Levels of Inflammatory Cytokines in Type 2 Diabetes Patients with Different Urinary Albumin Excretion Rates and Their Correlation with Clinical Variables
Although the pathogenetic mechanism of DN has not been elucidated, an inflammatory mechanism has been suggested as a potential contributor. This study was designed to explore the relationship between low-grade inflammation and renal microangiopathy in T2DM. A total of 261 diabetic subjects were divided into three groups according to UAE: a normal albuminuria group, a microalbuminuria group, and a macroalbuminuria group. A control group was also chosen. Levels of hs-CRP, TNF- , uMCP-1, SAA, SCr, BUN, serum lipid, blood pressure, and HbA1c were measured in all subjects. Compared with the normal controls, levels of hs-CRP, TNF- , uMCP-1, and SAA in T2DM patients were significantly higher. They were also elevated in the normal albuminuria group, . Compared with the normal albuminuria group, levels of these inflammatory cytokines were significantly higher in the microalbuminuria and macroalbuminuria group, . The macroalbuminuria group also showed higher levels than the microalbuminuria group, . Also they were positively correlated with UAE, SBP, DBP, LDL-C, and TC. We noted no significance correlated with course, TG, or HDL-C. Only TNF- ; was positively correlated with HbA1c. This study revealed the importance of these inflammatory cytokines in DN pathogenesis. Further studies are needed to fully establish the potential of these cytokines as additional biomarkers for the development of DN. 1. Introduction Diabetic nephropathy (DN) has been widely recognized as a major complication associated with type 2 diabetes and is a leading cause of end-stage renal disease. It is characterized functionally by proteinuria and albuminuria and pathologically by glomerular hypertrophy, mesangial expansion, and tubulointerstitial fibrosis [1]. In recent years, our knowledge of the pathophysiological processes that lead to DN has notably improved on a genetic and molecular level. Thus, the classic view of metabolic and hemodynamic alterations as the main causes of renal injury in diabetes has been transformed significantly, with clear evidence indicating that these traditional factors are only a partial view of a much more complex picture. One of the most important changes is related to the participation of immune-mediated inflammatory processes in the pathophysiology of diabetes mellitus and its complications [2, 3]. Whether inflammation plays a role in the pathogenesis of DN and understanding what the underlying mechanisms constitute, these are questions which have yet to be answered [4, 5]. Therefore, it is very important to find new pathogenic pathways that may provide
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