Diabetic nephropathy (DN) is a chronic disease characterized by proteinuria, glomerular hypertrophy, decreased glomerular filtration and renal fibrosis with loss of renal function. DN is the leading cause of end-stage renal disease, accounting for millions of deaths worldwide. Hyperglycemia is the driving force for the development of diabetic nephropathy. The exact cause of diabetic nephropathy is unknown, but various postulated mechanisms are: hyperglycemia (causing hyperfiltration and renal injury), advanced glycosylation products, activation of cytokines. In this review article, we have discussed a number of diabetes-induced metabolites such as glucose, advanced glycation end products, protein kinase C and oxidative stress and other related factors that are implicated in the pathophysiology of the DN. An understanding of the biochemical and molecular changes especially early in the DN may lead to new and effective therapies towards prevention and amelioration of DN.
Recent attention has focused on HIV prevention interventions that depend upon knowing one's serostatus, including viral load suppression, prevention with positives, pre-exposure prophylaxis and seroadaptation. Until the low level of testing and resulting high level of undiagnosed HIV infection are addressed, these tools are not likely to be effective for MSM in China.
The results showed that endothelial dysfunction and increased OS were present in subjects with IGT and IFG, indicating endothelial damage in these stages.
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