Cardiotoxicity of Uremic Toxins: A Driver of Cardiorenal Syndrome
Cardiovascular disease (CVD) is highly prevalent in the setting of chronic kidney disease (CKD). Such coexistence of CVD and CKD—the so-called “cardiorenal or renocardiac syndrome”—contributes to exponentially increased risk of cardiovascular (CV) mortality. U...
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| Format: | Article |
| Language: | English |
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MDPI AG
2018-09-01
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| Series: | Toxins |
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| Online Access: | http://www.mdpi.com/2072-6651/10/9/352 |
| _version_ | 1811307065905250304 |
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| author | Suree Lekawanvijit |
| author_facet | Suree Lekawanvijit |
| author_sort | Suree Lekawanvijit |
| collection | DOAJ |
| description | Cardiovascular disease (CVD) is highly prevalent in the setting of chronic kidney disease (CKD). Such coexistence of CVD and CKD—the so-called “cardiorenal or renocardiac syndrome”—contributes to exponentially increased risk of cardiovascular (CV) mortality. Uremic cardiomyopathy is a characteristic cardiac pathology commonly found in CKD. CKD patients are also predisposed to heart rhythm disorders especially atrial fibrillation. Traditional CV risk factors as well as known CKD-associated CV risk factors such as anemia are insufficient to explain CV complications in the CKD population. Accumulation of uremic retention solutes is a hallmark of impaired renal excretory function. Many of them have been considered inert solutes until their biological toxicity is unraveled and they become accepted as “uremic toxins”. Direct cardiotoxicity of uremic toxins has been increasingly demonstrated in recent years. This review offers a mechanistic insight into the pathological cardiac remodeling and dysfunction contributed by uremic toxins with a main focus on fibroblastic growth factor-23, an emerging toxin playing a central role in the chronic kidney disease–mineral bone disorder, and the two most investigated non-dialyzable protein-bound uremic toxins, indoxyl sulfate and p-cresyl sulfate. Potential therapeutic strategies that could address these toxins and their relevant mediated pathways since pre-dialysis stages are also discussed. |
| first_indexed | 2024-04-13T08:57:44Z |
| format | Article |
| id | doaj.art-b03400421a8e43fabb0e4cc37f6f2b4b |
| institution | Directory Open Access Journal |
| issn | 2072-6651 |
| language | English |
| last_indexed | 2024-04-13T08:57:44Z |
| publishDate | 2018-09-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Toxins |
| spelling | doaj.art-b03400421a8e43fabb0e4cc37f6f2b4b2022-12-22T02:53:15ZengMDPI AGToxins2072-66512018-09-0110935210.3390/toxins10090352toxins10090352Cardiotoxicity of Uremic Toxins: A Driver of Cardiorenal SyndromeSuree Lekawanvijit0Department of Pathology, Faculty of Medicine, Chiang Mai University, 110 Intawaroros Rd, Sribhoom, Chiang Mai 50200, ThailandCardiovascular disease (CVD) is highly prevalent in the setting of chronic kidney disease (CKD). Such coexistence of CVD and CKD—the so-called “cardiorenal or renocardiac syndrome”—contributes to exponentially increased risk of cardiovascular (CV) mortality. Uremic cardiomyopathy is a characteristic cardiac pathology commonly found in CKD. CKD patients are also predisposed to heart rhythm disorders especially atrial fibrillation. Traditional CV risk factors as well as known CKD-associated CV risk factors such as anemia are insufficient to explain CV complications in the CKD population. Accumulation of uremic retention solutes is a hallmark of impaired renal excretory function. Many of them have been considered inert solutes until their biological toxicity is unraveled and they become accepted as “uremic toxins”. Direct cardiotoxicity of uremic toxins has been increasingly demonstrated in recent years. This review offers a mechanistic insight into the pathological cardiac remodeling and dysfunction contributed by uremic toxins with a main focus on fibroblastic growth factor-23, an emerging toxin playing a central role in the chronic kidney disease–mineral bone disorder, and the two most investigated non-dialyzable protein-bound uremic toxins, indoxyl sulfate and p-cresyl sulfate. Potential therapeutic strategies that could address these toxins and their relevant mediated pathways since pre-dialysis stages are also discussed.http://www.mdpi.com/2072-6651/10/9/352uremic toxinsFGF23protein-bound uremic toxinindoxyl sulfatep-cresyl sulfatecardiotoxicitycardiorenal syndrome |
| spellingShingle | Suree Lekawanvijit Cardiotoxicity of Uremic Toxins: A Driver of Cardiorenal Syndrome Toxins uremic toxins FGF23 protein-bound uremic toxin indoxyl sulfate p-cresyl sulfate cardiotoxicity cardiorenal syndrome |
| title | Cardiotoxicity of Uremic Toxins: A Driver of Cardiorenal Syndrome |
| title_full | Cardiotoxicity of Uremic Toxins: A Driver of Cardiorenal Syndrome |
| title_fullStr | Cardiotoxicity of Uremic Toxins: A Driver of Cardiorenal Syndrome |
| title_full_unstemmed | Cardiotoxicity of Uremic Toxins: A Driver of Cardiorenal Syndrome |
| title_short | Cardiotoxicity of Uremic Toxins: A Driver of Cardiorenal Syndrome |
| title_sort | cardiotoxicity of uremic toxins a driver of cardiorenal syndrome |
| topic | uremic toxins FGF23 protein-bound uremic toxin indoxyl sulfate p-cresyl sulfate cardiotoxicity cardiorenal syndrome |
| url | http://www.mdpi.com/2072-6651/10/9/352 |
| work_keys_str_mv | AT sureelekawanvijit cardiotoxicityofuremictoxinsadriverofcardiorenalsyndrome |