Creatine Kinase Elevation in Autosomal Dominant Polycystic Kidney Disease Patients on Tolvaptan Treatment
Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary cause of end-stage kidney disease. Currently, tolvaptan is the only treatment that has proven to delay disease progression. The most notable side effect of this therapy is drug-induced liver injury; however, recently,...
| Autores: | , , , , , , , , , , , , , , |
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| Tipo de documento: | artigo |
| Data de publicação: | 2022 |
| País: | España |
| Recursos: | Universitat Autònoma de Barcelona |
| Repositório: | Dipòsit Digital de Documents de la UAB |
| Idioma: | inglês |
| OAI Identifier: | oai:ddd.uab.cat:281651 |
| Acesso em linha: | https://ddd.uab.cat/record/281651 https://dx.doi.org/urn:doi:10.1159/000526368 |
| Access Level: | Acceso aberto |
| Palavra-chave: | ADPKD Creatine-kinase Side effect Tolvaptan |
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Creatine Kinase Elevation in Autosomal Dominant Polycystic Kidney Disease Patients on Tolvaptan TreatmentRodríguez-Espinosa, DianaBroseta, José Jesús|||0000-0002-4559-9083Bastida, Carla|||0000-0003-0845-8107Álvarez Mora, María Isabel|||0000-0003-3788-8915Nicolau, Carlos|||0000-0002-1381-6442Alvarez, CristinaAgraz Pamplona, Irene|||0000-0002-4223-6834Sánchez-Baya, Maya|||0000-0003-1689-9383Furlano, Monica|||0000-0003-1025-3901Ruiz, CésarQuintana, Luis F.|||0000-0001-7582-8476Piñeiro, Gastón Julio|||0000-0003-3806-4731Poch, Esteban|||0000-0002-6492-024XTorra Balcells, Roser|||0000-0001-8714-2332Blasco Pelicano, Miquel|||0000-0003-0789-7992ADPKDCreatine-kinaseSide effectTolvaptanAutosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary cause of end-stage kidney disease. Currently, tolvaptan is the only treatment that has proven to delay disease progression. The most notable side effect of this therapy is drug-induced liver injury; however, recently, there have been two reports of creatine kinase (CK) elevation in ADPKD patients on tolvaptan treatment. We set out to monitor and determine the actual incidence of CK elevation and evaluate its potential association with other clinical factors. This is an observational retrospective multicenter study performed in rapidly progressive ADPKD patients on tolvaptan treatment from Barcelona, Spain. Laboratory tests, demographics, treatment dose, and reported symptoms were collected from October 2018 to March 2021. Ninety-five patients initiated tolvaptan treatment during follow-up. The medication had to be discontinued in 31 (32.6%) patients, primarily due to aquaretic effects (12.6%), elevated liver enzymes (8.4%), and symptomatic or persistently elevated CK levels (3.2%). Moreover, a total of 27 (28.4%) patients had elevated CK levels, with most of them being either transient (12.6%), mild and asymptomatic (4.2%), or resolved after dose reduction (3.2%) or temporary discontinuation (2.1%). We pre sent the largest cohort that has monitored CK levels in a real-life setting, finding them elevated in 28.4% of patients. More research and monitoring will help us understand the clinical implications and the pathophysiological mechanism of CK elevation in this population.Universitat Autònoma de Barcelona 22022-01-0120222022-01-01Articlehttp://purl.org/coar/resource_type/c_6501VoRhttp://purl.org/coar/version/c_970fb48d4fbd8a85info:eu-repo/semantics/articleapplication/pdfhttps://ddd.uab.cat/record/281651https://dx.doi.org/urn:doi:10.1159/000526368reponame:Dipòsit Digital de Documents de la UABinstname:Universitat Autònoma de BarcelonaInglésengopen accesshttp://purl.org/coar/access_right/c_abf2Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, sempre que no sigui amb finalitats comercials, i sempre que es reconegui l'autoria de l'obra original.https://creativecommons.org/licenses/by-nc/4.0/info:eu-repo/semantics/openAccessoai:ddd.uab.cat:2816512026-06-06T12:50:31Z |
| dc.title.none.fl_str_mv |
Creatine Kinase Elevation in Autosomal Dominant Polycystic Kidney Disease Patients on Tolvaptan Treatment |
| title |
Creatine Kinase Elevation in Autosomal Dominant Polycystic Kidney Disease Patients on Tolvaptan Treatment |
| spellingShingle |
Creatine Kinase Elevation in Autosomal Dominant Polycystic Kidney Disease Patients on Tolvaptan Treatment Rodríguez-Espinosa, Diana ADPKD Creatine-kinase Side effect Tolvaptan |
| title_short |
Creatine Kinase Elevation in Autosomal Dominant Polycystic Kidney Disease Patients on Tolvaptan Treatment |
| title_full |
Creatine Kinase Elevation in Autosomal Dominant Polycystic Kidney Disease Patients on Tolvaptan Treatment |
| title_fullStr |
Creatine Kinase Elevation in Autosomal Dominant Polycystic Kidney Disease Patients on Tolvaptan Treatment |
| title_full_unstemmed |
Creatine Kinase Elevation in Autosomal Dominant Polycystic Kidney Disease Patients on Tolvaptan Treatment |
| title_sort |
Creatine Kinase Elevation in Autosomal Dominant Polycystic Kidney Disease Patients on Tolvaptan Treatment |
| dc.creator.none.fl_str_mv |
Rodríguez-Espinosa, Diana Broseta, José Jesús|||0000-0002-4559-9083 Bastida, Carla|||0000-0003-0845-8107 Álvarez Mora, María Isabel|||0000-0003-3788-8915 Nicolau, Carlos|||0000-0002-1381-6442 Alvarez, Cristina Agraz Pamplona, Irene|||0000-0002-4223-6834 Sánchez-Baya, Maya|||0000-0003-1689-9383 Furlano, Monica|||0000-0003-1025-3901 Ruiz, César Quintana, Luis F.|||0000-0001-7582-8476 Piñeiro, Gastón Julio|||0000-0003-3806-4731 Poch, Esteban|||0000-0002-6492-024X Torra Balcells, Roser|||0000-0001-8714-2332 Blasco Pelicano, Miquel|||0000-0003-0789-7992 |
| author |
Rodríguez-Espinosa, Diana |
| author_facet |
Rodríguez-Espinosa, Diana Broseta, José Jesús|||0000-0002-4559-9083 Bastida, Carla|||0000-0003-0845-8107 Álvarez Mora, María Isabel|||0000-0003-3788-8915 Nicolau, Carlos|||0000-0002-1381-6442 Alvarez, Cristina Agraz Pamplona, Irene|||0000-0002-4223-6834 Sánchez-Baya, Maya|||0000-0003-1689-9383 Furlano, Monica|||0000-0003-1025-3901 Ruiz, César Quintana, Luis F.|||0000-0001-7582-8476 Piñeiro, Gastón Julio|||0000-0003-3806-4731 Poch, Esteban|||0000-0002-6492-024X Torra Balcells, Roser|||0000-0001-8714-2332 Blasco Pelicano, Miquel|||0000-0003-0789-7992 |
| author_role |
author |
| author2 |
Broseta, José Jesús|||0000-0002-4559-9083 Bastida, Carla|||0000-0003-0845-8107 Álvarez Mora, María Isabel|||0000-0003-3788-8915 Nicolau, Carlos|||0000-0002-1381-6442 Alvarez, Cristina Agraz Pamplona, Irene|||0000-0002-4223-6834 Sánchez-Baya, Maya|||0000-0003-1689-9383 Furlano, Monica|||0000-0003-1025-3901 Ruiz, César Quintana, Luis F.|||0000-0001-7582-8476 Piñeiro, Gastón Julio|||0000-0003-3806-4731 Poch, Esteban|||0000-0002-6492-024X Torra Balcells, Roser|||0000-0001-8714-2332 Blasco Pelicano, Miquel|||0000-0003-0789-7992 |
| author2_role |
author author author author author author author author author author author author author author |
| dc.contributor.none.fl_str_mv |
Universitat Autònoma de Barcelona |
| dc.subject.none.fl_str_mv |
ADPKD Creatine-kinase Side effect Tolvaptan |
| topic |
ADPKD Creatine-kinase Side effect Tolvaptan |
| description |
Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary cause of end-stage kidney disease. Currently, tolvaptan is the only treatment that has proven to delay disease progression. The most notable side effect of this therapy is drug-induced liver injury; however, recently, there have been two reports of creatine kinase (CK) elevation in ADPKD patients on tolvaptan treatment. We set out to monitor and determine the actual incidence of CK elevation and evaluate its potential association with other clinical factors. This is an observational retrospective multicenter study performed in rapidly progressive ADPKD patients on tolvaptan treatment from Barcelona, Spain. Laboratory tests, demographics, treatment dose, and reported symptoms were collected from October 2018 to March 2021. Ninety-five patients initiated tolvaptan treatment during follow-up. The medication had to be discontinued in 31 (32.6%) patients, primarily due to aquaretic effects (12.6%), elevated liver enzymes (8.4%), and symptomatic or persistently elevated CK levels (3.2%). Moreover, a total of 27 (28.4%) patients had elevated CK levels, with most of them being either transient (12.6%), mild and asymptomatic (4.2%), or resolved after dose reduction (3.2%) or temporary discontinuation (2.1%). We pre sent the largest cohort that has monitored CK levels in a real-life setting, finding them elevated in 28.4% of patients. More research and monitoring will help us understand the clinical implications and the pathophysiological mechanism of CK elevation in this population. |
| publishDate |
2022 |
| dc.date.none.fl_str_mv |
2 2022-01-01 2022 2022-01-01 |
| dc.type.none.fl_str_mv |
Article http://purl.org/coar/resource_type/c_6501 VoR http://purl.org/coar/version/c_970fb48d4fbd8a85 |
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info:eu-repo/semantics/article |
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article |
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https://ddd.uab.cat/record/281651 https://dx.doi.org/urn:doi:10.1159/000526368 |
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https://ddd.uab.cat/record/281651 https://dx.doi.org/urn:doi:10.1159/000526368 |
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Inglés eng |
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Inglés |
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eng |
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open access http://purl.org/coar/access_right/c_abf2 https://creativecommons.org/licenses/by-nc/4.0/ |
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info:eu-repo/semantics/openAccess |
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open access http://purl.org/coar/access_right/c_abf2 https://creativecommons.org/licenses/by-nc/4.0/ |
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openAccess |
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application/pdf |
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