الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
AKI is a clinical syndrome characterized by a rapid decrease in renal excretory function, with the accumulation of urea, creatinine and other nitrogenous waste products. Several consensus definitions have been developed in order to provide a uniform definition of AKI. The most recent is the KDIGO classification; according to which AKI is defined as an increase in serum creatinine by ≥0.3 mg/dl within 48 h, or increase in serum creatinine to ≥1.5 times baseline; which is known or presumed to have occurred within the prior 7 days, or urine volume <0.5 mL/kg/h for 6 h.
Acute Kidney Injury (AKI) affects over 13 million people per year globally, and results in 1.7 million deaths. AKI is diagnosed in up to 20% of hospitalized patients and in 30–60% of critically ill patients. It is the most frequent cause of organ dysfunction in intensive care units (ICUs) and the occurrence of even mild AKI is associated with a 50% higher risk of death.
Traditional tools to diagnose AKI and to determine etiology of AKI (clinical history, physical examination, renal ultrasound, fractional excretion of sodium (FeNa), fractional excretion of urea, serum creatinine (SCr), blood urea nitrogen (BUN), and urine microscopy) remain the cornerstone of diagnostic tools available to the clinician in the ICU.
Multiple risk factors for the development of AKI have been described in critically ill patients including: a significantly increased with older age, diabetes, higher baseline creatinine, heart failure, sepsis/SIRS, use of nephrotoxic drugs, higher severity of disease scores, use of vasopressors / inotropes, high risk surgery, emergency surgery, and possibly hypertension. In the critically ill, sepsis is the major cause of AKI, accounting for nearly 50% of cases.
Causes of AKI are frequently categorized as prerenal, intrinsic renal and postrenal; reflecting the overlapping pathologic mechanisms underlying AKI. Acute tubular necrosis (ATN) is the most common cause of intrinsic renal failure in the ICU; taking into consideration that many causes of AKI in ICU patients likely represent multifactorial etiologies.
Serum creatinine is a poor marker of AKI because patients are not in a steady state and changes in serum creatinine lag behind decrements in renal function. Accordingly, identification of biomarkers with the ability to detect early renal injury before histological or functional changes develop would be desirable. Recently, several candidate biomarkers of AKI have been identified including urinary KIM-1.
Urinary KIM-1, a type-1 transmembrane protein, was originally found as a putative epithelial cell adhesive molecule containing a novel immunoglobulin domain, which was absent in normal condition but elevated in the proximal tubule apical membrane cells after injury. Previous reports had proved KIM-1 in rat model as an outstanding indicator of kidney injury better than serum creatinine to predict proximal tubule injury. Urinary KIM-1 was a sensitive and specific marker of injury as well as a predictor of outcome, especially in the diagnosis of ischemic ATN.
The aim of this study was to identify risk factors for progression of AKI in critically ill adult patients in the medical ICU in Alexandria Main University Hospitals and to assess urinary KIM-1 as a marker for progression of AKI.
The study included 80 AKI patients who were followed during their ICU stay for primary outcome which was progression to severe AKI (KDIGO stage 2 or 3) and secondary outcomes which included the need for RRT, ICU mortality, length of ICU stay and serum creatinine at the time of discharge from the ICU.