Fabry病患者尿微小核糖核酸排泄谱相关变量提示肾纤维化。

International Journal of Chronic Diseases Pub Date : 2019-06-24 eCollection Date: 2019-01-01 DOI:10.1155/2019/4027606
Sebastián Jaurretche, Germán Perez, Norberto Antongiovanni, Fernando Perretta, Graciela Venera
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引用次数: 7

摘要

引言:在晚期Fabry肾病阶段,酶替代疗法(ERT)的疗效降低,因为它不可能逆转肾纤维化。因此,在受影响的患者中发现早期肾纤维化生物标志物是有意义的。在肾纤维化过程中,miR-21、miR-192和miR-433(纤维化启动子)被转化生长因子-β(TGF-β)激活,miR-29和miR-200家族(纤维化抑制剂)被TGF-β抑制。本研究的目的是通过逻辑回归分析,分析具有某些临床变量的法布里病(FD)患者出现尿微小RNA排泄谱指示肾纤维化的可能性。结果:包括34名参与者:24名FD患者和10名对照组。16/24(66.66%)FD患者出现微小RNA尿液排泄谱,表明肾纤维化。通过纤维化抑制因子miR-29和miR-200的减少而不是通过纤维化启动子miR-21、miR192和miR-433的增加来观察到这种情况。多汗症、血管角化瘤、神经性疼痛、听力损失、心脏受累、男性、αGalA活性降低和肾素-血管紧张素-醛固酮系统抑制剂治疗与指示肾纤维化的amicroRNAs尿液排泄谱的出现有关。在接受具有琼脂糖苷酶β的ERT的患者中观察到对尿微小RNA排泄谱的可能有益影响。研究了每个微小RNA家族的肾功能参数之间的相关性。miR-21与尿白蛋白-肌酐比值之间存在唯一具有统计学意义的相关性(p=0.021)。结论:应考虑可能的非TGF-β介导的微小RNA调节,或者TGF-β在FD中对微小RNA调节的影响与其他肾病不同。典型FD的典型临床表现与指示肾纤维化的尿液微小RNA谱的出现有关。FD患者在病理性蛋白尿发作前在尿液中表达肾纤维化生物标志物。观察到尿miR-21与蛋白尿程度之间存在直接相关性。
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Variables Associated with a Urinary MicroRNAs Excretion Profile Indicative of Renal Fibrosis in Fabry Disease Patients.

Introduction: In advanced Fabry nephropathy stages, enzyme replacement theraphy (ERT) efficacy decreases, due to its impossibility to reverse renal fibrosis. Therefore, the finding of early kidney fibrosis biomarkers in affected patients is of interest. During renal fibrosis miR-21, miR-192 and miR-433 (fibrosis promotors) are activated by transforming growth factor-β (TGF-β), and miR-29 and miR-200 family (fibrosis supressors) are inhibited by TGF-β. The aim of this study is to analyze the probability that Fabry disease (FD) patients with some clinical variables can present an urinary microRNAs excretion profile indicative of renal fibrosis through a logistic regression analysis.

Results: A population of 34 participants was included: 24 FD patients and 10 controls. 16/24 (66.66%) FD patients presented microRNAs urinary excretion profile indicative of renal fibrosis. This profile was observed by decrease of fibrosis suppresors miR-29 and miR-200 and not by increase of fibrosis promotors miR-21, miR192, and miR-433. Hypohidrosis, angiokeratomas, neuropathic pain, hearing loss, cardiac involvement, male gender, reduced αGalA activity, and renin-angiotensin-aldosterone system inhibitors treatment are associated with the appearance of amicroRNAs urinary excretion profile indicative of renal fibrosis. A probable beneficial effect on urinary microRNAs excretion profile was observed in patients receiving ERT with agalsidase beta. The correlation between parameters of renal function with each family of microRNAs was studied. The only association with statistical significance was found between miR-21 and urine albumin-creatinine ratio (p =0.021).

Conclusions: A probable microRNAs regulation not mediated by TGF-β should be considered or TGF-β has a different effect in FD than in other nephropathies on microRNAs regulation. Typical clinical manifestations of classic FD are associated with appearance of urinary microRNAs profile indicative of renal fibrosis. FD patients express renal fibrosis biomarkers in urine prior to onset of pathological albuminuria. A direct correlation between urinary miR-21 and degree of albuminuria was observed.

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