الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
One of the top concerns for worldwide public health is diabetes mellitus. It is described as the group of metabolic disorders that are characterized by persistent hyperglycemia. These disorders are typically caused by either impaired insulin secretion, impaired insulin action, or both, which are crucial for maintaining a normal euglycemic state. T2DM is primarily caused by IR and relative insulin insufficiency due to β-cell dysfunction.
One of the most significant microvascular consequences of type 2 diabetes is diabetic kidney disease (DKD). When other primary kidney disease symptoms are absent, the presence of albuminuria and/or a reduced GFR is used for clinical diagnosis of diabetic kidney disease (DKD). It is categorized into two phenotypes (albuminuric and non-albuminuric DKD.
It’s clear that tubulointerstitial inflammation of the kidney plays a crucial part in the pathophysiology of DKD, contrary to the conventional belief that glomerular injury is the primary cause of DKD and is followed by secondary tubular damage. Improved understanding of the early molecules implicated in tubulointerstitial damage may allow new therapeutic approaches and diagnostic tools to focus on early kidney’s proximal tubules damage.
Urinary kidney injury molecule-1 (uKIM-1) is a type I transmembrane glycoprotein. When kidney tissue is healthy, it is almost undetectable. The chronic inflammatory effect of T2DM causes dedifferentiated proximal renal epithelial cells in damaged regions leading to production of this protein. When it becomes detectable in the urine, it is highly specific for kidney damage, specifically renal proximal convoluted tubules. According to many suggested theories, the presence of uKIM-1 in the urine may act as a biomarker for renal proximal tubule damage, aiding in the early detection of the condition.
The goal of the current study was to identify diabetic kidney damage in patients with type 2 diabetes by using uKIM-1 as an early biomarker. Ninety participants were divided equally into three groups. Thirty T2DM patients with albuminuria included in group 1, thirty T2DM patients without albuminuria but with a different eGFR included in group 2, and thirty healthy participants with matched age and sex included in group 3 as a control group.
The results showed that, in comparison to the control group, the mean values of weight, BMI, hip circumference, and waist circumference were higher in all tested T2DM patients. moreover, their mean ABI value was lower than that of the control group. Regarding the laboratory data, the study’s patients had mean levels of FPG, HBA1c, HOMA-IR, total cholesterol,
LDL-C, TG, serum creatinine, and uKIM-1 that were greater than those of the control group. However, their mean levels of eGFR and HDL-C were lower than those of the controls.
The findings demonstrated that in comparison to non-DKD patients and controls, uKIM-1 was considerably greater in DKD patients. Furthermore, the findings showed that in T2DM patients, uKIM-1 is thought to be a reliable predictor of both DKD and albuminuria.
Additionally, the data showed a strong positive association between the uKIM-1 and serum creatinine level and uACR. Moreover, uKIM-1 and eGFR showed a strong negative correlation. In addition, the only significant predictors of DKD were ABI and uKim-1. On the other hand, uACR and serum creatinine level are significant indicators of uKIM-1.