Additional burden of iron deficiency in heart failure patients beyond the cardio-renal anaemia syndrome: findings from the BIOSTAT-CHF study.

Additional burden of iron deficiency in heart failure patients beyond the cardio-renal anaemia syndrome: findings from the BIOSTAT-CHF study.
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DOI:
10.1002/ejhf.2393
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发表时间:
2022-01
影响因子:
18.2
通讯作者:
--
中科院分区:
医学1区
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虽然贫血和慢性肾脏病(CKD)的组合已在心力衰竭(HF)患者中进行了广泛研究,但缺铁(ID)对这种功能失调的相互作用的贡献尚不清楚。我们的目的是评估与这种多病综合征中ID相关的临床联系和病理生理学途径。我们研究了来自BIOSTAT-CHF队列的2151例HF患者。根据ID(转铁蛋白饱和度<20%)、贫血(世界卫生组织定义)和/或CKD(估计肾小球滤过率<60 ml/min/1.73 m2)对患者进行分层。患者主要为男性(73.3%),中位年龄为70.5岁(四分位距61.4-78.1)。ID的患病率高于CKD和贫血(分别为63.3%、47.2%和35.6%),在伴有CKD和贫血的患者中患病率最高(77.5% vs. 59.3%; p < 0.001)。在患有孤立性ID、贫血或CKD的患者之间,或在共同途径中与免疫、炎症、细胞存活和癌症相关的过程的组合中,生物标志物和途径存在相当大的重叠。ID综合征之间共有的关键生物标志物包括转铁蛋白受体、白细胞介素-6、成纤维细胞生长因子-23和骨形态发生蛋白6。在多变量分析中,单独或在贫血和/或CKD的基础上患有ID与总体概括性堪萨斯城心肌病问卷评分较低、6分钟步行试验受损以及住院和/或死亡率增加相关(所有p < 0.05)。HF患者的缺铁、CKD和/或贫血在生物标志物特征方面有很大的重叠,表明与这些综合征相关的共同途径。单独或在CKD和贫血基础上的ID与HF恶化患者的生活质量、运动能力和预后较差相关。无论是否伴有贫血和/或慢性肾脏疾病(CKD),心力衰竭(HF)患者的缺铁(ID)仍与临床结局存在不良相关性。在对患有ID、CKD和/或贫血的HF患者进行的全面生物标志物和途径分析中,我们发现生物标志物谱广泛重叠,表明尽管临床定义不同,但这些综合征的潜在机制相似。BMP 6,骨形态发生蛋白6; CRAIDS,心肾性贫血缺铁综合征; CRAS,心肾性贫血综合征; CRIDS,心肾性缺铁综合征; FGF 23,成纤维细胞生长因子23; IDA,缺铁性贫血; IL-6,白细胞介素-6; TFRC,转铁蛋白受体。一些图形元素改编自www.flaticon.com。
Whereas the combination of anaemia and chronic kidney disease (CKD) has been extensively studied in patients with heart failure (HF), the contribution of iron deficiency (ID) to this dysfunctional interplay is unknown. We aimed to assess clinical associates and pathophysiological pathways related to ID in this multimorbid syndrome. We studied 2151 patients with HF from the BIOSTAT‐CHF cohort. Patients were stratified based on ID (transferrin saturation <20%), anaemia (World Health Organization definition) and/or CKD (estimated glomerular filtration rate <60 ml/min/1.73 m2). Patients were mainly men (73.3%), with a median age of 70.5 (interquartile range 61.4–78.1). ID was more prevalent than CKD and anaemia (63.3%, 47.2% and 35.6% respectively), with highest prevalence in those with concomitant CKD and anaemia (77.5% vs. 59.3%; p < 0.001). There was a considerable overlap in biomarkers and pathways between patients with isolated ID, anaemia or CKD, or in combination, with processes related to immunity, inflammation, cell survival and cancer amongst the common pathways. Key biomarkers shared between syndromes with ID included transferrin receptor, interleukin‐6, fibroblast growth factor‐23, and bone morphogenetic protein 6. Having ID, either alone or on top of anaemia and/or CKD, was associated with a lower overall summary Kansas City Cardiomyopathy Questionnaire score, an impaired 6‐min walk test and increased incidence of hospitalizations and/or mortality in multivariable analyses (all p < 0.05). Iron deficiency, CKD and/or anaemia in patients with HF have great overlap in biomarker profiles, suggesting common pathways associated with these syndromes. ID either alone or on top of CKD and anaemia is associated with worse quality of life, exercise capacity and prognosis of patients with worsening HF. Iron deficiency (ID) in patients with heart failure (HF) retains its adverse association with clinical outcomes regardless of concomitant anaemia and/or chronic kidney disease (CKD). In a comprehensive biomarker and pathway analysis of HF patients with ID, CKD and/or anaemia, we found an extensive overlap in biomarker profiles, suggesting similar underlying mechanisms of these syndromes despite different clinical definitions. BMP6, bone morphogenetic protein 6; CRAIDS, cardio‐renal anaemia iron deficiency syndrome; CRAS, cardio‐renal anaemia syndrome; CRIDS, cardio‐renal iron deficiency syndrome; FGF23, fibroblast growth factor 23; IDA, iron deficiency anaemia; IL‐6, interleukin‐6; TFRC, transferrin receptor. Several graphical elements were adapted from www.flaticon.com.
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