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Background: Diabetic nephropathy is the leading cause of End-Stage Renal Disease (ESRD) emerging in developed as well as developing countries, with the complicated pathogenesis. The study of expression of the genes related to kidney cells e.g. podocytes has been shown to be associated with the condition, helping in the elucidation of pathogenesis of the disease. Previously the gene expression associated was studied in urine samples. Material and Methods: In the present study, it was attempted to analyze the mRNA expression of podocyte related genes viz. podocalyxin, podocin and synaptopodin in Peripheral Blood Mononuclear Cells (PBMCs) in patients with diabetes with and without nephropathy in comparison with healthy controls by reverse transcriptase Polymerase Chain Reaction (PCR), followed by semi-quantitative PCR. Results: The expression of Synaptopodin (SYNPO) was increased in diabetics than the controls, while no significant difference was found for Podocalixyn (PODXL) and Podocin (NPHS2). The expression of PODXL and NPHS2 was significantly up-regulated; SYNPO was unaltered in microalbuminuric patients than healthy controls. PODXL and SYNPO were increased significantly in nephropathy subjects than controls, with no significant change in NPHS2. The expression of only PODXL was found to be upregulated in microalbuminuric patients as compared to T2DM patients without nephropathy. PODXL, SYNPO were significantly up-regulated and NPHS2 was significantly down-regulated in nephropathy subjects as compared to T2DM patients without nephropathy. A significant down-regulation was found for NPHS2 expression in nephropathy patients than microalbuminuric patients of T2DM with nephropathy. Conclusion: The detection of gene expression of these proteins can be used as an early marker for the detection of development of nephropathy in T2DM patients and preventive measures can be taken to prolong the onset of nephropathy in these patients, increasing the life expectancy. [ABSTRACT FROM AUTHOR]

Background: Diabetes Mellitus (DM) is one of the leading non-communicable disorders, leading to various complications viz. cardiovascular diseases, retinopathy, nephropathy, neuropathy and peripheral vascular disorders. Diabetic Nephropathy (DN) patients further develop into End Stage Renal Disease (ESRD) and they have to undergo the repeated blood transfusions, increasing the social and economic burden. The number of risk factors are known for causation of diabetic nephropathy including the environmental, biochemical as well as genetic factors. The association of nephropathy with various genes has been proved. Aim and Objectives: In the present study we attempted to check the association of Insertion/Deletion (I/D) polymorphism of Angiotensin Converting Enzyme (ACE) in diabetic patients with and without nephropathy and also with the biochemical markers. Material and Methods: Each group consisted of 110 individuals viz. diabetics with and without nephropathy and age and gender matched healthy controls. Results: The determination of I/D polymorphism by polymerase chain reaction revealed the significant increased 'D' allele frequencies in patients of diabetes with and without nephropathy than the controls, while no significant difference was noted in genotype frequencies. The odds ratios for this polymorphism were calculated to be 1.84 and 2.41 for DM and DN respectively in comparison with the healthy controls. The regression analysis indicated I/D polymorphism is associated positively with all the lipid parameters, except High Density Lipoprotein-Cholesterol (HDL-C) which was negatively associated with the polymorphism. The levels of lipid parameters were also significantly increased in patients of diabetes with and without nephropathy carriers for 'D' allele than the patients having 'I' allele, while the level of HDL-C was significantly decreased. Conclusion: The conclusion can be made from these results that, the presence of I/D polymorphism of ACE may increase the risk of development of nephropathy in general population, with the role of 'D' allele in its causation, along with its effect on the biochemical markers. [ABSTRACT FROM AUTHOR]