Pathophysiology of AKI to CKD progression

急性肾损伤 病理生理学 肾脏疾病 肾功能 医学 疾病 免疫系统 病理 内科学 重症监护医学 免疫学
作者
Yuki Sato,Masahiro Takahashi,Motoko Yanagita
出处
期刊:Seminars in Nephrology [Elsevier]
卷期号:40 (2): 206-215 被引量:132
标识
DOI:10.1016/j.semnephrol.2020.01.011
摘要

Summary: Acute kidney injury (AKI), defined as a rapid decrease in glomerular filtration rate, is a common and devastating pathologic condition. AKI is associated with significant morbidity and subsequent chronic kidney disease (CKD) development. Regardless of the initial insult, CKD progression after AKI involves multiple types of cells, including proximal tubular cells, fibroblasts, and immune cells. Although the mechanisms underlying this AKI to CKD progression have been investigated extensively over the past decade, therapeutic strategies still are lacking. One of the reasons for this stems from the fact that AKI and its progression toward CKD is multifactorial and variable because it is dependent on patient background. In this review, we describe the current understanding of AKI and its maladaptive repair with a focus on proximal tubules and resident fibroblasts. Subsequently, we discuss the unique pathophysiology of AKI in the elderly, highlighting our recent finding of age-dependent tertiary lymphoid tissues. Summary: Acute kidney injury (AKI), defined as a rapid decrease in glomerular filtration rate, is a common and devastating pathologic condition. AKI is associated with significant morbidity and subsequent chronic kidney disease (CKD) development. Regardless of the initial insult, CKD progression after AKI involves multiple types of cells, including proximal tubular cells, fibroblasts, and immune cells. Although the mechanisms underlying this AKI to CKD progression have been investigated extensively over the past decade, therapeutic strategies still are lacking. One of the reasons for this stems from the fact that AKI and its progression toward CKD is multifactorial and variable because it is dependent on patient background. In this review, we describe the current understanding of AKI and its maladaptive repair with a focus on proximal tubules and resident fibroblasts. Subsequently, we discuss the unique pathophysiology of AKI in the elderly, highlighting our recent finding of age-dependent tertiary lymphoid tissues. Erratum Regarding “Pathophysiology of AKI to CKD Progression” (Semin Nephrol. 2020;40:206-215)Seminars in NephrologyVol. 40Issue 3PreviewIn the article entitled “Pathophysiology of AKI to CKD Progression” that appeared in the March 2020 issue of Seminars in Nephrology (Sato et al, volume 40, issue 2, pages 206-215), there were reference errors regarding the reprint information in the Figure 2 and Figure 4 legends. The reprint information for each reference should have read as follows: Full-Text PDF
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