Heat shock proteins play an important role in immune inflammation and the formation and restoration of proteins. In recent years, the importance of heat shock protein 90 (Hsp90) in the activation of immune inflammation through nuclear factor kB (NFkB) has been discussed. To assess the activation of the Hsp90-NFkB system by measuring serum and urinary levels in patients with chronic glomerulonephritis (CGN). This study included 32 patients with active forms of CGN and 14 patients with Fabry nephropathy. The control group included 10 healthy individuals. Twenty-one out of 32 CGN patients had nephrotic syndrome (NS). Eleven out of 32 CGN patients had proteinuria levels from 1 to 3 g/day without nephrotic syndrome. A total of 17 patients had renal dysfunction (estimated glomerular filtration rate < 60 ml/min/1.73m²). Fourteen patients with Fabry nephropathy had proteinuria without nephrotic syndrome. Serum and urine HSP-90 and NFkB p65 levels were determined using an enzyme-linked immunosorbent assay. The levels of HSP-90 and NFkB in the serum of patients with CGN were significantly higher than in healthy individuals and patients with Fabry nephropathy. In patients with Fabry nephropathy, the HSP-90 and NFkB levels in the urine and serum did not significantly differ from those in the control subjects. Serum Hsp90 levels were significantly higher in the CGN patients with NS than in patients without NS, as well as in patients with normal renal function compared with patients with an eGFR < 60 ml/min/1.73 m² and patients with tubulo-interstitial fibrosis. Higher levels of HSP-90 and NFkB in serum were observed in patients with nephrotic forms of CGN, including focal segmental glomerulosclerosis, minimal change disease and membranous nephropathy. There were no correlations between the clinical signs of CGN and urinary HSP90/NFkB levels. Activation of the HSP-90-NFkB system, which is directly involved in the development of immune inflammation in CGN, was found in patients with an active course of CGN, especially in those with nephrotic syndrome.

中文翻译：

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慢性肾小球肾炎患者血清和尿液中热休克蛋白 90 和 NFkB 水平。


热休克蛋白在免疫炎症以及蛋白质的形成和恢复中发挥重要作用。近年来，人们讨论了热休克蛋白90（Hsp90）在通过核因子kB（NFkB）激活免疫炎症中的重要性。通过测量慢性肾小球肾炎 (CGN) 患者的血清和尿液水平来评估 Hsp90-NFkB 系统的激活情况。这项研究包括 32 名患有活动性 CGN 的患者和 14 名患有法布里肾病的患者。对照组包括 10 名健康个体。 32 名 CGN 患者中有 21 名患有肾病综合征 (NS)。 32 名 CGN 患者中有 11 名蛋白尿水平为 1 至 3 g/天，但不伴有肾病综合征。共有17名患者出现肾功能不全（估计肾小球滤过率<60 ml/min/1.73m ² ）。 14 名法布里肾病患者有蛋白尿，但无肾病综合征。使用酶联免疫吸附测定法测定血清和尿液 HSP-90 和 NFkB p65 水平。 CGN患者血清中HSP-90和NFkB的水平显着高于健康个体和法布里肾病患者。在法布里肾病患者中，尿液和血清中的 HSP-90 和 NFkB 水平与对照受试者没有显着差异。患有NS的CGN患者的血清Hsp90水平显着高于不患有NS的患者，以及肾功能正常的患者与eGFR < 60 ml/min/1.73 m ²的患者和肾小管间质纤维化患者相比。 在肾病型 CGN 患者中观察到血清中 HSP-90 和 NFkB 水平较高，包括局灶节段性肾小球硬化、微小病变和膜性肾病。 CGN 的临床症状与尿 HSP90/NFkB 水平之间没有相关性。在 CGN 活动性病程的患者中，尤其是肾病综合征患者中发现了 HSP-90-NFkB 系统的激活，该系统直接参与 CGN 免疫炎症的发展。