Acute kidney injury and chronic kidney disease: From the laboratory to the clinic.
Acute kidney injury and chronic kidney disease: From the laboratory to the clinic.
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DOI：
10.1016/j.nephro.2016.02.005
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发表时间：
2016-04
影响因子：
0.7
通讯作者：
Bonventre JV
中科院分区：
文献类型：
--
作者：
Ferenbach DA;Bonventre JV
慢性肾脏疾病和急性肾损伤传统上被认为是具有不同病因的独立实体。近年来，这一观点发生了变化，慢性肾脏疾病被认为是发生新的急性肾损伤的主要风险因素，而急性肾损伤现在被认为会导致新发或加速的慢性和终末期肾脏疾病。患有现有慢性肾脏疾病的患者在急性损伤后似乎不太能够进行完全的“适应性”修复，而是不适应地修复，加速纤维化和肾功能下降。本文回顾了人类的流行病学研究，证明了这两个过程之间的联系。我们还检查了临床和实验研究领域的重要性，急性和慢性疾病：急性和慢性肾损伤的血管，周细胞和白细胞群体，涉及损伤和修复的信号通路，细胞应激和生长停滞和衰老细胞的水平增加的影响。讨论了这些过程对急性和慢性损伤的重要性和治疗潜力。
Chronic Kidney Disease and Acute Kidney Injury have traditionally been considered as separate entities with different etiologies. This view has changed in recent years, with chronic kidney disease recognized as a major risk factor for the development of new acute kidney injury, and acute kidney injury now accepted to lead to de novo or accelerated chronic and end stage kidney diseases. Patients with existing chronic kidney disease appear to be less able to mount a complete ‘adaptive’ repair after acute insults, and instead repair maladaptively, with accelerated fibrosis and rates of renal functional decline. This article reviews the epidemiological studies in man that have demonstrated the links between these two processes. We also examine clinical and experimental research in areas of importance to both acute and chronic disease: acute and chronic renal injury to the vasculature, the pericyte and leukocyte populations, the signaling pathways implicated in injury and repair, and the impact of cellular stress and increased levels of growth arrested and senescent cells. The importance and therapeutic potential raised by these processes for acute and chronic injury are discussed.