蛋白尿
医学
肾功能
内科学
糖尿病前期
糖尿病肾病
糖尿病
炎症
肌酐
肾脏疾病
2型糖尿病
发病机制
疾病
胃肠病学
内分泌学
肾
作者
Kuppuswami Jayashree,Gandhipuram Periyasamy Senthilkumar,Sreejith Parameswaran,Vadivelan Mehalingam
标识
DOI:10.1016/j.clinbiochem.2023.110682
摘要
Sub-clinical inflammation in hyperglycemia is tied to the pathogenesis of diabetic kidney disease (DKD). Though well known for its immunostimulatory function, the significance of extracellular heat shock protein 72 (eHSP72) in DKD is not well studied. We aimed to determine the association of extracellular HSP72 with systemic inflammation and the progression of DKD, and explore its possible clinical significance in DKD.160 type 2 diabetic individuals were enrolled in the study. Their anthropometric data, routine biochemical parameters, urinary renal function parameters, and blood count parameters were estimated. Plasma from patients' blood samples were used to estimate HSP72 and interleukin 1β (IL-1β) using sandwich immunoassays.Plasma eHSP72 is elevated in DKD. Pairwise comparisons showed the drastic elevation of eHSP72 in the presence of albuminuria. A significant positive relationship was observed between plasma levels of eHSP72 and IL-1β. eHSP72 levels did not statistically differ between micro and macro-albuminuric DKD. However, it was inversely associated with estimated glomerular filtration rate, the index of disease severity, independent of age, gender, diabetes duration and absolute monocyte count. At a cutoff of 0.52 ng/ml, with sensitivity of 64.1 % and specificity of 69.2 %, plasma eHSP72 differentiated the presence of DKD in type 2 diabetics with statistical significance.The positive relationship of eHSP72 and IL-1β with worsening DKD likely indicates their participation in immunostimulatory pathways of renal fibrosis. eHSP72 may be closely linked to albuminuria-induced tubular injury and likely contributes to fibrotic changes in the progression of DKD. From our study, we infer the possible clinical significance of eHSP72 as a marker of sub-clinical renal damage in DKD, and the implication of IL-1β-associated mechanisms in DKD progression.
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