Acute Kidney Injury (AKI)

AKI is a common syndrome, especially in hospitalised patients, and is independently and strongly associated with increased morbidity and mortality. CKD increases the risk of AKI, and an episode of AKI in turn increases the likelihood of subsequent CKD — a two-way relationship that justifies ongoing surveillance in both directions.

Diagnosis

• Increase in serum creatinine ≥26.5 µmol/L within 48 hours, or
• Increase in serum creatinine to ≥1.5× baseline, known or presumed to have occurred within the prior 7 days, or
• Significant reduction in urine output compared with normal (persistent oliguria)

Risk factors

Pre-existing: CKD, other chronic disease (diabetes, heart/lung/liver disease, cancer, anaemia), advanced age, female sex.

Modifiable kidney insults: hypovolaemia (sepsis, critical illness, circulatory shock, burns, trauma), drugs (the “triple whammy” — see below), radiocontrast agents, venomous animal bites/stings, heatwave.

Prevention and management plan

Identify those at risk: all people with CKD stage 3–5 are at increased risk. Minimise NSAIDs and other nephrotoxic drugs in CKD. Identify at-risk patients early in acute illness and consider temporarily ceasing ACEi/ARB/diuretics with hypovolaemia or hypotension.

During an AKI episode:

• Remove risk factors early in the illness
• Seek specialist advice early
• Systematic fluid assessment and medication review for all at-risk patients when acute illness occurs

After an AKI episode:

• Annual Kidney Health Check for the subsequent 3 years
• Education and self-management to monitor and reduce risk of subsequent exposures
• Record in practice records as “AKI (resolved)“

Sick-day medication guidance (SADMANS)

If a patient becomes unwell and can’t maintain adequate fluid intake (e.g. gastrointestinal upset, dehydration), advise withholding medications that either increase the risk of worsening kidney function or have reduced clearance with increased adverse-effect risk:

Increase risk of kidney function decline: ACE inhibitors, ARBs, NSAIDs, diuretics, SGLT2 inhibitors.

Reduced clearance / increased adverse-effect risk: metformin, sulfonylureas.

Mnemonic — SADMANS: Sulfonylureas, ACE inhibitors, Diuretics, Metformin, Angiotensin receptor blockers, NSAIDs, SGLT2 inhibitors.

Post-AKI follow-up — the period after AKI is a genuine care opportunity

AKI’s effects extend well beyond the acute illness. Survivors face increased risk of hospital readmission (20–29% by 90 days), chronic disease (kidney and cardiovascular), frailty and death — AKI approximately doubles the risk of subsequent death, with adverse associations persisting for up to 10 years even once GFR returns to baseline. In one large cohort, 12-month mortality after AKI was 28%, with cancer and cardiovascular disease the leading causes.

Roughly half of AKI diagnoses in Australian inpatient settings are missed or poorly communicated at discharge — explicitly documenting “AKI (resolved)” in the record (above) matters for exactly this reason.

Management priorities after an episode:

• Documentation — confirm the patient/carer understands the AKI diagnosis; document it in the record and treatment plan
• Address complexity — clarify patient priorities (holistic care, education, quality of life); recognise problems “beyond GFR” (persistent effects of acute illness, anaemia, cognitive impairment, frailty)
• Case-finding — screen for unrecognised CKD, cardiovascular disease (especially heart failure), diabetes and hypertension; AKI is a trigger for ongoing Kidney Health Checks
• Preventive healthcare — revisit lifestyle measures, immunisation, and standard CVD/CKD/ malignancy screening
• Medication interruptions — clarify why medications were interrupted if unclear; make timely adjustments as GFR changes (antimicrobials, anticoagulants, analgesia, diabetes therapies)
• “Permissive AKI” — in some chronic disease management contexts, tolerating an acute GFR reduction is appropriate to permit longer-term benefit
• Sick-day advice — identify medications that could accumulate dangerously or worsen hypoperfusion/toxicity/hyperkalaemia with acute illness; ensure prompt review after any sick-day interruption (watch for unmasked hypertension/hyperglycaemia). See Electrolyte Disorders for managing the hyperkalaemia this can precipitate.

If AKI features persist between 7 and 90 days, the term acute kidney disease applies (though not yet widely used in practice) — eGFR/albuminuria assessment at 3 months post-AKI is appropriate, though earlier review may uncover previously unrecognised CKD.