الفهرس 
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Abstract
Acute kidney injury (AKI) is defined as a daily urine output < 0.5 ml/kg/h and/or an increase in serum creatinine ≥ 0.3 mg/dl from admission value within 48 h or a 1.5-fold increase from baseline level) (Heller T, et al., 2018).
Acute kidney injury (AKI) is a serious clinical problem due to its high morbidity and mortality Therefore, early diagnosis and treatment for condition is of critical importance.
Acute kidney injury (AKI) is common among hospitalized and critically ill patients, and its incidence is increasing. Approximately 30-60 % of critically ill patients and 20% of hospitalized patients develop AKI. This results in increased hospital stays, infectious complications, and increased mortality (Cuma et al., 2018).
Recent studies have linked AKI with future development of chronic kidney disease multiple factors contribute to the development, causes of AKI including sepsis, ischemia, drugs, intravenous contrast, and infection, (Cuma et al., 2018)
Diagnosis of AKI is based on the level of the plasma creatinine However, creatinine is an insensitive and non-specific marker that is affected by several variables such as age, gender, muscle density and hepatic functions Plasma creatinine may not increase until days after injury or 50% of renal function is lost,many search for alternative markers for early diagnosis of AKI has been increasing (Gaut et el., 2014).
Biomarkers of AKI can identify the injury to the tubular system and to identify patients who are going to develop AKI earlier. Also, biomarkers help evaluation severity of injury and the effect of interventions on recovery. Of these biomarkers that can be measured in urine or serum, neutrophil gelatinase associated lipocalin (NGAL), kidney injury molecule1(KIM-1),myo_inositol oxygenase (miox), IL-18, calprotectin, urine angiotensinogen, microRNA and tissue inhibitor metalloproteinase2 with insulin like growth factor binding protein7 (TIMP-2&IGFBP7) (Kashani et al., 2017).
Myoinositol oxygenase (MIOX) is a renal-specific enzyme that catalyzes the first committed step in myo-inositol metabolis and kidney-specific protein highly concentrated in the proximal tubule that could be released from proximal tubule during AKI (Schrezenmeier et al., 2016).
Konvalinka, (2014) In a murine model of ischemic renal injury, serum MIOX was increased 24 h postinjury, at the time when histologic injury was profound. In critically ill patients, plasma MIOX was increased 54 h earlier than creatinine, although the timing of injury was unclear. Furthermore, it seemed that plasma MIOX was able to segregate patients with oliguric (traditionally more severe) and nonoliguric AKI. MIOX might thus fit several requirements of novel biomarker development, including an early increase, and specificity to renal tissue and nephron segments (Konvalinka, 2014).
Myoinositol oxygenase. resembles structural enzyme biomarkers such as N-acetyl-- glucosaminidase, alkaline phosphatase, -glutamyltranspeptidase, However, MIOX appears to be uniquely expressed in the kidney, unlike any of the other enzymes. Thus its release into the circulation, and potentially into the urine, may represent a specific and early measure of injury (Konvalinka A, 2014)
The aim of this study to assess myo-inositol oxygenase as predictor marker in acute kidney injury in critically ill patient.
Study groups:
1- group 1:
The study group consist of 40 critically ill patients were admitted in ICU in Ain shams university and followed up regarding development of Aki in ICU categorize into two subgroups.
- 1a-subgroup; this group include patients developed AKI in our hospital that were diagnosed with AKI by the same nephrologist in icu between 2018 to 2019. AKI etiology of the patients was different, there were hypovolemia/ prerenal factors in 3 patients, renal factor in 16patients and postrenal/obstructive factors in 1 patients.
- 1b-subgroup; this group include patients not developed acute kidney injury
2-group 2:
20 control healthy volunteers
Laboratory investigation included: complet blood count, serum creatinine, serum urea, serum albumin sodium and potassium level, liver enzymes and
i- Myo-inositol oxygenase level: The blood samples were collected and immediately centrifuged. The extracted serum samples were kept at –80 °C until use in biochemical tests. The results were recorded in pg/mL and ng/mL. This test did at time of admission and repeated in patients group which develop AKI within 24-48 hours.
Our result showed
Patients that were diagnosed with AKI based on increased serum creatinine and urine output were evaluated in terms of their MIOX values. The MIOX levels of the patients that were measured three days previously were found to precede the increase in creatinine levels by two days.
The results of our study showed that patients who developed AKI had a higher mean of MIOX which ranged from 900-3200 with mean 1525,000±582,079 in comparison with non-AKI group which ranged from 500-800 with mean 620,000 ±89,443 And control group range from 300 to 700 with mean 550,000±145,999. And mean of increase in MIOX level in patients who developed AKI (2-3) days later (4850.000 ± 2182.104); which was statistically significant (P≤ 0.001).
Miox as marker in the present study, showing highly significance correlation between serum MIOX at time of admission and after development of AKI.
The present study showed MIOX as highly predictor of AKI with highly specificity 100%and sensitivity 100%.
MIOX was found to be significant parameters in the diagnosis of AKI. MIOX presents as a promising potential biomarker that needs to be further investigated in terms of its role in the early diagnosis of AKI.