. Across all stages, KHA-CARI recommends: discontinuing all nephrotoxic agents where possible, ensuring adequate volume status and perfusion pressure, monitoring SCr and urine output closely, avoiding hyperglycaemia, and considering alternatives to radiocontrast procedures. For volume resuscitation, isotonic crystalloids are preferred over colloids in the absence of haemorrhagic shock; hydroxyethyl starch (HES) solutions must not be used for volume resuscitation given evidence of significantly increased AKI incidence and requirement for renal replacement therapy compared with crystalloids in large RCTs conducted in Australasian ICUs. Protocolised haemodynamic management targeting tissue perfusion is recommended in high-risk perioperative patients and those with septic shock. For glycaemic control in critical illness, insulin should not be used to target glucose below 6.1 mmol/L (risk of hypoglycaemia), but hyperglycaemia above 10.0 mmol/L should be treated with insulin targeting 8.0 to 10.0 mmol/L. Micronutrient losses caused by renal replacement therapy require active replacement. Specific causes requiring urgent treatment include rapidly progressive glomerulonephritis, vasculitis, interstitial nephritis, thrombotic microangiopathy, and urinary tract obstruction; these must be identified early and treated concurrently with general AKI measures. In Stage 2 and Stage 3 disease, drug dosing for renally cleared medications must be reviewed and adjusted. ICU admission should be considered for Stage 3 AKI. Renal replacement therapy (intermittent haemodialysis or continuous renal replacement therapy in haemodynamically unstable patients) is indicated for refractory hyperkalaemia, severe metabolic acidosis, fluid overload unresponsive to diuretics, or uraemic complications.

6. Pharmacology and AU PBS notes

There are no PBS-listed disease-modifying drugs specific to AKI. Pharmacological management is supportive and prophylactic. Insulin (e.g., Actrapid) is used for hyperkalaemia management (10 units IV with 50 mL 50% dextrose) and for glycaemic control targeting 8.0 to 10.0 mmol/L in critically ill patients. Calcium gluconate 10% (10 mL IV over 2 to 3 minutes) is used for cardioprotection in severe hyperkalaemia and is not PBS-restricted in the inpatient setting. Sodium bicarbonate may be used for severe metabolic acidaemia as a temporising measure. Frusemide (furosemide) is sometimes used to convert oliguric to non-oliguric AKI to facilitate fluid management, though it does not reduce the need for renal replacement therapy or improve survival and should not be used for this indication per se. Nephrotoxic drugs requiring cessation or dose adjustment include NSAIDs, aminoglycosides, vancomycin (target trough monitoring required), ACE inhibitors and angiotensin receptor blockers, metformin, and radiocontrast agents. Aminoglycoside monitoring via extended-interval dosing with AUC-guided or trough-guided adjustment is standard practice in Australian hospitals.

7. Complications and monitoring

Major complications include hyperkalaemia (risk of fatal arrhythmia, monitor ECG), metabolic acidaemia, fluid overload with pulmonary oedema, hyponatraemia, uraemic pericarditis, uraemic encephalopathy, and increased susceptibility to infection. AKI is an independent risk factor for the subsequent development of chronic kidney disease (CKD) and end-stage renal disease; survivors should be followed up with eGFR and urine albumin-to-creatinine ratio at 3 months post-discharge. Monitoring during admission includes at minimum 4-hourly urine output in catheterised patients, daily or twice-daily SCr and electrolytes in Stages 2 to 3, continuous cardiac monitoring for hyperkalaemia, and daily fluid balance with weight. In patients on renal replacement therapy, micronutrient (trace element and water-soluble vitamin) levels require regular assessment and active replacement. All patients with AKI Stage 1 or above should have a documented plan for nephrology review at discharge or outpatient follow-up.

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.