الفهرس 
Introduction and Aim of the WorkOnly 14 pages are availabe for public view
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Abstract
Diabetes mellitus burden is high and rising in every country, driven by the global rise in the prevalence of obesity and unhealthy lifestyles.
Diabetic nephropathy is a major microvascular complication and a foremost cause of chronic kidney failure in individuals with both T1DM and T2DM.
Periostin is a type of secreted ECM protein. Periostin is undetected in the normal renal tubules, and is released when distal tubules are damaged. It was found that during the renal injury periostin was prominently expressed in tubulointerstitial areas.
E-Cadherin is a transmembrane integral protein which is found at the adherent junction of the epithelial cells. E-cadherin is abundant in the distal tubules but doesn’t exist or is present only at very low levels in the proximal tubules
Besides, it has been suggested that tubular injury could precede glomerular injury in DN, which may explain the early appearance of an increase in several urinary biomarker excretion compared with albumin. One-third of patients with DN lost renal function even during normal albuminuria or without any marker of glomerular injury which makes us look for prevention or early treatment.
Thus we aimed to investigate the circulatory level of E-cadherin and periostin in type 2 diabetic patient with nephropathy. Moreover, the second goal was to examine possible relation between them in order to address the role of EMT in the pathophysiology of DN. Further to study the association between E-cadherin and periostin with the degree of renal impairment in DN patient. Finally, explore the possibility for using both E-cadherin and periostin as early biomarkers for DN.
In order to fulfil our aim, this study was conducted on 90 subjects divided into the following four groups:
group I: This group comprised 19 healthy adult volunteers; 9 males and 10 postmenopausal females
group II a: This group involved 19 DN patients with normoalbuminura (UACR <30 mg/g); 12 males and 7 postmenopausal females. Their mean age was 55.00 ± 1.79 years. Their UACR median was 19.9(17-22).
group II b: This group involved 37 DN patients with microalbuminuria (UACR 30-300) mg/g); 23 males and 14 postmenopausal females. Their mean age was 54.97 ± 1.16 years. Their UACR median was 51(39-104).
group II c: This group involved 15 DN patients with macroalbuminuria (UACR>300 mg/g); 7 males and 8 postmenopausal females. Their mean age was 56.67 ± 1.67 years. Their UACR median was 400(320-473).
from results obtained we can summarize the following:
1- Serum periostin, in comparison to the control group, there was a significant increase in DN group.
2- Although there was no significant difference between normoalbuminuria and control group in periostin level, a tendency towards higher values was observed in normoalbuminuria patients.
3- Serum E-cadherin, in comparison to the control group, there was a significant decrease in DN group.
4- Serum E-cadherin dramatically decreased in normoalbuminuria, microalbuminuria and macroalbuminuria respectively from the control group.
5- Spearman’s correlation analysis revealed highly significant positive correlations of levels of periostin with UACR and urea.
6- There were highly negative correlations between the level of E-cadherin with UACR and urea.
7- Interestingly, periostin and E-cadherin were significantly negatively correlated (p value= 0.001).
8- Multiple linear backward regression analysis using E-cadherin as the dependent variable and periostin, urea and FPG as independent variables, all showed significantly negative associations with E-cadherin.
9- Regarding periostin, considering E-cadherin and UACR as independent variables, there was a significant positive correlation between periostin with UACR and a significant negative correlation with E-cadherin.
10- The ROC curve analysis of serum periostin and E-cadherin detected high values for AUC that confirmed high sensitivity and specificity for diagnosing DN.