Pathophysiology of AKI to CKD progression
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 in...
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| Veröffentlicht in: | Seminars in nephrology 2020-03, Vol.40 (2), p.206-215 |
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| creator | Sato, Yuki Takahashi, Masahiro Yanagita, Motoko |
| description | 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. |
| doi_str_mv | 10.1016/j.semnephrol.2020.01.011 |
| format | Article |
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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.</description><identifier>ISSN: 0270-9295</identifier><identifier>EISSN: 1558-4488</identifier><identifier>DOI: 10.1016/j.semnephrol.2020.01.011</identifier><identifier>PMID: 32303283</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Acute kidney injury ; Acute Kidney Injury - immunology ; Acute Kidney Injury - metabolism ; Acute Kidney Injury - physiopathology ; Age Factors ; Aged ; Animals ; chronic inflammation ; Disease Progression ; Disease Susceptibility ; fibroblast ; Fibroblasts - immunology ; Fibroblasts - metabolism ; Fibrosis ; Glomerular Filtration Rate ; Humans ; Inflammation - immunology ; Inflammation - metabolism ; Inflammation - physiopathology ; Ischemia - metabolism ; Ischemia - physiopathology ; Kidney - pathology ; Kidney - physiology ; Kidney Tubules, Proximal - immunology ; Kidney Tubules, Proximal - metabolism ; Kidney Tubules, Proximal - physiopathology ; Mitochondria - metabolism ; Monocytes - immunology ; Neutrophils - immunology ; proximal tubule ; Regeneration ; Renal Insufficiency, Chronic - immunology ; Renal Insufficiency, Chronic - metabolism ; Renal Insufficiency, Chronic - physiopathology ; T-Lymphocytes - immunology ; Tertiary Lymphoid Structures - immunology ; tertiary lymphoid tissues</subject><ispartof>Seminars in nephrology, 2020-03, Vol.40 (2), p.206-215</ispartof><rights>2020 Elsevier Inc.</rights><rights>Copyright © 2020 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c374t-ab1b40f2d5ebf32624b567cbcb573ee9b3b5def17834363226410ae0cdb108933</citedby><cites>FETCH-LOGICAL-c374t-ab1b40f2d5ebf32624b567cbcb573ee9b3b5def17834363226410ae0cdb108933</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.semnephrol.2020.01.011$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32303283$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sato, Yuki</creatorcontrib><creatorcontrib>Takahashi, Masahiro</creatorcontrib><creatorcontrib>Yanagita, Motoko</creatorcontrib><title>Pathophysiology of AKI to CKD progression</title><title>Seminars in nephrology</title><addtitle>Semin Nephrol</addtitle><description>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.</description><subject>Acute kidney injury</subject><subject>Acute Kidney Injury - immunology</subject><subject>Acute Kidney Injury - metabolism</subject><subject>Acute Kidney Injury - physiopathology</subject><subject>Age Factors</subject><subject>Aged</subject><subject>Animals</subject><subject>chronic inflammation</subject><subject>Disease Progression</subject><subject>Disease Susceptibility</subject><subject>fibroblast</subject><subject>Fibroblasts - immunology</subject><subject>Fibroblasts - metabolism</subject><subject>Fibrosis</subject><subject>Glomerular Filtration Rate</subject><subject>Humans</subject><subject>Inflammation - immunology</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - physiopathology</subject><subject>Ischemia - metabolism</subject><subject>Ischemia - physiopathology</subject><subject>Kidney - pathology</subject><subject>Kidney - physiology</subject><subject>Kidney Tubules, Proximal - immunology</subject><subject>Kidney Tubules, Proximal - metabolism</subject><subject>Kidney Tubules, Proximal - physiopathology</subject><subject>Mitochondria - metabolism</subject><subject>Monocytes - immunology</subject><subject>Neutrophils - immunology</subject><subject>proximal tubule</subject><subject>Regeneration</subject><subject>Renal Insufficiency, Chronic - immunology</subject><subject>Renal Insufficiency, Chronic - metabolism</subject><subject>Renal Insufficiency, Chronic - physiopathology</subject><subject>T-Lymphocytes - immunology</subject><subject>Tertiary Lymphoid Structures - immunology</subject><subject>tertiary lymphoid tissues</subject><issn>0270-9295</issn><issn>1558-4488</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkEtPwzAQhC0EoqXwF1COcEjw2nEex1JeVSvBAc5W7GzaVEkc7BSp_x5XLXBEGmkP-82OdggJgEZAIbnbRA7bDvu1NU3EKKMRBS84IWMQIgvjOMtOyZiylIY5y8WIXDi3oZRByuCcjDjjlLOMj8ntWzGsTb_eudo0ZrULTBVMF_NgMMFs8RD01qwsOr_sLslZVTQOr45zQj6eHt9nL-Hy9Xk-my5DzdN4CAsFKqYVKwWqirOExUokqVZaiZQj5oorUWIFacZjnnDGkhhogVSXCmiWcz4hN4e7Pvtzi26Qbe00Nk3Rodk6yXgOeSqSWHg0O6DaGucsVrK3dVvYnQQq90XJjfwrSu6LkhS8wFuvjylb1WL5a_xpxgP3BwD9r181Wul0jZ3GsraoB1ma-v-Ub8HffVM</recordid><startdate>202003</startdate><enddate>202003</enddate><creator>Sato, Yuki</creator><creator>Takahashi, Masahiro</creator><creator>Yanagita, Motoko</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>202003</creationdate><title>Pathophysiology of AKI to CKD progression</title><author>Sato, Yuki ; Takahashi, Masahiro ; Yanagita, Motoko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c374t-ab1b40f2d5ebf32624b567cbcb573ee9b3b5def17834363226410ae0cdb108933</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Acute kidney injury</topic><topic>Acute Kidney Injury - immunology</topic><topic>Acute Kidney Injury - metabolism</topic><topic>Acute Kidney Injury - physiopathology</topic><topic>Age Factors</topic><topic>Aged</topic><topic>Animals</topic><topic>chronic inflammation</topic><topic>Disease Progression</topic><topic>Disease Susceptibility</topic><topic>fibroblast</topic><topic>Fibroblasts - immunology</topic><topic>Fibroblasts - metabolism</topic><topic>Fibrosis</topic><topic>Glomerular Filtration Rate</topic><topic>Humans</topic><topic>Inflammation - immunology</topic><topic>Inflammation - metabolism</topic><topic>Inflammation - physiopathology</topic><topic>Ischemia - metabolism</topic><topic>Ischemia - physiopathology</topic><topic>Kidney - pathology</topic><topic>Kidney - physiology</topic><topic>Kidney Tubules, Proximal - immunology</topic><topic>Kidney Tubules, Proximal - metabolism</topic><topic>Kidney Tubules, Proximal - physiopathology</topic><topic>Mitochondria - metabolism</topic><topic>Monocytes - immunology</topic><topic>Neutrophils - immunology</topic><topic>proximal tubule</topic><topic>Regeneration</topic><topic>Renal Insufficiency, Chronic - immunology</topic><topic>Renal Insufficiency, Chronic - metabolism</topic><topic>Renal Insufficiency, Chronic - physiopathology</topic><topic>T-Lymphocytes - immunology</topic><topic>Tertiary Lymphoid Structures - immunology</topic><topic>tertiary lymphoid tissues</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sato, Yuki</creatorcontrib><creatorcontrib>Takahashi, Masahiro</creatorcontrib><creatorcontrib>Yanagita, Motoko</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Seminars in nephrology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sato, Yuki</au><au>Takahashi, Masahiro</au><au>Yanagita, Motoko</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pathophysiology of AKI to CKD progression</atitle><jtitle>Seminars in nephrology</jtitle><addtitle>Semin Nephrol</addtitle><date>2020-03</date><risdate>2020</risdate><volume>40</volume><issue>2</issue><spage>206</spage><epage>215</epage><pages>206-215</pages><issn>0270-9295</issn><eissn>1558-4488</eissn><abstract>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. 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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Acute kidney injury Acute Kidney Injury - immunology Acute Kidney Injury - metabolism Acute Kidney Injury - physiopathology Age Factors Aged Animals chronic inflammation Disease Progression Disease Susceptibility fibroblast Fibroblasts - immunology Fibroblasts - metabolism Fibrosis Glomerular Filtration Rate Humans Inflammation - immunology Inflammation - metabolism Inflammation - physiopathology Ischemia - metabolism Ischemia - physiopathology Kidney - pathology Kidney - physiology Kidney Tubules, Proximal - immunology Kidney Tubules, Proximal - metabolism Kidney Tubules, Proximal - physiopathology Mitochondria - metabolism Monocytes - immunology Neutrophils - immunology proximal tubule Regeneration Renal Insufficiency, Chronic - immunology Renal Insufficiency, Chronic - metabolism Renal Insufficiency, Chronic - physiopathology T-Lymphocytes - immunology Tertiary Lymphoid Structures - immunology tertiary lymphoid tissues |
| title | Pathophysiology of AKI to CKD progression |
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