الفهرس 
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Abstract
Diabetes is a fast-growing health problem globally with a significant impact on morbidity, mortality (Ramu et al., 2015). Diabetic nephropathy, the major microvascular complication of diabetes mellitus (DM), has been widely considered as the central cause of morbidity and mortality in diabetic patients (Molitch, 2004), (KDOQI, 2007). Until recently, diabetic nephropathy has been exclusively attributed to the interaction between metabolic parameters and advanced glycosylated end products-AGEs (Goh and Cooper, 2008) hemodynamic factors and oxidative stress, governed by genetic and environmental factors. However, recent evidence suggest that chronic subclinical inflammation may play a key role in the initiation and progression of diabetic nephropathy (Navarro-González, et al., 2011).
Microalbuminuria prevalence ranges from 8–47% in type-2 diabetes mellitus, the presence of microalbuminuria (MA) was originally thought to be predictive of future overt DN in 80% of patients. However more recent evidence suggests that only around 30% of microalbuminuric patients progress to overt nephropathy after 10 years of follow up. Detection of microalbuminuria is not as sensitive as more invasive techniques, such as renal biopsy. There is an urgent need to identify non-invasive biomarkers of DKD in its early stages (Currie et al., 2014).
Growth differentiation factor (GDF)-15, a member of the transforming growth factor β family discovered in a broad range of cells (Lind, et al., 2009). High glucose increases GDF-15 expression and its secretion, which modulates cell apoptosis in negative feedback manner. GDF-15 is expressed by the adipose tissue through p53, a transcriptional factor that links GDF-15 with obesity and insulin resistance.serum GDF-15 measurement is used for the diagnosis and management of cancer and cardiovascular diseases. Also, GDF-15 was thought to be associated with renal outcome and a faster decline of estimated glomerular filtration rate (eGFR) (Li, et al., 2013).
The elevated levels of glucose starts forming covalent adducts with plasma proteins through a non-enzymatic process known as glycation. Protein glycation reactions leading toformation of AGEs. Advanced Glycation End Products (AGEs) are a group of heterogeneous compounds which thought to be the major causes of different diabetic complications (Negre-Salvayre et al., 2009).
This study included a total of 180 subjects (150 type 2 diabetic patients and 30 healthy subjects as control group).
group (I): Normoalbuminuria, included 50 patients with type 2 diabetes.
group (II): Microalbuminuria, included 50 diabetic patients.
group (III): Macroalbuminuria included 50 diabetic patients.
group (IV): Included 30 apparently healthy subjects.
Aim of the work:
The objective of this study is to detect the plasma level of growth differentiation factor 15 and advanced glycation end products in patients of type 2 diabetic nephropathy and to assess their value in diagnosis and evaluation of type 2 diabetic nephropathy.
All included subjects were subjected to the following:
1. History taking and Clinical examination:
2. Laboratory investigations:
Hemoglobin A1c (glycated hemoglobin) was assayed using boronate affinity by NycoCard READER II
Serum urea & serum creatinine are measured by fully automated clinical chemistry auto-analyzer system Konelab 60i (Thermo-Electron Incorporation, Finland).
Estimated GFR was calculated using CKD-EPI.
GFR, in mL/minute =141 ×min (Serum Creat /kappa, 1) alpha
× Max (Serum Creat /kappa, 1) −1.209 × 0.993Age × Sex × Race
For females, the following values are used: Sex =1.018; alpha =−0.329; kappa =0.7. For males, the following values are used: Sex =1; alpha = −0.411; kappa =0.9. (Levey, et al, 2009).
We used also El minia equation for estimation of glomerular filtration rate in different stages of chronic kidney disease which is [CKD- EPI × (BSA) 0.1 ](El-Minshawy, El-Bassuoni, 2012).