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• W3016622249 abstract "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" @default.
• W3016622249 created "2020-04-24" @default.
• W3016622249 creator A5051981873 @default.
• W3016622249 creator A5053240410 @default.
• W3016622249 creator A5085413862 @default.
• W3016622249 date "2020-03-01" @default.
• W3016622249 modified "2023-10-13" @default.
• W3016622249 title "Pathophysiology of AKI to CKD progression" @default.
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• W3016622249 doi "https://doi.org/10.1016/j.semnephrol.2020.01.011" @default.
• W3016622249 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32303283" @default.

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