الفهرس 
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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.
While being generally uncommon in the community-dwelling population, AKI is more common in hospitalized individuals with a reported incidence ranging from 2-20% increasing up to 20-60% in critically ill patients, in whom it is associated with adverse outcomes including increased length of ICU and hospital stay, development of CKD, and increased short- and long-term mortality risk.
Multiple risk factors for the development of AKI have been described in critically ill patients. However, the risk for AKI represents the interaction between susceptibility (i.e. features intrinsic to the patient) and exposure (i.e. the causative factor or factors). Exposures known to produce AKI in susceptible populations include sepsis, ischemia, heart failure, liver disease, major surgery (especially vascular and cardiac), myonecrosis, urinary tract obstruction and various nephrotoxins. 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.
The initial step in the evaluation of patients with AKI is a careful history and physical examination to identify events and/or disease processes that result in decreased tissue perfusion that can lead to prerenal disease or post-ischemic ATN. Clinically, many patients are asymptomatic and present only with an increase in serum creatinine or a decrease in urine output.
AKI is potentially preventable with the fundamental principle of prevention being treatment of the cause or trigger. No specific drug-based intervention has been shown to be protective.
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 neutrophil gelatinase-associated lipocalin (NGAL), cystatin C, interleukin-18,L-type fatty acid–binding protein (L-FABP) and kidney injury moleclue-1 (KIM-1).
NGAL is a member of lipocalin superfamily with a small molecular weight of only 25 kDa. NGAL was first found in human neutrophils. NGAL is very stable, so it can be easily detected in serum. Under normal conditions, low NGAL expression levels can be detected in a variety of tissues (lung, kidney, large intestine and stomach). High expression levels of NGAL can be induced by cell apoptosis after epithelial cell damage. The expression of NGAL rises 1000-fold in humans and rodents in response to renal tubular injury, and it appears so rapidly in the urine and serum that it is useful as an early biomarker of renal failure.
Urinalysis is a simple and widely available tool for evaluating renal disease. The presence of renal epithelial cells, renal epithelial cell casts and granular casts are traditional markers of acute tubular necrosis. Urine sediment is especially helpful in assessing patients with acute kidney injury (AKI), as well as those with proteinuria, hematuria, and leukocyturia identified on dipstick urinalysis. Based on the information garnered from this bedside test, urine sediment provides a window into the kidneys such that it has been viewed as the noninvasive “liquid biopsy”.
The aim of this work is to study the diagnostic utility of urinary sediment cast scoring index in comparison to serum NGAL as markers for early detection of acute kidney injury in intensive care unit.
The study included 60 ICU patients who were followed during their ICU stay for the occurrence of acute kidney injury according to AKIN criteria and regrouped into AKI and non-AKI group according to that.
All participants in the present study were subjected to history taking, full clinical examination and laboratory investigations including routine and specific investigations. Urine samples were collected for all patients at the time of ICU admission and after 24 hour of admission, examined within a 30 min period for urinary sediment cast score index. Also serum samples were taken at the same time and NGAL were measured.
The results of this study showed that: AKI group has a significant urinary sediment cast score index at presentation (p<0.001) and after 24 hour (p<0.001) and also higher serum NGAL level at presentation (p<0.001), higher serum NGAL level after 24 hour (p<0.001).
Urinary sediment cast score at presentation has a higher level among patients with hypotension (p=0.001), nephrotoxic drug (p=0.042) and those with sepsis (p<0.001).
Urinary sediment cast score at had a significant positive correlations with blood lactate level (p<0.001), WBC (p<0-001), temperature (p=0.019), heart rate (p=0.044) and respiratory rate (p<0.001) . On the other hand, it had a negative correlations with urine output (p<0.001), level of bicarbonate (p<0.001), systolic blood pressure (p=0.003), diastolic blood pressure (p=0.008), mean blood pressure (p=0.005).
Urinary sediment cast score index and serum NGAL level at presentation had a high sensitivity and a high specificity in early diagnosis of AKI (AUC=0.960, p<0.001), (AUC=0.969, p<0.001) respectively, in comparison between two parameters they have approximately the same sensitivity and specificity.
We concluded that urinary sediment cast score index is an easy, cheap and practical way that could be used for prediction of hospital acquired AKI in developing countries. It also had a specificity and sensitivity a proximately equal to that of NGAL for prediction of hospital acquired AKI.