Calcimimetics and Vascular Calcification
In patients with chronic kidney disease (CKD), cardiovascular events (CVA) are the main cause of morbidity and mortality. Vascular calcification, linked to bone mineral metabolism disorders such as elevated serum phosphate, parathyroid hormone (PTH), and FGF23, well-known uremic toxins, aggravate th...
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| Format: | Article |
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MDPI AG
2025-06-01
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| Series: | Toxins |
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| Online Access: | https://www.mdpi.com/2072-6651/17/6/297 |
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| author | Avinash Chandu Carolt Arana Juan Daniel Díaz-García Mario Cozzolino Paola Ciceri José-Vicente Torregrosa |
| author_facet | Avinash Chandu Carolt Arana Juan Daniel Díaz-García Mario Cozzolino Paola Ciceri José-Vicente Torregrosa |
| author_sort | Avinash Chandu |
| collection | DOAJ |
| description | In patients with chronic kidney disease (CKD), cardiovascular events (CVA) are the main cause of morbidity and mortality. Vascular calcification, linked to bone mineral metabolism disorders such as elevated serum phosphate, parathyroid hormone (PTH), and FGF23, well-known uremic toxins, aggravate this risk. Calcimimetics are allosteric activators of the calcium-sensing receptor (CaSR), a G protein-coupled receptor that regulates PTH secretion and synthesis in response to changes in extracellular calcium in the parathyroid glands. Through direct and indirect mechanisms, they have demonstrated their efficacy in reducing the progression of vascular, valvular, and soft tissue calcification in experimental studies. Although clinical studies in dialysis patients did not achieve statistical significance in their primary objectives, positive results in subgroup analyses suggest that the lack of significance may be attributable to the short follow-up period. This finding highlights the need to consider early treatment strategies, especially in advanced stages of chronic kidney disease, to more effectively address the progression of vascular calcification through serum uremic toxins control. |
| format | Article |
| id | doaj-art-647bd287f31441f2b5cf7b253f82075e |
| institution | OA Journals |
| issn | 2072-6651 |
| language | English |
| publishDate | 2025-06-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Toxins |
| spelling | doaj-art-647bd287f31441f2b5cf7b253f82075e2025-08-20T02:21:58ZengMDPI AGToxins2072-66512025-06-0117629710.3390/toxins17060297Calcimimetics and Vascular CalcificationAvinash Chandu0Carolt Arana1Juan Daniel Díaz-García2Mario Cozzolino3Paola Ciceri4José-Vicente Torregrosa5Nephrology and Renal Transplant Department, Hospital Clínic, 08036 Barcelona, SpainNephrology and Renal Transplant Department, Hospital Clínic, 08036 Barcelona, SpainNephrology and Renal Transplant Department, Hospital Clínic, 08036 Barcelona, SpainDepartment of Health Sciences, University of Milan, 20142 Milan, ItalyDepartment of Health Sciences, University of Milan, 20142 Milan, ItalyNephrology and Renal Transplant Department, Hospital Clínic, 08036 Barcelona, SpainIn patients with chronic kidney disease (CKD), cardiovascular events (CVA) are the main cause of morbidity and mortality. Vascular calcification, linked to bone mineral metabolism disorders such as elevated serum phosphate, parathyroid hormone (PTH), and FGF23, well-known uremic toxins, aggravate this risk. Calcimimetics are allosteric activators of the calcium-sensing receptor (CaSR), a G protein-coupled receptor that regulates PTH secretion and synthesis in response to changes in extracellular calcium in the parathyroid glands. Through direct and indirect mechanisms, they have demonstrated their efficacy in reducing the progression of vascular, valvular, and soft tissue calcification in experimental studies. Although clinical studies in dialysis patients did not achieve statistical significance in their primary objectives, positive results in subgroup analyses suggest that the lack of significance may be attributable to the short follow-up period. This finding highlights the need to consider early treatment strategies, especially in advanced stages of chronic kidney disease, to more effectively address the progression of vascular calcification through serum uremic toxins control.https://www.mdpi.com/2072-6651/17/6/297vascular calcificationaortic calcificationcalcimimeticscinacalcetetelecatetideevocaletide |
| spellingShingle | Avinash Chandu Carolt Arana Juan Daniel Díaz-García Mario Cozzolino Paola Ciceri José-Vicente Torregrosa Calcimimetics and Vascular Calcification Toxins vascular calcification aortic calcification calcimimetics cinacalcet etelecatetide evocaletide |
| title | Calcimimetics and Vascular Calcification |
| title_full | Calcimimetics and Vascular Calcification |
| title_fullStr | Calcimimetics and Vascular Calcification |
| title_full_unstemmed | Calcimimetics and Vascular Calcification |
| title_short | Calcimimetics and Vascular Calcification |
| title_sort | calcimimetics and vascular calcification |
| topic | vascular calcification aortic calcification calcimimetics cinacalcet etelecatetide evocaletide |
| url | https://www.mdpi.com/2072-6651/17/6/297 |
| work_keys_str_mv | AT avinashchandu calcimimeticsandvascularcalcification AT caroltarana calcimimeticsandvascularcalcification AT juandanieldiazgarcia calcimimeticsandvascularcalcification AT mariocozzolino calcimimeticsandvascularcalcification AT paolaciceri calcimimeticsandvascularcalcification AT josevicentetorregrosa calcimimeticsandvascularcalcification |