Acute kidney injury (AKI), formerly known as acute renal failure, is a syndrome characterized by an abrupt (within hours to days) deterioration in renal function. It is defined by a rise in serum creatinine or reduction in urine output, or both (Box 25.1 and 25.2). AKI occurs in around 10–20% of patients admitted to hospital, and is most often due to hypovolaemia/hypotension, sepsis and nephrotoxins (Tables 25.1 and 25.2).

Stage-based management of AKI is summarized in Figure 25.1. Consider and address potentially correctable causes or contributory factors (Tables 25.1 and 25.2):

• Obtain a full set of physiological observations.
• Review the medical record, and drug, observation and fluid balance charts.
• Make a focused clinical assessment (Table 25.3).
• Arrange urgent investigation (Table 25.4), which must include urinalysis and urine microscopy.

1. Correct hypovolaemia/hypotension
   • Prompt and vigorous correction of hypovolaemia and hypotension will often reverse AKI. If there is clinically obvious hypovolaemia, give IV fluid (crystalloid or blood, as appropriate to the cause of hypovolaemia). A CVP line may be helpful (to avoid over-replacement of fluid), but the patient should be resuscitated first before this is placed.
   • If the evidence for hypovolaemia is less certain, but there are no clinical signs of fluid overload, give a fluid challenge, ideally with monitoring of the CVP, especially if the JVP is difficult to assess. Target CVP is 5–10cm water, measured from a mid-axillary line zero reference point (p. 662). Ultrasonography of the inferior vena cava is an alternative method of assessing the CVP.
   • If the systolic BP remains <90 mmHg despite correction or exclusion of hypovolaemia, search for and treat other causes of hypotension, of which sepsis is the most likely (Chapter 35). If the BP remains low, inotropic-vasopressor therapy will be needed (p. 13 Table 2.7).
2. Search for and treat sepsis
   • Suspect sepsis if AKI is associated with fever or reduced body temperature (<36°C), or there is an obvious focus of infection (e.g. signs of pneumonia or recent instrumentation of urinary or biliary tract). Bear in mind that many patients with neutropenic sepsis (Chapter 101) have no detectable clinical focus. Obtain a surgical opinion if you suspect an abdominal or pelvic source.
   • The diagnosis and management of sepsis is described in Chapter 35. Start antibiotic therapy as soon as blood has been taken for culture and within one hour. Choice of antibiotic therapy should take account of the source of sepsis, if known, whether the infection is community or hospital acquired, results of previous isolates from the patient and the local pattern of antibiotic resistance.
3. Exclude urinary tract obstruction
   • Ultrasonography should be performed within 24h if obstruction is suspected or there is no identified cause of AKI. It should be performed as soon as possible in case of suspected pyonephrosis or obstruction of a solitary kidney. Non-contrast CT is an alternative to ultrasonography.
   • AKI beginning in hospital is rarely due to urinary tract obstruction, once bladder outflow obstruction has been excluded by catheterization. The hallmark of obstruction is dilatation of the urinary tract above the obstruction, although this is not an invariable feature.
4. Treat immediate complications of AKI

Monitoring and supportive care in AKI is summarized in Table 25.5. Three common scenarios are encountered: