The reported incidences of AKI vary, and are confounded by differences in diagnosis, definition criteria, or hospital discharge coding. UK Renal Registry data, covering a population of 9.1 million people 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). AKI is seen in 10% to 20% of people admitted to hospital as emergencies, with an inpatient mortality >20%. The overall incidence of AKI in the ICU is higher at 20% to 50% and it is associated with mortality over 50%. 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. 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. Prediction scores have been developed for outcomes of AKI, but have had variable success.
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.
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.
Up to 7% of patients hospitalised with AKI require renal replacement therapy. In the ICU, the mortality rate exceeds 50% in patients with multi-organ failure who require dialysis. 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.
Advanced age is associated with chronic kidney disease, underlying vascular disease of the kidneys, and other comorbid medical conditions that predispose to AKI.
Associated with increased susceptibility to AKI, particularly contrast-related AKI. Risks increase with increasing severity of chronic kidney disease.
AKI incidence rates of 9% to 38% have been reported in patients with diabetes and chronic kidney disease undergoing contrast exposure.
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.
Intravenous iodinated contrast has previously been reported to cause contrast-induced AKI. However, the association has been questioned more recently by large population studies that have failed to demonstrate this risk. Risk of contrast-induced AKI increases with intra-arterial administration and with increasing volume of contrast medium.
exposure to nephrotoxins (e.g., aminoglycosides, vancomycin + piperacillin-tazobactam, cancer therapies, non-steroidal anti-inflammatory drugs, or ACE inhibitors)
From haemorrhage, vomiting, diarrhoea, or sweating; hospitalised patients may have insufficient replacement fluids.
May precede AKI from pre-kidney, intrinsic, or post-kidney causes. Cardiothoracic surgery is particularly high risk, although off-pump approaches may limit this risk.
The resulting impaired kidney perfusion supports pre-kidney AKI as cause of AKI or ischaemia resulting in acute tubular necrosis.
May be associated with atheroembolic injury or contrast-induced AKI.
May precede pre-kidney AKI or acute tubular necrosis, especially if there is severe and prolonged kidney ischaemia.
There may be severe third spacing of fluid leading to intravascular volume depletion resulting in pre-kidney failure.
There may be impaired kidney perfusion causing pre-kidney AKI, rhabdomyolysis predisposing to pigment-induced injury, or ischaemia causing acute tubular necrosis.
Malignant hypertension may cause AKI.
May present with AKI (e.g., systemic lupus erythematosus, scleroderma, anti-neutrophil cytoplasmic antibody-associated glomerulonephritis, anti-glomerular basement membrane disease).
Associated with chronic kidney disease, but may present with AKI.
May precede AKI due to direct toxicity, rhabdomyolysis, and volume depletion.
May lead to AKI if significant obstruction is present.
AKI from nephrotoxicity, ischaemia.
Suspect pigment-induced AKI if rhabdomyolysis is present (e.g., after prolonged loss of consciousness).
Suspect pigment-induced AKI due to rhabdomyolysis.
AKI may be present from intravascular haemolytic transfusion reaction, deposition of immune complexes.
May lead to post-kidney AKI if mass effect is causing outflow obstruction, or AKI may result in association with myeloproliferative disorders or chemotherapy-related toxicities (i.e., tumour lysis). Immune complex glomerulonephritis may result from the malignancy.
Found to be a predictor of risk of postoperative AKI, but may be a marker rather than a mediator of risk. It is unclear whether there is any benefit to stopping agents prior to surgery in high-risk patients.
Proton pump inhibitors may increase risk of AKI; however, more studies are needed to clarify this association.
Case reports suggest that herbs and dietary supplements could potentially contribute to kidney injuries.
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