Effectiveness of myo-inositol oxygenase in the early diagnosis of experimental acute kidney injury

Abstract

OBJECTIVES: The effectiveness of the myo-inositol oxygenase (MIOX) enzyme was investigated in the diagnosis of acute kidney injury (AKI). METHODS: In total, 40 rats were divided into 5 groups (n = 8, for each group) while left kidney ischemiareperfusion was implemented in groups 2, 3, 4 and 5. Group 1 was the control group. Group 2 underwent 1-hour ischemia and 2-hour reperfusion. Group 3 underwent 1-hour ischemia and 4-hour reperfusion. Group 4 underwent 2-hour ischemia and 2-hour reperfusion. Group 5 underwent 2-hour ischemia and 4-hour reperfusion. RESULTS: Serum creatinine and blood urea nitrogen levels in all ischemia-reperfusion groups were higher than in the control group (p < 0.001). Serum MIOX level was higher in groups 2, 3 and 4 than in group 1 (p =0.002). Tissue MIOX level was lower in groups 2, 4, and 5 than in group 1 (p = 0.039). Serum and tissue neutrophil gelatinase-associated lipocalin levels were not signifi cantly different between the groups. The injury level in histopathologic examination was as follows: group 1 < group 3 < group 2 = group 4 < group 5. CONCLUSION: The serum MIOX level increases in the early stages of AKI, however, decreases subsequently. Therefore, the serum MIOX may be a potential promising biomarker in the early diagnosis of AKI (Tab. 5, Fig. 6, Ref. 30).

Serum myo-inositol oxygenase levels at hospital discharge predict progression to chronic kidney disease in community-acquired acute kidney injury

“…High levels of serum MIOX has been associated with AKI, and levels of serum MIOX increased even before the rise in serum creatinine suggestive of markers for detection of AKI 11 , 12 . A recent study investigated the effectiveness of MIOX in the early diagnosis in ischemia–reperfusion mice models and found increased serum MIOX levels in the early stages of AKI 19 . In another study, overexpression of MIOX led to worsening of AKI in cisplatin-induced injury, and disruption in MIOX gene seemed to be protective against cisplatin-induced AKI 20 , Further, in type 2 diabetic nephropathy (T2DN), expression of MIOX correlates with tubulointerstitial damage 21 A few studies have explored pathways that might explain the mechanism of the role of MIOX in AKI-CKD progression.…”