A case of crescentic glomerulonephritis induced by afatinib for lung adenocarcinoma
Afatinib is a second-generation, oral, epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI). One of the most common adverse effects of affatinib is diarrhea, which may lead to acute kidney injury (AKI) due to severe plasma volume loss; however, no case of glomerular injury directly...
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creator | Morita, Daisuke Ito, Kenji Ikeuchi, Nobumitsu Nishida, Yoshihiro Igata, Fumiyasu Nakamura, Tsubasa Murayama, Hiroyuki Watanabe, Maho Takahashi, Koji Yasuno, Tetsuhiko Uesugi, Noriko Fujita, Masaki Oda, Takashi Masutani, Kosuke |
description | Afatinib is a second-generation, oral, epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI). One of the most common adverse effects of affatinib is diarrhea, which may lead to acute kidney injury (AKI) due to severe plasma volume loss; however, no case of glomerular injury directly induced by afatinib has been reported to date. Here, we describe the case of a 53-year-old Japanese male patient with advanced lung adenocarcinoma who twice developed AKI requiring dialysis, once after starting and once after increasing the dose of afatinib. Although serum anti-neutrophil cytoplasmic antibodies were negative, crescentic glomerulonephritis with no immune deposits was confirmed on kidney biopsy. No vasculitis-like signs were observed in other organs, such as lung, skin, or peripheral nerves. Afatinib was considered the cause of glomerular damage and was immediately discontinued; corticosteroids were administered. Renal function gradually recovered thereafter, with serum creatinine levels at ~ 2.3 mg/dL after second-line therapy with bevacizumab and atezolizumab. Several cases of cutaneous leukocytoclastic vasculitis have been reported in patients treated with other EGFR-TKIs; therefore, afatinib-induced vasculitis may lead to crescentic glomerulonephritis. Although afatinib-induced glomerular injury is extremely rare and has an unclear mechanism, renal function and urinary findings need to be closely monitored. |
doi_str_mv | 10.1007/s13730-022-00737-8 |
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One of the most common adverse effects of affatinib is diarrhea, which may lead to acute kidney injury (AKI) due to severe plasma volume loss; however, no case of glomerular injury directly induced by afatinib has been reported to date. Here, we describe the case of a 53-year-old Japanese male patient with advanced lung adenocarcinoma who twice developed AKI requiring dialysis, once after starting and once after increasing the dose of afatinib. Although serum anti-neutrophil cytoplasmic antibodies were negative, crescentic glomerulonephritis with no immune deposits was confirmed on kidney biopsy. No vasculitis-like signs were observed in other organs, such as lung, skin, or peripheral nerves. Afatinib was considered the cause of glomerular damage and was immediately discontinued; corticosteroids were administered. Renal function gradually recovered thereafter, with serum creatinine levels at ~ 2.3 mg/dL after second-line therapy with bevacizumab and atezolizumab. Several cases of cutaneous leukocytoclastic vasculitis have been reported in patients treated with other EGFR-TKIs; therefore, afatinib-induced vasculitis may lead to crescentic glomerulonephritis. Although afatinib-induced glomerular injury is extremely rare and has an unclear mechanism, renal function and urinary findings need to be closely monitored.</description><identifier>ISSN: 2192-4449</identifier><identifier>EISSN: 2192-4449</identifier><identifier>DOI: 10.1007/s13730-022-00737-8</identifier><identifier>PMID: 36180718</identifier><language>eng</language><publisher>Singapore: Springer Nature Singapore</publisher><subject>Adenocarcinoma - drug therapy ; Adenocarcinoma of Lung - drug therapy ; Afatinib - therapeutic use ; Case Report ; ErbB Receptors - metabolism ; Glomerulonephritis - drug therapy ; Humans ; Lung Neoplasms - pathology ; Male ; Medicine ; Medicine & Public Health ; Middle Aged ; Nephrology ; Quinazolines - pharmacology ; Quinazolines - therapeutic use ; Renal Dialysis ; Urology</subject><ispartof>CEN case reports, 2023-05, Vol.12 (2), p.152-158</ispartof><rights>The Author(s) under exclusive licence to The Japan Society of Nephrology 2022. 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The Author(s) under exclusive licence to The Japan Society of Nephrology.</rights><rights>The Author(s) under exclusive licence to The Japan Society of Nephrology 2022, Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c471t-70a5fd63b62346aec87e540e39416749a1bb8bbee0e9c20334ab6f06d6bd9dbb3</citedby><cites>FETCH-LOGICAL-c471t-70a5fd63b62346aec87e540e39416749a1bb8bbee0e9c20334ab6f06d6bd9dbb3</cites><orcidid>0000-0003-2082-9871</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10151294/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10151294/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,728,781,785,886,27929,27930,41493,42562,51324,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36180718$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Morita, Daisuke</creatorcontrib><creatorcontrib>Ito, Kenji</creatorcontrib><creatorcontrib>Ikeuchi, Nobumitsu</creatorcontrib><creatorcontrib>Nishida, Yoshihiro</creatorcontrib><creatorcontrib>Igata, Fumiyasu</creatorcontrib><creatorcontrib>Nakamura, Tsubasa</creatorcontrib><creatorcontrib>Murayama, Hiroyuki</creatorcontrib><creatorcontrib>Watanabe, Maho</creatorcontrib><creatorcontrib>Takahashi, Koji</creatorcontrib><creatorcontrib>Yasuno, Tetsuhiko</creatorcontrib><creatorcontrib>Uesugi, Noriko</creatorcontrib><creatorcontrib>Fujita, Masaki</creatorcontrib><creatorcontrib>Oda, Takashi</creatorcontrib><creatorcontrib>Masutani, Kosuke</creatorcontrib><title>A case of crescentic glomerulonephritis induced by afatinib for lung adenocarcinoma</title><title>CEN case reports</title><addtitle>CEN Case Rep</addtitle><addtitle>CEN Case Rep</addtitle><description>Afatinib is a second-generation, oral, epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI). One of the most common adverse effects of affatinib is diarrhea, which may lead to acute kidney injury (AKI) due to severe plasma volume loss; however, no case of glomerular injury directly induced by afatinib has been reported to date. Here, we describe the case of a 53-year-old Japanese male patient with advanced lung adenocarcinoma who twice developed AKI requiring dialysis, once after starting and once after increasing the dose of afatinib. Although serum anti-neutrophil cytoplasmic antibodies were negative, crescentic glomerulonephritis with no immune deposits was confirmed on kidney biopsy. No vasculitis-like signs were observed in other organs, such as lung, skin, or peripheral nerves. Afatinib was considered the cause of glomerular damage and was immediately discontinued; corticosteroids were administered. Renal function gradually recovered thereafter, with serum creatinine levels at ~ 2.3 mg/dL after second-line therapy with bevacizumab and atezolizumab. Several cases of cutaneous leukocytoclastic vasculitis have been reported in patients treated with other EGFR-TKIs; therefore, afatinib-induced vasculitis may lead to crescentic glomerulonephritis. Although afatinib-induced glomerular injury is extremely rare and has an unclear mechanism, renal function and urinary findings need to be closely monitored.</description><subject>Adenocarcinoma - drug therapy</subject><subject>Adenocarcinoma of Lung - drug therapy</subject><subject>Afatinib - therapeutic use</subject><subject>Case Report</subject><subject>ErbB Receptors - metabolism</subject><subject>Glomerulonephritis - drug therapy</subject><subject>Humans</subject><subject>Lung Neoplasms - pathology</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Nephrology</subject><subject>Quinazolines - pharmacology</subject><subject>Quinazolines - therapeutic use</subject><subject>Renal Dialysis</subject><subject>Urology</subject><issn>2192-4449</issn><issn>2192-4449</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9UU1P3DAQtaoiQAt_gEPlYy8p44-N41OFUGmRkHoAzpbtTBajxN7aSSX-PYalK7j0NDN6b96M3iPkjME3BqDOCxNKQAOcN3UUquk-kWPONG-klPrzu_6InJbyCABMSFiDPiRHomUdKNYdk9sL6m1BmgbqMxaPcQ6ebsY0YV7GFHH7kMMcCg2xXzz21D1RO9g5xODokDIdl7ihtseYvM0-xDTZE3Iw2LHg6VtdkfurH3eXv5qb3z-vLy9uGi8VmxsFdj30rXAtF7K16DuFawkotGStktoy5zrnEAG15yCEtK4doO1b1-veObEi33e628VN2L_8nu1otjlMNj-ZZIP5iMTwYDbpr2HA1oxrWRW-vink9GfBMpspVA_G0UZMSzFccZBcaSUqle-oPqdSMg77OwzMSyJml4ipiZjXRExXl768_3C_8s__ShA7QqlQ3GA2j2nJsbr2P9lnkC-YgA</recordid><startdate>20230501</startdate><enddate>20230501</enddate><creator>Morita, Daisuke</creator><creator>Ito, Kenji</creator><creator>Ikeuchi, Nobumitsu</creator><creator>Nishida, Yoshihiro</creator><creator>Igata, Fumiyasu</creator><creator>Nakamura, Tsubasa</creator><creator>Murayama, Hiroyuki</creator><creator>Watanabe, Maho</creator><creator>Takahashi, Koji</creator><creator>Yasuno, Tetsuhiko</creator><creator>Uesugi, Noriko</creator><creator>Fujita, Masaki</creator><creator>Oda, Takashi</creator><creator>Masutani, Kosuke</creator><general>Springer Nature Singapore</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><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-2082-9871</orcidid></search><sort><creationdate>20230501</creationdate><title>A case of crescentic glomerulonephritis induced by afatinib for lung adenocarcinoma</title><author>Morita, Daisuke ; Ito, Kenji ; Ikeuchi, Nobumitsu ; Nishida, Yoshihiro ; Igata, Fumiyasu ; Nakamura, Tsubasa ; Murayama, Hiroyuki ; Watanabe, Maho ; Takahashi, Koji ; Yasuno, Tetsuhiko ; Uesugi, Noriko ; Fujita, Masaki ; Oda, Takashi ; Masutani, Kosuke</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c471t-70a5fd63b62346aec87e540e39416749a1bb8bbee0e9c20334ab6f06d6bd9dbb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Adenocarcinoma - drug therapy</topic><topic>Adenocarcinoma of Lung - drug therapy</topic><topic>Afatinib - therapeutic use</topic><topic>Case Report</topic><topic>ErbB Receptors - metabolism</topic><topic>Glomerulonephritis - drug therapy</topic><topic>Humans</topic><topic>Lung Neoplasms - pathology</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Nephrology</topic><topic>Quinazolines - pharmacology</topic><topic>Quinazolines - therapeutic use</topic><topic>Renal Dialysis</topic><topic>Urology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Morita, Daisuke</creatorcontrib><creatorcontrib>Ito, Kenji</creatorcontrib><creatorcontrib>Ikeuchi, Nobumitsu</creatorcontrib><creatorcontrib>Nishida, Yoshihiro</creatorcontrib><creatorcontrib>Igata, Fumiyasu</creatorcontrib><creatorcontrib>Nakamura, Tsubasa</creatorcontrib><creatorcontrib>Murayama, Hiroyuki</creatorcontrib><creatorcontrib>Watanabe, Maho</creatorcontrib><creatorcontrib>Takahashi, Koji</creatorcontrib><creatorcontrib>Yasuno, Tetsuhiko</creatorcontrib><creatorcontrib>Uesugi, Noriko</creatorcontrib><creatorcontrib>Fujita, Masaki</creatorcontrib><creatorcontrib>Oda, Takashi</creatorcontrib><creatorcontrib>Masutani, Kosuke</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>CEN case reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Morita, Daisuke</au><au>Ito, Kenji</au><au>Ikeuchi, Nobumitsu</au><au>Nishida, Yoshihiro</au><au>Igata, Fumiyasu</au><au>Nakamura, Tsubasa</au><au>Murayama, Hiroyuki</au><au>Watanabe, Maho</au><au>Takahashi, Koji</au><au>Yasuno, Tetsuhiko</au><au>Uesugi, Noriko</au><au>Fujita, Masaki</au><au>Oda, Takashi</au><au>Masutani, Kosuke</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A case of crescentic glomerulonephritis induced by afatinib for lung adenocarcinoma</atitle><jtitle>CEN case reports</jtitle><stitle>CEN Case Rep</stitle><addtitle>CEN Case Rep</addtitle><date>2023-05-01</date><risdate>2023</risdate><volume>12</volume><issue>2</issue><spage>152</spage><epage>158</epage><pages>152-158</pages><issn>2192-4449</issn><eissn>2192-4449</eissn><abstract>Afatinib is a second-generation, oral, epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI). One of the most common adverse effects of affatinib is diarrhea, which may lead to acute kidney injury (AKI) due to severe plasma volume loss; however, no case of glomerular injury directly induced by afatinib has been reported to date. Here, we describe the case of a 53-year-old Japanese male patient with advanced lung adenocarcinoma who twice developed AKI requiring dialysis, once after starting and once after increasing the dose of afatinib. Although serum anti-neutrophil cytoplasmic antibodies were negative, crescentic glomerulonephritis with no immune deposits was confirmed on kidney biopsy. No vasculitis-like signs were observed in other organs, such as lung, skin, or peripheral nerves. Afatinib was considered the cause of glomerular damage and was immediately discontinued; corticosteroids were administered. Renal function gradually recovered thereafter, with serum creatinine levels at ~ 2.3 mg/dL after second-line therapy with bevacizumab and atezolizumab. Several cases of cutaneous leukocytoclastic vasculitis have been reported in patients treated with other EGFR-TKIs; therefore, afatinib-induced vasculitis may lead to crescentic glomerulonephritis. Although afatinib-induced glomerular injury is extremely rare and has an unclear mechanism, renal function and urinary findings need to be closely monitored.</abstract><cop>Singapore</cop><pub>Springer Nature Singapore</pub><pmid>36180718</pmid><doi>10.1007/s13730-022-00737-8</doi><tpages>7</tpages><orcidid>https://orcid.org/0000-0003-2082-9871</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Adenocarcinoma - drug therapy Adenocarcinoma of Lung - drug therapy Afatinib - therapeutic use Case Report ErbB Receptors - metabolism Glomerulonephritis - drug therapy Humans Lung Neoplasms - pathology Male Medicine Medicine & Public Health Middle Aged Nephrology Quinazolines - pharmacology Quinazolines - therapeutic use Renal Dialysis Urology |
title | A case of crescentic glomerulonephritis induced by afatinib for lung adenocarcinoma |
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