Acute kidney injury (AKI) is an abrupt decline in renal function, occurring over hours to days, defined by a rapid rise in serum creatinine, a fall in urine output, or both. It reflects the kidney's vulnerability to ischemic, toxic, and obstructive insults, and is classified by mechanism into prerenal causes from re…
Acute kidney injury (AKI) is an abrupt decline in renal function, occurring over hours to days, defined by a rapid rise in serum creatinine, a fall in urine output, or both. It reflects the kidney's vulnerability to ischemic, toxic, and obstructive insults, and is classified by mechanism into prerenal causes from reduced perfusion, intrinsic injury affecting tubules, glomeruli, or interstitium, and postrenal obstruction. Common precipitants include hypotension and altered intraoperative hemodynamics, nephrotoxic exposures such as iodinated radiographic contrast agents, sepsis, and systemic illnesses including severe COVID-19, where microthrombi within the renal microvasculature can contribute to damage. AKI frequently arises within the broader physiology of cardiorenal interaction, in which heart failure and impaired renal perfusion reinforce one another, and it intersects with chronic kidney disease and conditions such as delayed graft function after transplantation. Clinically, AKI matters because it raises the risk of fluid and electrolyte disturbance, prolonged hospitalization, and progression to chronic impairment. Prevention centers on maintaining perfusion, judicious use of nephrotoxins, and early recognition in at-risk patients, while management addresses the underlying cause and supports renal recovery.
11 peer-reviewed articles, ranked by relevance. Each links to its DOI.
The 11 articles above have been cited 56 times in the scholarly literature. Citation data via OpenAlex and Crossref, updated Jun 2026.
A sample of recent works citing this journal's research on Acute Kidney Injury, linking to each citing work.