Summary
Commonly associated with sepsis, hypovolaemia, and/or hypotension (pre-kidney AKI and intrinsic AKI);
nephrotoxins such as aminoglycoside antibiotics (e.g., gentamicin), intravenous iodinated contrast, ethylene
OVERVIEW
glycol, or rarer forms of AKI such as vasculitis or interstitial nephritis (intrinsic AKI); or urinary outflow
obstruction (post-kidney AKI).
Usually occurs in patients with intercurrent illness, without symptoms or signs specific to the kidneys, and is
only diagnosed when kidney function tests are performed. Patients may present in many different ways (e.g.,
with sepsis, hypotension, decreased urine output, lower urinary tract symptoms, or oedema).
Suspect AKI when there is an acute rise in serum creatinine and/or a fall in urine output. More severe AKI
can be complicated by hyperkalaemia and acidaemia along with uraemic encephalopathy or pericarditis.
Pulmonary oedema can also occur in patients with AKI secondary to obstructive uropathy or renal artery
stenosis (flash pulmonary oedema) but is usually iatrogenic due to over-enthusiastic fluid resuscitation.
The mainstay of management is supportive care, with treatment of the underlying cause. Give particular
attention to the prompt treatment of sepsis, optimisation of volume status, correction of acidaemia or
electrolyte complications, avoidance of nephrotoxins, and relief of any obstruction.
Renal replacement therapy may be needed for severe AKI with complications that do not respond to medical
management.
Prompt recognition and treatment is important; AKI occurs in 10% to 20% of emergency admissions and has
an inpatient mortality >20% (>35% for stage 3 AKI).
Definition
Acute kidney injury (AKI), previously known as acute renal failure (ARF), is an acute decline in kidney
function, leading to a rise in serum creatinine and/or a fall in urine output.[1] The change in terminology
emphasises that kidney injury presents as a disease spectrum from mild kidney injury to severe kidney
failure.[1] [2] [3] A standardised definition is important to facilitate clinical care and research.[4] AKI may
be due to various insults such as impaired kidney perfusion, exposure to nephrotoxins, outflow obstruction,
or intrinsic kidney disease. The resulting effects include impaired clearance and regulation of metabolic
homeostasis, altered acid/base and electrolyte regulation, and impaired volume regulation.
Epidemiology
The reported incidences of AKI vary, and are confounded by differences in diagnosis, definition criteria,
or hospital discharge coding.[6] [7] UK Renal Registry data, covering a population of 9.1 million people
THEORY
in England over a 3 month period in 2017, produced an annual estimated AKI rate of 10,400 per million
population (95% CI 10,000 to 10,400).[8] AKI is seen in 10% to 20% of people admitted to hospital as
emergencies, with an inpatient mortality >20%.[3] [9] [10] The overall incidence of AKI in the ICU is higher
at 20% to 50% and it is associated with mortality over 50%.[11] [12] There is some evidence to suggest that
AKI is becoming more common, perhaps because of more aggressive medical and surgical interventions in
older patients who are at higher risk of developing AKI as a complication.[13] One study found the incidence
of AKI not requiring dialysis among a large population of hospitalised patients to have increased from 323
to 522 per 100,000 person-years between 1996 and 2003.[14] Prediction scores have been developed for
outcomes of AKI, but have had variable success.[15] [16]
Acute tubular necrosis (ATN) accounts for 45% of cases of AKI. ATN is caused by sepsis in 19% of ICU
patients. Pre-kidney AKI, obstruction, glomerulonephritis, vasculitis, acute interstitial nephritis, acute on
chronic kidney disease and atheroembolic injury account for most of the remainder.[17] [18]
The incidence of contrast nephropathy varies, and is reported to be the third most common cause of AKI in
hospitalised patients. In a study of 7500 patients undergoing percutaneous intervention for coronary artery
disease, 3.3% of all patients experienced AKI, defined as a rise in serum creatinine of 38 micromols/L (0.5
mg/dL) or more, and 25% of patients with a baseline creatinine of at least 153 micromols/L (2.0 mg/dL)
experienced AKI.[19]
Up to 7% of patients hospitalised with AKI require renal replacement therapy.[20] In the ICU, the mortality
rate exceeds 50% in patients with multi-organ failure who require dialysis.[17] [18] [20] Minor rises in
creatinine (≥26.5 micromols/L [0.3 mg/dL]) are associated with an increased risk of hospital mortality,
increased risk of chronic kidney disease, and higher odds of progressing to end-stage kidney failure.
Risk factors
Strong
advanced age
Advanced age is associated with chronic kidney disease, underlying vascular disease of the kidneys,
and other comorbid medical conditions that predispose to AKI.
underlying kidney disease
Associated with increased susceptibility to AKI, particularly contrast-related AKI. Risks increase with
increasing severity of chronic kidney disease.[5]
diabetes mellitus
AKI incidence rates of 9% to 38% have been reported in patients with diabetes and chronic kidney
disease undergoing contrast exposure.[49]
sepsis
May result in acute tubular necrosis, infectious glomerulonephritis, pre-kidney AKI from hypotension, or
drug-induced injury from medicines used in treatment. Highest risk with bacteraemia.
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