Inflammatory activation: cardiac, renal, and cardio-renal interactions in patients with the cardiorenal syndrome.
Inflammatory activation: cardiac, renal, and cardio-renal interactions in patients with the cardiorenal syndrome.
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DOI：
10.1007/s10741-011-9261-3
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发表时间：
2012-03
影响因子：
4.6
通讯作者：
Cotter, Gad
中科院分区：
文献类型：
--
作者：
Colombo, Paolo C.;Ganda, Anjali;Lin, Jeffrey;Onat, Duygu;Harxhi, Ante;Iyasere, Julia E.;Uriel, Nir;Cotter, Gad
虽然炎症是一种旨在保护我们免受感染的生理反应，但如果不加以控制和持续，它可能会造成实质性的伤害。已知慢性心力衰竭（CHF）和慢性肾脏疾病（CKD）都会引起几种促炎介质的精细化，这些介质可以在组织和血流中高浓度检测到。导致慢性心力衰竭和慢性肾病慢性炎症状态的生物来源尚未完全确定。传统的炎症来源包括心脏和肾脏，它们在神经激素和交感神经激活的作用下产生广泛的促炎细胞因子。然而，越来越多的证据表明，非传统的生物力学机制，如体积过载引起的静脉和组织充血，也很重要，因为它们刺激肠道和外周的内毒素吸收和促炎介质的合成和释放。无论是在慢性期，还是在慢性心力衰竭和慢性肾病的急性加重期，炎症和充血似乎都相互放大，导致心脏、血管和肾脏功能恶化的恶性循环，这可能会对患者的预后产生负面影响。迄今为止，旨在减轻心肾综合征终末器官损伤和改善临床预后的抗炎治疗策略令人失望。可能需要一种新的治疗模式，包括针对CHF和CKD的不同病因和阶段的不同抗炎策略。它也可能包括特定的（短期）抗炎治疗，在临床失代偿的不稳定阶段抵消炎症。最后，它将需要更多地关注容量过载作为心肾综合征系统性炎症的日益重要的来源。
Although inflammation is a physiologic response designed to protect us from infection, when unchecked and ongoing it may cause substantial harm. Both chronic heart failure (CHF) and chronic kidney disease (CKD) are known to cause elaboration of several pro-inflammatory mediators that can be detected at high concentrations in the tissues and blood stream. The biologic sources driving this chronic inflammatory state in CHF and CKD are not fully established. Traditional sources of inflammation include the heart and the kidneys which produce a wide range of proinflammatory cytokines in response to neurohormones and sympathetic activation. However, growing evidence suggests that non-traditional biomechanical mechanisms such as venous and tissue congestion due to volume overload are also important as they stimulate endotoxin absorption from the bowel and peripheral synthesis and release of proinflammatory mediators. Both during the chronic phase and, more rapidly, during acute exacerbations of CHF and CKD, inflammation and congestion appear to amplify each other resulting in a downward spiral of worsening cardiac, vascular, and renal functions that may negatively impact patients’ outcome. Anti-inflammatory treatment strategies aimed at attenuating end organ damage and improving clinical prognosis in the cardiorenal syndrome have been disappointing to date. A new therapeutic paradigm may be needed, which involves different anti-inflammatory strategies for individual etiologies and stages of CHF and CKD. It may also include specific (short-term) anti-inflammatory treatments that counteract inflammation during the unsettled phases of clinical decompensation. Finally, it will require greater focus on volume overload as an increasingly significant source of systemic inflammation in the cardiorenal syndrome.
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影响因子：
4.4
作者：
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通讯作者：
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影响因子：
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通讯作者：
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影响因子：
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作者：
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Purcaro, A