Physiological and pathophysiological role of reactive oxygen species and reactive nitrogen species in the kidney
Summary End‐stage renal disease is a leading cause of morbidity and mortality worldwide. The prevalence of the disease and the number of patients who receive renal replacement therapy are expected to increase in the next decade. Accumulating evidence suggests that chronic hypoxia in the tubulointers...
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| Veröffentlicht in: | Clinical and experimental pharmacology & physiology 2018-11, Vol.45 (11), p.1097-1105 |
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| container_title | Clinical and experimental pharmacology & physiology |
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| creator | Ishimoto, Yu Tanaka, Tetsuhiro Yoshida, Yoko Inagi, Reiko |
| description | Summary
End‐stage renal disease is a leading cause of morbidity and mortality worldwide. The prevalence of the disease and the number of patients who receive renal replacement therapy are expected to increase in the next decade. Accumulating evidence suggests that chronic hypoxia in the tubulointerstitium represents the final common pathway to end‐stage renal failure, and that reactive oxygen species (ROS) and reactive nitrogen species (RNS) are the key players in kidney injury. However, ROS and RNS that exceed the physiological levels associated with the pathophysiology of most kidney diseases. The molecules that comprise ROS and RNS play an important role in regulating solute and water reabsorption in the kidney, which is vital for maintaining electrolyte homeostasis and the volume of extracellular fluid. This article reviews the physiological and pathophysiological role of ROS and RNS in normal kidney function and in various kidney diseases. |
| doi_str_mv | 10.1111/1440-1681.13018 |
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End‐stage renal disease is a leading cause of morbidity and mortality worldwide. The prevalence of the disease and the number of patients who receive renal replacement therapy are expected to increase in the next decade. Accumulating evidence suggests that chronic hypoxia in the tubulointerstitium represents the final common pathway to end‐stage renal failure, and that reactive oxygen species (ROS) and reactive nitrogen species (RNS) are the key players in kidney injury. However, ROS and RNS that exceed the physiological levels associated with the pathophysiology of most kidney diseases. The molecules that comprise ROS and RNS play an important role in regulating solute and water reabsorption in the kidney, which is vital for maintaining electrolyte homeostasis and the volume of extracellular fluid. This article reviews the physiological and pathophysiological role of ROS and RNS in normal kidney function and in various kidney diseases.</description><identifier>ISSN: 0305-1870</identifier><identifier>EISSN: 1440-1681</identifier><identifier>DOI: 10.1111/1440-1681.13018</identifier><identifier>PMID: 30051924</identifier><language>eng</language><publisher>Australia: Wiley Subscription Services, Inc</publisher><subject>acute kidney injury ; Acute Kidney Injury - metabolism ; Acute Kidney Injury - physiopathology ; chronic kidney disease ; Homeostasis ; Humans ; Hypoxia ; Kidney - metabolism ; Kidney - physiology ; Kidney - physiopathology ; Kidney diseases ; Kidneys ; Morbidity ; Nitrogen ; oxidative and nitrosative stress ; Oxidative Stress ; Physiology ; Reabsorption ; Reactive nitrogen species ; Reactive Nitrogen Species - metabolism ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Renal failure ; Renal Insufficiency, Chronic - metabolism ; Renal Insufficiency, Chronic - physiopathology ; Review</subject><ispartof>Clinical and experimental pharmacology & physiology, 2018-11, Vol.45 (11), p.1097-1105</ispartof><rights>2018 The Authors. Published by John Wiley & Sons Australia, Ltd</rights><rights>2018 The Authors. Clinical and Experimental Pharmacology and Physiology Published by John Wiley & Sons Australia, Ltd.</rights><rights>Copyright © 2018 John Wiley & Sons Australia, Ltd</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5338-96ed089ffa8c080701dc6e6358924d9c7156d3302065d79ba72c7861ac2ae1343</citedby><cites>FETCH-LOGICAL-c5338-96ed089ffa8c080701dc6e6358924d9c7156d3302065d79ba72c7861ac2ae1343</cites><orcidid>0000-0001-7032-7736 ; 0000-0001-5773-8637</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2F1440-1681.13018$$EPDF$$P50$$Gwiley$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2F1440-1681.13018$$EHTML$$P50$$Gwiley$$Hfree_for_read</linktohtml><link.rule.ids>230,315,781,785,886,1418,27929,27930,45579,45580</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30051924$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ishimoto, Yu</creatorcontrib><creatorcontrib>Tanaka, Tetsuhiro</creatorcontrib><creatorcontrib>Yoshida, Yoko</creatorcontrib><creatorcontrib>Inagi, Reiko</creatorcontrib><title>Physiological and pathophysiological role of reactive oxygen species and reactive nitrogen species in the kidney</title><title>Clinical and experimental pharmacology & physiology</title><addtitle>Clin Exp Pharmacol Physiol</addtitle><description>Summary
End‐stage renal disease is a leading cause of morbidity and mortality worldwide. The prevalence of the disease and the number of patients who receive renal replacement therapy are expected to increase in the next decade. Accumulating evidence suggests that chronic hypoxia in the tubulointerstitium represents the final common pathway to end‐stage renal failure, and that reactive oxygen species (ROS) and reactive nitrogen species (RNS) are the key players in kidney injury. However, ROS and RNS that exceed the physiological levels associated with the pathophysiology of most kidney diseases. The molecules that comprise ROS and RNS play an important role in regulating solute and water reabsorption in the kidney, which is vital for maintaining electrolyte homeostasis and the volume of extracellular fluid. This article reviews the physiological and pathophysiological role of ROS and RNS in normal kidney function and in various kidney diseases.</description><subject>acute kidney injury</subject><subject>Acute Kidney Injury - metabolism</subject><subject>Acute Kidney Injury - physiopathology</subject><subject>chronic kidney disease</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Kidney - metabolism</subject><subject>Kidney - physiology</subject><subject>Kidney - physiopathology</subject><subject>Kidney diseases</subject><subject>Kidneys</subject><subject>Morbidity</subject><subject>Nitrogen</subject><subject>oxidative and nitrosative stress</subject><subject>Oxidative Stress</subject><subject>Physiology</subject><subject>Reabsorption</subject><subject>Reactive nitrogen species</subject><subject>Reactive Nitrogen Species - metabolism</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Renal failure</subject><subject>Renal Insufficiency, Chronic - metabolism</subject><subject>Renal Insufficiency, Chronic - physiopathology</subject><subject>Review</subject><issn>0305-1870</issn><issn>1440-1681</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><recordid>eNqFkUFP3DAQha2Kqmxpz72hSFx6CczYieNckNAKaCWkcmjPlnEmu6ZZO9hZIP--2V26gl7qi0fzvnma0WPsC8IpTu8MiwJylApPUQCqd2y27xywGQgoc1QVHLKPKd0DQAlSfGCHYqqw5sWM9bfLMbnQhYWzpsuMb7LeDMvQv2nH0FEW2iySsYN7nOrncUE-Sz1ZR2k7tte8G2J4rTqfDUvKfrvG0_iJvW9Nl-jzy3_Efl1d_px_y29-XH-fX9zkthRC5bWkBlTdtkZZUFABNlaSFKWa1m5qW2EpGyGAgyybqr4zFbeVkmgsN4SiEEfsfOfbr-9W1FjyQzSd7qNbmTjqYJx-q3i31IvwqCXnCFuDry8GMTysKQ165ZKlrjOewjppDpUqa1HwDXryD3of1tFP52mOvJACpRQTdbajbAwpRWr3yyDoTZp6k53eZKe3aU4Tx69v2PN_45uAcgc8uY7G__np-eXtzvgPI9yqtQ</recordid><startdate>201811</startdate><enddate>201811</enddate><creator>Ishimoto, Yu</creator><creator>Tanaka, Tetsuhiro</creator><creator>Yoshida, Yoko</creator><creator>Inagi, Reiko</creator><general>Wiley Subscription Services, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><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>7QP</scope><scope>7TK</scope><scope>7U7</scope><scope>C1K</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-7032-7736</orcidid><orcidid>https://orcid.org/0000-0001-5773-8637</orcidid></search><sort><creationdate>201811</creationdate><title>Physiological and pathophysiological role of reactive oxygen species and reactive nitrogen species in the kidney</title><author>Ishimoto, Yu ; Tanaka, Tetsuhiro ; Yoshida, Yoko ; Inagi, Reiko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5338-96ed089ffa8c080701dc6e6358924d9c7156d3302065d79ba72c7861ac2ae1343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>acute kidney injury</topic><topic>Acute Kidney Injury - metabolism</topic><topic>Acute Kidney Injury - physiopathology</topic><topic>chronic kidney disease</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>Kidney - metabolism</topic><topic>Kidney - physiology</topic><topic>Kidney - physiopathology</topic><topic>Kidney diseases</topic><topic>Kidneys</topic><topic>Morbidity</topic><topic>Nitrogen</topic><topic>oxidative and nitrosative stress</topic><topic>Oxidative Stress</topic><topic>Physiology</topic><topic>Reabsorption</topic><topic>Reactive nitrogen species</topic><topic>Reactive Nitrogen Species - metabolism</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Renal failure</topic><topic>Renal Insufficiency, Chronic - metabolism</topic><topic>Renal Insufficiency, Chronic - physiopathology</topic><topic>Review</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ishimoto, Yu</creatorcontrib><creatorcontrib>Tanaka, Tetsuhiro</creatorcontrib><creatorcontrib>Yoshida, Yoko</creatorcontrib><creatorcontrib>Inagi, Reiko</creatorcontrib><collection>Wiley-Blackwell Open Access Titles</collection><collection>Wiley Free Content</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Clinical and experimental pharmacology & physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ishimoto, Yu</au><au>Tanaka, Tetsuhiro</au><au>Yoshida, Yoko</au><au>Inagi, Reiko</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Physiological and pathophysiological role of reactive oxygen species and reactive nitrogen species in the kidney</atitle><jtitle>Clinical and experimental pharmacology & physiology</jtitle><addtitle>Clin Exp Pharmacol Physiol</addtitle><date>2018-11</date><risdate>2018</risdate><volume>45</volume><issue>11</issue><spage>1097</spage><epage>1105</epage><pages>1097-1105</pages><issn>0305-1870</issn><eissn>1440-1681</eissn><abstract>Summary
End‐stage renal disease is a leading cause of morbidity and mortality worldwide. The prevalence of the disease and the number of patients who receive renal replacement therapy are expected to increase in the next decade. Accumulating evidence suggests that chronic hypoxia in the tubulointerstitium represents the final common pathway to end‐stage renal failure, and that reactive oxygen species (ROS) and reactive nitrogen species (RNS) are the key players in kidney injury. However, ROS and RNS that exceed the physiological levels associated with the pathophysiology of most kidney diseases. The molecules that comprise ROS and RNS play an important role in regulating solute and water reabsorption in the kidney, which is vital for maintaining electrolyte homeostasis and the volume of extracellular fluid. This article reviews the physiological and pathophysiological role of ROS and RNS in normal kidney function and in various kidney diseases.</abstract><cop>Australia</cop><pub>Wiley Subscription Services, Inc</pub><pmid>30051924</pmid><doi>10.1111/1440-1681.13018</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0001-7032-7736</orcidid><orcidid>https://orcid.org/0000-0001-5773-8637</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | acute kidney injury Acute Kidney Injury - metabolism Acute Kidney Injury - physiopathology chronic kidney disease Homeostasis Humans Hypoxia Kidney - metabolism Kidney - physiology Kidney - physiopathology Kidney diseases Kidneys Morbidity Nitrogen oxidative and nitrosative stress Oxidative Stress Physiology Reabsorption Reactive nitrogen species Reactive Nitrogen Species - metabolism Reactive oxygen species Reactive Oxygen Species - metabolism Renal failure Renal Insufficiency, Chronic - metabolism Renal Insufficiency, Chronic - physiopathology Review |
| title | Physiological and pathophysiological role of reactive oxygen species and reactive nitrogen species in the kidney |
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