PDF(Pubmed)
Abstract：
The role of plasma soluble tumor necrosis factor receptor 1 (sTNFR1) and sTNFR2 in the prognosis of clinical events after hospitalization with or without acute kidney injury (AKI) is unknown.
Prospective cohort.
Hospital survivors from the ASSESS-AKI (Assessment, Serial Evaluation, and Subsequent Sequelae of Acute Kidney Injury) and ARID (AKI Risk in Derby) studies with and without AKI during the index hospitalization who had baseline serum samples for biomarker measurements.
We measured sTNFR1 and sTNFR2 from plasma samples obtained 3 months after discharge.
The associations of biomarkers with longitudinal kidney disease incidence and progression, heart failure, and death were evaluated.
Cox proportional hazard models.
Among 1,474 participants with plasma biomarker measurements, 19% had kidney disease progression, 14% had later heart failure, and 21% died during a median follow-up of 4.4 years. For the kidney outcome, the adjusted HRs (AHRs) per doubling in concentration were 2.9 (95% CI, 2.2-3.9) for sTNFR1 and 1.9 (95% CI, 1.5-2.5) for sTNFR2. AKI during the index hospitalization did not modify the association between biomarkers and kidney events. For heart failure, the AHRs per doubling in concentration were 1.9 (95% CI, 1.4-2.5) for sTNFR1 and 1.5 (95% CI, 1.2-2.0) for sTNFR2. For mortality, the AHRs were 3.3 (95% CI, 2.5-4.3) for sTNFR1 and 2.5 (95% CI, 2.0-3.1) for sTNFR2. The findings in ARID were qualitatively similar in terms of the magnitude of association between biomarkers and outcomes.
Different biomarker platforms and AKI definitions; limited generalizability to other ethnic groups.
Plasma sTNFR1 and sTNFR2 measured 3 months after hospital discharge were independently associated with clinical events regardless of AKI status during the index admission. sTNFR1 and sTNFR2 may assist with the risk stratification of patients during follow-up.
Prospective cohort.
Hospital survivors from the ASSESS-AKI (Assessment, Serial Evaluation, and Subsequent Sequelae of Acute Kidney Injury) and ARID (AKI Risk in Derby) studies with and without AKI during the index hospitalization who had baseline serum samples for biomarker measurements.
We measured sTNFR1 and sTNFR2 from plasma samples obtained 3 months after discharge.
The associations of biomarkers with longitudinal kidney disease incidence and progression, heart failure, and death were evaluated.
Cox proportional hazard models.
Among 1,474 participants with plasma biomarker measurements, 19% had kidney disease progression, 14% had later heart failure, and 21% died during a median follow-up of 4.4 years. For the kidney outcome, the adjusted HRs (AHRs) per doubling in concentration were 2.9 (95% CI, 2.2-3.9) for sTNFR1 and 1.9 (95% CI, 1.5-2.5) for sTNFR2. AKI during the index hospitalization did not modify the association between biomarkers and kidney events. For heart failure, the AHRs per doubling in concentration were 1.9 (95% CI, 1.4-2.5) for sTNFR1 and 1.5 (95% CI, 1.2-2.0) for sTNFR2. For mortality, the AHRs were 3.3 (95% CI, 2.5-4.3) for sTNFR1 and 2.5 (95% CI, 2.0-3.1) for sTNFR2. The findings in ARID were qualitatively similar in terms of the magnitude of association between biomarkers and outcomes.
Different biomarker platforms and AKI definitions; limited generalizability to other ethnic groups.
Plasma sTNFR1 and sTNFR2 measured 3 months after hospital discharge were independently associated with clinical events regardless of AKI status during the index admission. sTNFR1 and sTNFR2 may assist with the risk stratification of patients during follow-up.
摘要：
目的：血浆可溶性肿瘤坏死因子受体1（sTNFR1）和sTNFR2在有或没有急性肾损伤（AKI）住院后临床事件预后中的作用尚不清楚。
方法：前瞻性队列。
方法：来自ASSESS-AKI的医院幸存者(评估，串行评估，以及随后的急性肾损伤后遗症）和ARID（Derby中的AKI风险）研究，在住院期间是否有AKI，他们有基线血清样本进行生物标志物测量。
方法：我们从放电后3个月获得的血浆样品中测量了sTNFR1和sTNFR2。
结果：生物标志物与纵向肾脏疾病发病率和进展的关系，心力衰竭,并对死亡进行了评估。
方法：Cox比例风险模型。
结果：在1,474名进行血浆生物标志物测量的参与者中，19%有肾脏疾病进展，14%的人后来出现心力衰竭，21%在4.4年的中位随访期间死亡.对于肾脏的结果，sTNFR1和sTNFR2每倍增一次的校正HR(AHRs)分别为2.9(95%CI,2.2-3.9)和1.9(95%CI,1.5-2.5).住院期间的AKI并未改变生物标志物与肾脏事件之间的关联。对于心力衰竭，sTNFR1和sTNFR2的每倍增浓度的AHR分别为1.9(95%CI,1.4-2.5)和1.5(95%CI,1.2-2.0).对于死亡率，sTNFR1的AHR为3.3（95%CI，2.5-4.3），sTNFR2为2.5（95%CI，2.0-3.1）。就生物标志物与结果之间的关联程度而言，ARID的发现在质量上相似。
结论：不同的生物标志物平台和AKI定义；对其他种族群体的普适性有限。
结论：出院后3个月测量的血浆sTNFR1和sTNFR2与指示入院期间的AKI状况无关，与临床事件独立相关。sTNFR1和sTNFR2可能有助于随访期间患者的风险分层。
方法：前瞻性队列。
方法：来自ASSESS-AKI的医院幸存者(评估，串行评估，以及随后的急性肾损伤后遗症）和ARID（Derby中的AKI风险）研究，在住院期间是否有AKI，他们有基线血清样本进行生物标志物测量。
方法：我们从放电后3个月获得的血浆样品中测量了sTNFR1和sTNFR2。
结果：生物标志物与纵向肾脏疾病发病率和进展的关系，心力衰竭,并对死亡进行了评估。
方法：Cox比例风险模型。
结果：在1,474名进行血浆生物标志物测量的参与者中，19%有肾脏疾病进展，14%的人后来出现心力衰竭，21%在4.4年的中位随访期间死亡.对于肾脏的结果，sTNFR1和sTNFR2每倍增一次的校正HR(AHRs)分别为2.9(95%CI,2.2-3.9)和1.9(95%CI,1.5-2.5).住院期间的AKI并未改变生物标志物与肾脏事件之间的关联。对于心力衰竭，sTNFR1和sTNFR2的每倍增浓度的AHR分别为1.9(95%CI,1.4-2.5)和1.5(95%CI,1.2-2.0).对于死亡率，sTNFR1的AHR为3.3（95%CI，2.5-4.3），sTNFR2为2.5（95%CI，2.0-3.1）。就生物标志物与结果之间的关联程度而言，ARID的发现在质量上相似。
结论：不同的生物标志物平台和AKI定义；对其他种族群体的普适性有限。
结论：出院后3个月测量的血浆sTNFR1和sTNFR2与指示入院期间的AKI状况无关，与临床事件独立相关。sTNFR1和sTNFR2可能有助于随访期间患者的风险分层。
