الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Acute kidney injury is a clinical illness that is complex and variable and has several subtypes. Different molecular, cellular, and functional alterations result from different types of main insults, subsequent effects, and mitigating responses in the kidney. The precise mechanism causing sepsis-related AKI is still being researched. It has been suggested that aberrant cellular responses to damage, immunological and autonomic dysregulation, and macrovascular and microvascular dysfunction exist.
The traditional diagnosis of AKI is based on functional indicators such oliguria and elevated serum creatinine, which have a number of significant drawbacks. Oliguria is not highly selective for renal failure, and serum creatinine increase typically occurs with a decreased GFR of more than 30% and several hours after the renal insult. Despite difficulties with diagnosis, it is still not possible to early determine if an AKI is temporary or persistent.