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国家卫生健康委员会
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英文作者:Ding Dong1 Chen Leilei2 Li Tao1 Wang Yong1
单位:1徐州医科大学附属淮安医院心血管内科,淮安223002;2江苏省人民医院心血管内科,南京210029
英文单位:1Department of Cardiovascular Medicine the Affiliated Huaian Hospital of Xuzhou Medical University Huaian 223002 China; 2Department of Cardiovascular Medicine Jiangsu Province Hospital Nanjing 210029 China
英文关键词:Hypertensivenephropathy;Elabela;Gastrin
目的 探讨高血压肾病患者血清Elabela和胃泌素水平变化及其临床意义。方法 选择2016年1月至2020年1月徐州医科大学附属淮安医院诊治的82例高血压肾病患者为高血压肾病组,另选取同期诊治的单纯高血压病患者50例为单纯高血压组,选取同期体检的健康者40例为健康对照组。比较各组血清Elabela、胃泌素水平。分析血清Elabela、胃泌素水平与高血压肾病患者临床病理特征的关系及与肾功能指标的相关性。采用Kaplan-Meier生存分析方法 分析不同血清Elabela、胃泌素表达的高血压肾病患者肾脏存活率的差异。采用Cox回归方法 分析高血压肾病患者发生终末期肾病的危险因素。结果 高血压肾病组患者的血清胃泌素、血尿素氮、血肌酐水平均明显高于单纯高血压组和健康对照组,而Elabela水平、估算肾小球滤过率(eGFR)明显低于单纯高血压组和健康对照组(均P<0.05)。高血压肾病患者血清Elabela、胃泌素水平与肾小球球性硬化及肾小管萎缩/间质纤维化有关(均P<0.001)。高血压肾病患者血清Elabela水平与血尿素氮、血肌酐水平呈负相关,与eGFR呈正相关;血清胃泌素水平与血尿素氮、血肌酐水平呈正相关,与eGFR呈负相关(均P<0.001)。所有患者随访13~60个月,随访期间22.0%(18/82)的高血压肾病患者发展为终末期肾病。Elabela低表达患者肾脏存活率明显低于Elabela高表达患者[62.5%(25/40)比92.9%(39/42),Log-rank χ2=6.214,P<0.001]。胃泌素高表达患者肾脏存活率明显低于胃泌素低表达患者[65.9%(27/41)比90.2%(37/41),Log-rank χ2=5.966,P<0.001]。肾小管萎缩/间质纤维化,低eGFR,低水平Elabela,高水平胃泌素是高血压肾病患者发生终末期肾病的独立危险因素(均P<0.05)。结论 高血压肾病患者血清Elabela水平降低,胃泌素水平升高,Elabela、胃泌素与肾小球球性硬化、肾小管萎缩/间质纤维化有关。低水平Elabela、高水平胃泌素是高血压肾病患者发生终末期肾病的独立危险因素。
Objective To detect the levels of serum Elabela and gastrin (GAS) in patients with hypertensive nephropathy, and to explore their clinical significance. Methods From January 2016 to January 2020, 82 patients with hypertensive nephropathy admitted to the Affiliated Huaian Hospital of Xuzhou Medical University were selected as hypertensive nephropathy group, 50 patients with simple hypertension were selected as simple hypertension group, and 40 healthy people examined in the same period were selected as healthy control group. The levels of serum Elabela and GAS were compared among three groups. The relationship of the levels of serum Elabela and GAS with the clinicopathological characteristics of hypertensive nephropathy and renal function indexes was analyzed. Kaplan-Meier survival analysis was used to analyze the difference in renal survival rate in patients with different serum levels of Elabela and GAS. Cox regression analysis was used to analyze the risk factors of end-stage renal disease in patients with hypertensive nephropathy. Results Compared with simple hypertension group and healthy control group, levels of serum GAS, blood urea nitrogen (BUN) and serum creatinine (SCr) in hypertensive nephropathy group were significantly higher, while the level of Elabela and estimated glomerular fiktration rate (eGFR) were significantly lower (all P<0.05). The levels of serum Elabela and GAS in patients with hypertensive nephropathy were related to glomerulosclerosis and renal tubular atrophy/interstitial fibrosis (all P<0.001). Serum Elabela level in patients with hypertensive nephropathy was significantly negatively correlated with BUN and SCr, and positively correlated with eGFR; serum GAS level was significantly positively correlated with BUN and SCr, and negatively correlated with eGFR (all P<0.001). During the follow-up period (13-60 months), 22.0%(18/82) of patients with hypertensive nephropathy developed end-stage renal disease. The renal survival rate of patients with low Elabela expression was significantly lower than patients with high Elabela expression [62.5%(25/40) vs 92.9%(39/42), Log-rank χ2=6.214, P<0.001]. The renal survival rate of patients with high GAS expression was significantly lower than patients with low GAS expression [65.9%(27/41) vs 90.2%(37/41), Log-rank χ2=5.966, P<0.001]. Renal tubular atrophy/interstitial fibrosis, low levels of eGFR and Elabela, and high level of GAS were independent risk factors for end-stage renal disease in patients with hypertensive nephropathy. Conclusions The level of serum Elabela decreases and the level of GAS increases in patients with hypertensive nephropathy. Elabela and GAS are related to glomerulosclerosis and renal tubular atrophy/interstitial fibrosis. Low level of Elabela and high level of GAS are independent risk factors for end-stage renal disease.
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