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首页> 外文期刊>Kidney and blood pressure research >Serum Fas Ligand, Serum Myostatin and Urine TGF-β1 Are Elevated in Autosomal Dominant Polycystic Kidney Disease Patients with Impaired and Preserved Renal Function
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Serum Fas Ligand, Serum Myostatin and Urine TGF-β1 Are Elevated in Autosomal Dominant Polycystic Kidney Disease Patients with Impaired and Preserved Renal Function

机译：肾功能受损和保留的常染色体显性多囊肾病患者血清Fas配体，血清肌生长抑制素和尿液中的TGF-β1升高

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Background/Aims: The pathophysiology of renal disease progression in autosomal dominant polycystic disease (ADPKD) is largely unknown. Recent evidence suggests microvascular dysfunction leading to renal ischemia, as an additional pathway for renal function decline. This study examined the levels of serum Fas ligand (FasL), serum myostatin and urine transforming growth factor-beta 1 (TGF-β1) and their association with markers of endothelial dysfunction, in ADPKD patients with preserved or impaired renal function. Methods: Seventy-eight participants were enrolled in the study, divided in three groups: Group A consisted of 26 ADPKD patients with impaired renal function (eGFR 45-70 ml/min/1.73m2), Group B of 26 ADPKD patients with preserved renal function (eGFR > 70 ml/min/1.73m2), and Group C of 26 age- and sex- matched controls with no history of renal disease. Serum FasL, myostatin and urine levels of TGF-β1 were measured as biomarkers of vascular dysfunction, apoptosis and fibrosis with ELISA techniques. Results: Group A patients had significantly higher levels of FasL (13.12±1.69 ng/mL), myostatin (4.62±0.59 ng/mL) and urine logTGF-β1 (3.56±0.49 ng/24h) compared to Group B (9.6±1.28 ng/mL, 3.06±0.35, and 2.09±0.37, respectively, p< 0.001 for all comparisons) or controls (6.59±1.17 ng/mL, 2.18±0.45 ng/ml, and 1.58±0.21, respectively, p< 0.001 for all comparisons). Patients in Group B had also higher levels of all markers compared to controls (p< 0.001), despite having similar renal function. In ADKPD patients negative associations of eGFR with FasL (r=-0.799, p< 0.001), myostatin (r=-0.856, p< 0.001) and TGF-β1 (r=-0.476, p< 0.001) but positive correlations of these markers with asymmetric dimethylarginine (ADMA) (r=0.825; r=0.749; and r=0.599, respectively p< 0.001) were noted. Multivariate analysis demonstrated that FasL was independently associated with high urine TGF-β1 (OR 3.774, 95%CI 1.180-12.072, p=0.025). Conclusions: ADPKD patients with moderately preserved renal function have higher levels of FasL, myostatin and urine TGF-β1 than controls. These results indicate that an interplay between endothelial dysfunction and renal ischemia with mechanisms linked to apoptosis and fibrosis may be present even in early stages of ADPKD.
机译：背景/目的：常染色体显性遗传多囊性疾病（ADPKD）中肾脏疾病进展的病理生理机制尚不清楚。最近的证据表明，导致肾缺血的微血管功能障碍是肾功能下降的另一途径。这项研究检查了肾功能受损或受损的ADPKD患者的血清FasL（FasL），肌生长抑制素和尿液转化生长因子-β1（TGF-β1）的水平及其与内皮功能障碍标志物的关系。方法：78名受试者参加了研究，分为三组：A组由26例肾功能受损（eGFR 45-70 ml / min / 1.73m 2 ）的ADPKD患者组成。 B组26例肾功能保留（eGFR> 70 ml / min / 1.73m 2 ）的ADPKD患者，C组26例年龄和性别相匹配的对照组，无肾脏疾病史。 ELISA法检测了血清FasL，肌生长抑制素和尿液中TGF-β1的水平，以此作为血管功能障碍，凋亡和纤维化的生物标志物。结果：与B组（9.6±1.28）相比，A组患者的FasL（13.12±1.69 ng / mL），肌生长抑制素（4.62±0.59 ng / mL）和尿logTGF-β1（3.56±0.49 ng / 24h）显着更高。 ng / mL，3.06±0.35和2.09±0.37，对于所有比较，p <0.001）或对照（分别为6.59±1.17 ng / mL，2.18±0.45 ng / ml和1.58±0.21，p <0.001所有比较）。尽管肾功能相似，但B组患者的所有标志物水平均高于对照组（p <0.001）。在ADKPD患者中，eGFR与FasL（r = -0.799，p <0.001），肌生长抑制素（r = -0.856，p <0.001）和TGF-β1（r = -0.476，p <0.001）呈负相关，但它们之间呈正相关标记了具有不对称二甲基精氨酸（ADMA）的标记（r = 0.825; r = 0.749;和r = 0.599，分别p <0.001）。多变量分析表明FasL与高尿液TGF-β1独立相关（OR 3.774，95％CI 1.180-12.072，p = 0.025）。结论：肾功能中度保留的ADPKD患者的FasL，肌生长抑制素和尿液中的TGF-β1水平高于对照组。这些结果表明，即使在ADPKD的早期，内皮功能障碍和肾缺血之间的相互作用也可能与细胞凋亡和纤维化有关。

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