The reported incidences of AKI vary, and are confounded by differences in diagnosis, definition criteria, or hospital discharge coding.[6][7]​​​ The rate of hospitalizations for AKI in US Medicare patients increased by approximately 35% between 2010 and 2019.[8]​ Patients with diabetes were hospitalized with AKI at a greater than 2-fold higher rate compared with those without diabetes, and patients with chronic kidney disease (CKD) and diabetes were hospitalized with AKI at a more than 7.5-fold higher rate compared to patients with neither pre-existing condition.[8] Overall incidence of AKI among hospitalized patients ranges from 13% to 22%.[3][9]​​​​ In the intensive care unit (ICU), the incidence of AKI is higher.[10] Prediction scores have been developed for outcomes of AKI, but have had variable success in terms of reproducibility or utility.[11][12]

Acute tubular necrosis (ATN) accounts for 45% of cases of AKI. ATN is caused by sepsis in approximately 20% of ICU patients. Prerenal azotemia, obstruction, glomerulonephritis, vasculitis, acute interstitial nephritis, acute on chronic kidney disease, and atheroembolic injury account for most of the remainder.[13][14]

The incidence of contrast nephropathy varies, and is reported to be the third most common cause of AKI in hospitalized patients. One large systematic review and meta-analysis reported a 9% incidence of contrast-induced nephropathy in patients undergoing angiography for any reason, including percutaneous intervention for coronary artery disease, with 0.5% of patients requiring dialysis.[15]

​Up to 7% of patients hospitalized with AKI require renal replacement therapy.[16] In the ICU, the mortality rate exceeds 50% in patients with multiorgan failure who require dialysis.[13][14][16]​ Minor rises in creatinine (≥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 renal failure.

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