Acute renal and fluid problems

Acute kidney injury

Overview and approach

AKI is acute renal dysfunction assessed by creatinine change and/or urine output; seek cause and complications.

  • AKI is common in hospitalised patients and is strongly associated with morbidity and mortality. CKD increases AKI risk and AKI increases later CKD, kidney failure and death (1).
  • Diagnosis (Kidney Health Australia): a rise in serum creatinine to 1.5 times baseline within the prior 7 days, or a significant fall in urine output (1). The KDIGO definition also includes a rise of 26.5 micromol/L within 48 hours and urine output below 0.5 mL/kg/h for 6 hours.
  • Think pre-kidney (hypovolaemia, blood loss, hypotension, shock), kidney (critical illness, drug toxicity) and post-kidney (obstruction) causes (1).
Assessment and clinical features

Volume/perfusion, urine output, medicines/nephrotoxins, infection, obstruction and prior renal baseline.

  • Assess volume status and perfusion, urine output, recent illness, and drugs: NSAIDs, ACE inhibitors/ARBs, diuretics, metformin, sulfonylureas, SGLT2 inhibitors, nephrotoxins and contrast (1).
  • Risk factors: CKD (all with stage 3-5), diabetes, heart, lung or liver disease, cancer, anaemia and advanced age (1).
Differentials and investigations

Serial renal/electrolytes, urinalysis/microscopy and imaging for possible obstruction; creatinine may lag injury.

  • Compare with the baseline creatinine; repeat EUC serially. Urinalysis and microscopy; renal tract ultrasound for obstruction (1).
  • eGFR is unreliable during AKI: use the creatinine trend over several measurements to judge change and to guide drug dosing (not read directly; see Check below).
  • Distinguish AKI from CKD by prior results. A rapid eGFR fall (more than 5 mL/min/1.73 m2 over 3 months) or acute nephritis signs needs urgent referral (1).
Management and follow-up

Treat cause, review renally cleared drugs and individualise fluids; involve nephrology for severity or uncertain cause.

  • Treat the cause, seek specialist advice early, and do a systematic fluid assessment and medicine review for people at risk when they are acutely unwell (1).
  • Temporarily stop ACE inhibitors, ARBs, diuretics, NSAIDs, metformin, sulfonylureas and SGLT2 inhibitors during hypovolaemia or hypotension (SADMANS) and restart when stable (1).
  • After an AKI episode: kidney health check at 3 months and then yearly for 3 years; record "AKI (resolved)"; educate about sick day rules (1).
Red flags and clinical pearls

Hyperkalaemia, pulmonary oedema, severe acidosis, uraemic complications or anuria needs urgent review. Do not give fluid reflexively to a congested patient.

  • Obstruction is a reversible cause: image early if no clear pre-renal cause.
  • Avoid NSAIDs with ACE inhibitor/ARB plus diuretic ("triple whammy") (1).
  • Primary care can prevent AKI by early recognition of people at risk and sick day plans (1).
References
  1. Kidney Health Australia: CKD Management in Primary Care handbook, 5th edition (2024), Acute kidney injury section

Last updated from Sen’s notes on 9 October 2026.