Abstract：
The development of new drugs and device therapies has led to remarkable advancements in heart failure (HF) treatment in the past couple of decades. However, it becomes increasingly evident that guideline-directed medical therapy cannot be one-size-fits-all across a wide range of ejection fractions (EFs) and various aetiologies. Therefore, classifications solely relying on EF and natriuretic peptide make optimization of treatment challenging, and there is a growing exploration of new indicators that enable efficient risk stratification of HF patients. Particularly when considering HF as a multi-organ interaction syndrome, the cardiorenal interaction plays a central role in its pathophysiology, and albuminuria has gained great prominence as its biomarker, independent from glomerular filtration rate. Albuminuria has been shown to exhibit a linear correlation with cardiovascular disease and HF prognosis in multiple epidemiological studies, ranging from normal (<30 mg/g) to high levels (>300 mg/g). However, on the other hand, it is only recently that the details of the pathological mechanisms that give rise to albuminuria have begun to be elucidated, including the efficient compaction/tightening of the glomerular basement membrane by podocytes and mesangial cells. Interestingly, renal disease, diabetes, and HF damage these components associated with albuminuria, and experimental models have demonstrated that recently developed HF drugs reduce albuminuria by ameliorating these pathological phenotypes. In this review, facing the rapid expansion of horizons in HF treatment, we aim to clarify the current understanding of the pathophysiology of albuminuria and explore the comprehensive understanding of albuminuria by examining the clinically established evidence to date, the pathophysiological mechanisms leading to its occurrence, and the outcomes of clinical studies utilizing various drug classes committed to specific pathological mechanisms to put albuminuria as a novel axis to depict the pathophysiology of HF.
摘要：
在过去的几十年中，新药和设备疗法的开发导致了心力衰竭（HF）治疗的显着进步。然而,越来越明显的是,指南指导的药物治疗不能在广泛的射血分数(EF)和各种病因中一刀切.因此,仅依靠EF和利钠肽的分类使得治疗的优化具有挑战性，越来越多的新指标能够有效地对HF患者进行风险分层。特别是当将HF视为多器官相互作用综合征时，心肾相互作用在其病理生理学中起着核心作用，蛋白尿作为其生物标志物已经非常突出，与肾小球滤过率无关。在多项流行病学研究中，白蛋白尿与心血管疾病和HF预后呈线性相关。范围从正常（<30mg/g）到高水平（>300mg/g）。然而,另一方面,直到最近，引起蛋白尿的病理机制的细节才开始阐明，包括足细胞和肾小球系膜细胞对肾小球基底膜的有效压实/收紧。有趣的是,肾脏疾病,糖尿病,HF会损害这些与蛋白尿相关的成分，和实验模型已经证明，最近开发的HF药物通过改善这些病理表型来减少蛋白尿。在这次审查中,面对HF治疗的视野迅速扩大，我们的目的是澄清目前对蛋白尿的病理生理学的理解，并通过检查迄今为止临床建立的证据来探索对蛋白尿的全面理解，导致其发生的病理生理机制，以及使用致力于特定病理机制的各种药物类别的临床研究结果，将蛋白尿作为描述HF病理生理学的新轴。
