Acute kidney injury (AKI), is characterised by a sudden, but sometimes reversible, disruption to renal function. The 2009 NCEPOD report noted an incidence of AKI in 13–19% of people admitted to hospital, especially in older patients.¹ All patients admitted to hospital as an emergency, regardless of clinical condition, require: assessment for renal dysfunction risk factors, electrolyte monitoring, track and trigger scoring of physiological parameters and consultant review within 12 h of admission. Prevention, detection and optimal management of patients at risk of acute kidney injury is essential.² Acute care nurses need to understand the signs and of risk factors associated with AKI (see red flag box) as these are exacerbated by late recognition and, inappropriate or delayed treatment. Normally around 1L to 2L of urine is produced in 24 h. A minimum of 0.5–1 mL/kg/h is required to indicate good renal perfusion and function with, for example, a person weighing 70 kg, producing between 35 and 70 mL/h of urine.

AKI is defined as low urine output (oliguria) accompanied by rising serum creatinine. For normal ranges see illustration page opposite. The severity of AKI is dependent on the duration of the problem and degree to which abnormal biochemistry is evident. The RIFLE and the AKIN criteria (Table 42.1) describe levels of renal impairment,^3,4 whilst the KDIGO criteria (Box 42.1) refines the staging by highlighting more specific time frames.⁵ Causes of AKI fall into three categories: prerenal, intrinsic and postrenal (Figure 42.1).