The incidence of acute kidney injury (AKI) is rising reflecting an increasingly elderly at-risk population, with multiple comorbidities, coupled with improved detection of AKI following introduction of clinical chemistry laboratory algorithms. AKI is potentially reversible so improvements in its recognition and early interventions could have a major impact on patient outcomes. AKI occurs when there is a rapid decrease in GFR within hours to days. The loss of kidney function results in the retention of urea and creatinine and subsequent dysregulation of electrolytes and fluid balance. Individuals in the community with pre-existing CKD and/or patients treated with an ACE inhibitor or angiotensin receptor blocker are at increased risk of AKI if they develop an illness associated with hypovolaemia or hypotension. Potential clues in the history for AKI include reduced fluid intake and/or increased fluid losses, urinary tract symptoms and recent drug ingestion. Postural changes in pulse and BP are more sensitive indicators of hypovolaemia than supine observations. Once an unexplained raised serum creatinine is identified this should trigger a careful review of the patient's history including the common AKI risk factors, medication record, baseline renal function and clinical examination. The severity of the AKI should be considered by evaluating the extent of rise of serum creatinine from baseline. Reagent strip urinalysis should be performed, if possible, on any patient with suspected AKI. Positive protein and blood indicators of 2+ to 4+ on urinalysis suggest intrinsic glomerular disease and should trigger more urgent referral to hospital. The focus of AKI management is correcting the conditions causing or contributing to it.