الفهرس 
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Abstract
Acute renal failure (ARF) has traditionally been defined as the abrupt loss of kidney function that results in the retention of urea and other nitrogenous waste products and dysregulation of extracellular volume and electrolytes. (Mehta et Chertow, 2003). The causes of acute kidney injury are commonly categorized into prerenal, intrinsic, and postrenal. Prerenal causes of AKI (”pre-renal azotemia”) are those that decrease effective blood flow to the kidney. Intrinsic AKI can be due to damage to the glomeruli, renal tubules, or interstitium. Common causes of each are glomerulonephritis, acute tubular necrosis (ATN), acute interstitial nephritis (AIN) and tumor lysis syndrome. Postrenal AKI is a consequence of urinary tract obstruction. This may be related to benign prostatic hyperplasia, kidney stones, obstructed urinary catheter, bladder stone, bladder, ureteral or renal malignancy acute Kidney Failure Symptoms (Jim et al., 2010). Rifle criteria consists of three graded levels of injury (Risk, Injury, and Failure) based upon either the magnitude of elevation in serum creatinine or urine output, and two outcome measures (Loss and End-stage renal disease) (Mehta et al., 2007). The management of AKI hinges on identification and treatment of the underlying cause. In addition to treatment of the underlying disorder, management of AKI routinely includes the avoidance of substances that are toxic to the kidneys, called nephrotoxins. These include NSAIDs such as ibuprofen, iodinated contrasts such as those used for CT scans, many antibiotics such as gentamicin, and a range of other substances (Palevsky et al., 2008). Renal replacement therapy, such as with hemodialysis, may be instituted in some cases of AKI . Acute kidney injury (AKI) is common in hospitalised patients, especially in those who are critically ill (Bagshaw et al., 2007). Vitamin D is a group of fat-soluble secosteroids responsible for intestinal absorption of calcium and phosphate. In humans, the most important related compounds of vitamin D are vitamin D2 and vitamin D3. Cholecalciferol (vitamin D3) and ergocalciferol (vitamin D2) are unique as they constitute what we know as vitamin D and can be ingested from the diet and/or supplements. The body can also synthesize vitamin D (from cholesterol) when sun exposure is adequate (Holick, 2007). In the liver vitamin D is converted to calcidiol, which is also known as calcifediol (INN), 25-hydroxycholecalciferol, or 25-hydroxyvitamin D — abbreviated 25(OH)D; and which is the specific vitamin D metabolite that is measured in serum to determine a person’s vitamin D status. Part of the calcidiol is converted by the kidneys to calcitirol, the biologically active form of vitamin D Calcitriol circulates as ahormone in the blood, regulating the concentration of calcium and phosphate in the bloodstream and promoting the healthy growth and remodeling of bone. Calcidiol is also converted to calcitriol outside of the kidneys for other purposes, such as the proliferation, differentiation and apoptosis of cells; calcitriol also affects neuromuscular function and inflammation (Norman, 2008). Potential mechanisms of how a deficiency in vitamin D could predispose individuals to increased risk of acute renal failure include dysregulation of the immune system, predisposing patients to sepsis, endothelial dysfunction and prevention of healing of renal ischemia reperfusion injury. Toll-like receptors and the renin-angiotensin-aldosterone system are mediators of vitamin D effects (Levey et al., 2003). The aim of this work is to study serum 25-hydroxyvitamin D3 level as a predictor of acute kidney injury in the critically ill patient. Our study is a cohort study which is conducted on eighty patients over 6 months selected from ICU of Ahmed Maher Teaching Hospital in Cairo, and informed consent was obtained from all patients and the local authority of the hospital This study is approved ethically and the patients are concented to do this study. The paients were divided according to the presence or absence of acute kidney injury into: 1- AKI group: 20 patients (9 females and 11 males) with mean age 58.2±10.6 years. 2- Non AKI group:60 patients (29 females and 31 males) with mean age 65.1±11.3 years. And according to the presence or absence of 25-OH-D3 deficiency into: 1- 25 (OH)D Deficiency group: : 15patients (7 females and 8 males) with mean age 58.8±10.8 years. 2- Non 25 (OH)D Deficiency group: 65 patients (31 females and 34 males) with mean age 64.8±11.5 years. The selected patients were subjected to: history taking, full clinical examination, laboratory investigations, urea, creatinine, eGFR, CBC, serum calcium, serum phosphorus, lipid profile, serum albumin, fasting and 2h postprandial blood sugar, urine analysis and serum 25-hydroxyvitamin D. This study shows that there was significant association between 25 (OH)D deficiency and AKI as 75% of AKI group had 25 (OH)D deficiency while other group hadn’t any one. This study also shows there was significant association between mortality and 25 (OH)D deficiency as 26.7% of 25 (OH)D deficiency group died while no one in other group died.