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Bellamy CO, Burt AD. Liver in Systemic Disease. MACSWEEN'S PATHOLOGY OF THE LIVER 2024:1039-1095. [DOI: 10.1016/b978-0-7020-8228-3.00015-6] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/05/2025]
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Cozzolino M, Maffei Faccioli F, Cara A, Boni Brivio G, Rivela F, Ciceri P, Magagnoli L, Galassi A, Barbuto S, Speciale S, Minicucci C, Cianciolo G. Future treatment of vascular calcification in chronic kidney disease. Expert Opin Pharmacother 2023; 24:2041-2057. [PMID: 37776230 DOI: 10.1080/14656566.2023.2266381] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/07/2023] [Accepted: 09/29/2023] [Indexed: 10/02/2023]
Abstract
INTRODUCTION Cardiovascular disease (CVD) is one of the global leading causes of morbidity and mortality in chronic kidney disease (CKD) patients. Vascular calcification (VC) is a major cause of CVD in this population and is the consequence of complex interactions between inhibitor and promoter factors leading to pathological deposition of calcium and phosphate in soft tissues. Different pathological landscapes are associated with the development of VC, such as endothelial dysfunction, oxidative stress, chronic inflammation, loss of mineralization inhibitors, release of calcifying extracellular vesicles (cEVs) and circulating calcifying cells. AREAS COVERED In this review, we examined the literature and summarized the pathophysiology, biomarkers and focused on the treatments of VC. EXPERT OPINION Even though there is no consensus regarding specific treatment options, we provide the currently available treatment strategies that focus on phosphate balance, correction of vitamin D and vitamin K deficiencies, avoidance of both extremes of bone turnover, normalizing calcium levels and reduction of inflammatory response and the potential and promising therapeutic approaches liketargeting cellular mechanisms of calcification (e.g. SNF472, TNAP inhibitors).Creating novel scores to detect in advance VC and implementing targeted therapies is crucial to treat them and improve the future management of these patients.
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Affiliation(s)
- Mario Cozzolino
- Renal Division, Department of Health Sciences, ASST Santi Paolo e Carlo, University of Milan, Milan, Italy
| | - Federico Maffei Faccioli
- Renal Division, Department of Health Sciences, ASST Santi Paolo e Carlo, University of Milan, Milan, Italy
| | - Anila Cara
- Renal Division, Department of Health Sciences, ASST Santi Paolo e Carlo, University of Milan, Milan, Italy
| | - Giulia Boni Brivio
- Renal Division, Department of Health Sciences, ASST Santi Paolo e Carlo, University of Milan, Milan, Italy
| | - Francesca Rivela
- Renal Division, Department of Health Sciences, ASST Santi Paolo e Carlo, University of Milan, Milan, Italy
| | - Paola Ciceri
- Renal Division, Department of Health Sciences, ASST Santi Paolo e Carlo, University of Milan, Milan, Italy
| | - Lorenza Magagnoli
- Renal Division, Department of Health Sciences, ASST Santi Paolo e Carlo, University of Milan, Milan, Italy
| | - Andrea Galassi
- Renal Division, Department of Health Sciences, ASST Santi Paolo e Carlo, University of Milan, Milan, Italy
| | - Simona Barbuto
- Nephrology, Dialysis and Renal Transplant Unit, IRCCS-Azienda Ospedaliero-Universitaria di Bologna, Alma Mater Studiorum University of Bologna, Bologna, Italy
| | - Serena Speciale
- Nephrology, Dialysis and Renal Transplant Unit, IRCCS-Azienda Ospedaliero-Universitaria di Bologna, Alma Mater Studiorum University of Bologna, Bologna, Italy
| | - Carlo Minicucci
- Nephrology, Dialysis and Renal Transplant Unit, IRCCS-Azienda Ospedaliero-Universitaria di Bologna, Alma Mater Studiorum University of Bologna, Bologna, Italy
| | - Giuseppe Cianciolo
- Nephrology, Dialysis and Renal Transplant Unit, IRCCS-Azienda Ospedaliero-Universitaria di Bologna, Alma Mater Studiorum University of Bologna, Bologna, Italy
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Marreiros C, Viegas C, Simes D. Targeting a Silent Disease: Vascular Calcification in Chronic Kidney Disease. Int J Mol Sci 2022; 23:16114. [PMID: 36555758 PMCID: PMC9781141 DOI: 10.3390/ijms232416114] [Citation(s) in RCA: 18] [Impact Index Per Article: 6.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/11/2022] [Revised: 12/09/2022] [Accepted: 12/15/2022] [Indexed: 12/23/2022] Open
Abstract
Chronic kidney disease (CKD) patients have a higher risk of developing early cardiovascular disease (CVD). Although vascular calcification (VC) is one of the strongest predictors of CVD risk, its diagnosis among the CKD population remains a serious clinical challenge. This is mainly due to the complexity of VC, which results from various interconnected pathological mechanisms occurring at early stages and at multiples sites, affecting the medial and intimal layers of the vascular tree. Here, we review the most used and recently developed imaging techniques, here referred to as imaging biomarkers, for VC detection and monitoring, while discussing their strengths and limitations considering the specificities of VC in a CKD context. Although imaging biomarkers have a crucial role in the diagnosis of VC, with important insights into CVD risk, circulating biomarkers represent an added value by reflecting the molecular dynamics and mechanisms involved in VC pathophysiological pathways, opening new avenues into the early detection and targeted interventions. We propose that a combined strategy using imaging and circulating biomarkers with a role in multiple VC molecular mechanisms, such as Fetuin-A, Matrix Gla protein, Gla-rich protein and calciprotein particles, should represent high prognostic value for management of CVD risk in the CKD population.
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Affiliation(s)
- Catarina Marreiros
- Centre of Marine Sciences (CCMAR), University of Algarve, Campus de Gambelas, 8005-139 Faro, Portugal
| | - Carla Viegas
- Centre of Marine Sciences (CCMAR), University of Algarve, Campus de Gambelas, 8005-139 Faro, Portugal
- GenoGla Diagnostics, Centre of Marine Sciences (CCMAR), University of Algarve, Campus de Gambelas, 8005-139 Faro, Portugal
| | - Dina Simes
- Centre of Marine Sciences (CCMAR), University of Algarve, Campus de Gambelas, 8005-139 Faro, Portugal
- GenoGla Diagnostics, Centre of Marine Sciences (CCMAR), University of Algarve, Campus de Gambelas, 8005-139 Faro, Portugal
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Xiao Q, Tang Y, Xia J, Luo H, Yu M, Chen S, Wang W, Pu L, Wang L, Li G, Li Y. Ubiquitin-specific protease 47 is associated with vascular calcification in chronic kidney disease by regulating osteogenic transdifferentiation of vascular smooth muscle cells. Ren Fail 2022; 44:752-766. [PMID: 35509185 PMCID: PMC9090392 DOI: 10.1080/0886022x.2022.2072337] [Citation(s) in RCA: 4] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/09/2021] [Revised: 04/14/2022] [Accepted: 04/15/2022] [Indexed: 12/31/2022] Open
Abstract
Chronic kidney disease (CKD) has recently become a serious health and social concern. Vascular calcification, a common complication of CKD, is a risk factor that increases the incidence and mortality of cardiovascular events in patients with CKD. However, there are currently no effective therapeutic targets that can facilitate treatment with fewer side effects for vascular calcification in CKD. To identify potential therapeutic targets, we performed label-free quantification (LFQ) analyses of protein samples from rat aortic vascular smooth muscle cells (RASMCs) after high-phosphorus treatment by nano-UPLC-MS/MS. We determined that ubiquitin-specific protease 47 (USP47) may be associated with CKD vascular calcification by regulating the osteogenic transdifferentiation of the vascular smooth muscle cell (VSMC) phenotype, thus suggesting a novel and potentially effective therapeutic target for CKD vascular calcification. USP47 knockdown significantly reduced the expression of β-transducin repeat-containing protein (BTRC), serine/threonine-protein kinase akt-1 (AKT1), Klotho, fibroblast growth factor (FGF23), and matrix Gla protein (MGP) in RASMCs after high-phosphorus treatment. Consistent with the results of protein-protein interaction (PPI) analyses, USP47 may be involved in regulating osteogenic transdifferentiation markers, such as runt-related transcription factor 2 (RUNX2), Klotho, FGF23, and MGP through the BTRC/AKT1 pathway upon CKD vascular calcification. These data indicate that USP47 may be associated with vascular calcification in CKD by regulating osteogenic differentiation of VSMCs. USP47 may regulate osteogenic transdifferentiation in VSMCs upon CKD vascular calcification through a process involving the BTRC/AKT1 pathway. This study identified a novel potential therapeutic target for the treatment of vascular calcification in CKD.
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Affiliation(s)
- Qiong Xiao
- Department of Nephrology, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
- Sichuan Clinical Research Center for Kidney Diseases, Clinical Immunology Translational Medicine Key Laboratory of Sichuan Province, School of Medicine, University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
- Chinese Academy of Sciences Sichuan Translational Medicine Research Hospital, Chengdu, People’s Republic of China
- The First Affiliated Hospital of Chongqing Medical and Pharmaceutical College, Chongqing, People’s Republic of China
| | - Yun Tang
- Department of Nephrology, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
- Sichuan Clinical Research Center for Kidney Diseases, Clinical Immunology Translational Medicine Key Laboratory of Sichuan Province, School of Medicine, University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
- Chinese Academy of Sciences Sichuan Translational Medicine Research Hospital, Chengdu, People’s Republic of China
| | - Juhua Xia
- Jintang First People’s Hospital, Chengdu, People’s Republic of China
| | - Haojun Luo
- Department of Nephrology, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
- Sichuan Clinical Research Center for Kidney Diseases, Clinical Immunology Translational Medicine Key Laboratory of Sichuan Province, School of Medicine, University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
- Chinese Academy of Sciences Sichuan Translational Medicine Research Hospital, Chengdu, People’s Republic of China
| | - Meidie Yu
- Department of Nephrology, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
- Sichuan Clinical Research Center for Kidney Diseases, Clinical Immunology Translational Medicine Key Laboratory of Sichuan Province, School of Medicine, University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
- Chinese Academy of Sciences Sichuan Translational Medicine Research Hospital, Chengdu, People’s Republic of China
| | - Sipei Chen
- Department of Nephrology, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
- Sichuan Clinical Research Center for Kidney Diseases, Clinical Immunology Translational Medicine Key Laboratory of Sichuan Province, School of Medicine, University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
- Chinese Academy of Sciences Sichuan Translational Medicine Research Hospital, Chengdu, People’s Republic of China
| | - Wei Wang
- Department of Nephrology, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
- Sichuan Clinical Research Center for Kidney Diseases, Clinical Immunology Translational Medicine Key Laboratory of Sichuan Province, School of Medicine, University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
- Chinese Academy of Sciences Sichuan Translational Medicine Research Hospital, Chengdu, People’s Republic of China
| | - Lei Pu
- Department of Nephrology, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
- Sichuan Clinical Research Center for Kidney Diseases, Clinical Immunology Translational Medicine Key Laboratory of Sichuan Province, School of Medicine, University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
- Chinese Academy of Sciences Sichuan Translational Medicine Research Hospital, Chengdu, People’s Republic of China
| | - Li Wang
- Department of Nephrology, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
- Sichuan Clinical Research Center for Kidney Diseases, Clinical Immunology Translational Medicine Key Laboratory of Sichuan Province, School of Medicine, University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
- Chinese Academy of Sciences Sichuan Translational Medicine Research Hospital, Chengdu, People’s Republic of China
| | - Guisen Li
- Department of Nephrology, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
- Sichuan Clinical Research Center for Kidney Diseases, Clinical Immunology Translational Medicine Key Laboratory of Sichuan Province, School of Medicine, University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
- Chinese Academy of Sciences Sichuan Translational Medicine Research Hospital, Chengdu, People’s Republic of China
| | - Yi Li
- Department of Nephrology, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
- Sichuan Clinical Research Center for Kidney Diseases, Clinical Immunology Translational Medicine Key Laboratory of Sichuan Province, School of Medicine, University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
- Chinese Academy of Sciences Sichuan Translational Medicine Research Hospital, Chengdu, People’s Republic of China
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Xiao Q, Tang Y, Luo H, Chen S, Chen R, Yan Z, Pu L, Wang L, Li G, Li Y. Sclerostin is involved in osteogenic transdifferentiation of vascular smooth muscle cells in chronic kidney disease-associated vascular calcification with non-canonical Wnt signaling. Ren Fail 2022; 44:1426-1442. [PMID: 36017689 PMCID: PMC9423850 DOI: 10.1080/0886022x.2022.2114370] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/02/2022] Open
Abstract
Vascular calcification is prominent in patients with chronic kidney disease (CKD) and is a strong predictor of cardiovascular mortality in the CKD population. However, the mechanism underlying CKD-associated vascular calcification remains unclear. To identify potential therapeutic targets, a 5/6 nephrectomy rat model was established by feeding of a high-phosphorous diet as the CKD group and compared with sham group rats at 4 and 16 weeks. Sequencing analyses of the rat aorta revealed 643 upregulated and 1023 downregulated genes at 4 weeks, as well as 899 upregulated and 1185 downregulated genes at 16 weeks in the CKD group compared to the sham group. Bioinformatics analyses suggested that SOST (which encodes sclerostin) and Wnt signaling are involved in CKD-associated vascular calcification. Furthermore, protein-protein interactions analysis revealed interactions between SOST, WNT5A, and WNT5B, that involved runt-related transcription factor 2 (RUNX2) and transgelin (TAGLN). SOST was increased in CKD-associated vascular calcification following reduction of the Wnt signaling, including WNT5A and WNT5B, both in vivo and in vitro. TargetScan was used to predict the microRNAs (miRNAs) targeting WNT5A and WNT5B. The expression levels of miR-542-3p, miR-298-3p, miR-376b-5p, and miR-3568 were significantly reduced, whereas that of miR-742-3p was significantly increased in calcified rat aortic vascular smooth muscle cells (VSMCs). In CKD rat aortas, the expression of miR-542-3p, miR-298-3p, miR-376b-5p, miR-3568, miR-742-3p, and miR-22-5p were significantly reduced at both 4 and 16 weeks. Altogether, owing to several assessments, potentially diagnostic and prognostic biomarkers for improving common CKD diagnostic tools were identified in this study. Abbreviations: BUN: blood urea nitrogen; CKD: chronic kidney disease; CKD-MBD: chronic kidney disease-mineral bone disorder; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GO: the Gene Ontology; HE: hematoxylin-eosin; HRP: horseradish peroxidase; KEGG: Kyoto Encyclopedia of Genes and Genomes; MiRNAs: microRNAs; PAS: periodic acid-Schiff; RUNX2: runt-related transcription factor 2; SCr: serum creatinine; STRING: the Search Tool for the Retrieval of Interacting Genes/Proteins; TAGLN: transgelin; VSMC: vascular smooth muscle cell.
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Affiliation(s)
- Qiong Xiao
- Department of Nephrology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, PR China.,Sichuan Clinical Research Center for Kidney Diseases, Clinical Immunology Translational Medicine Key Laboratory of Sichuan Province, School of Medicine, University of Electronic Science and Technology of China, Chengdu, PR China.,Chinese Academy of Sciences, Sichuan Translational Medicine Research Hospital, Chengdu, PR China.,The First Affiliated Hospital of Chongqing Medical and Pharmaceutical College, Chongqing, PR China
| | - Yun Tang
- Department of Nephrology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, PR China.,Sichuan Clinical Research Center for Kidney Diseases, Clinical Immunology Translational Medicine Key Laboratory of Sichuan Province, School of Medicine, University of Electronic Science and Technology of China, Chengdu, PR China.,Chinese Academy of Sciences, Sichuan Translational Medicine Research Hospital, Chengdu, PR China
| | - Haojun Luo
- Department of Nephrology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, PR China.,Sichuan Clinical Research Center for Kidney Diseases, Clinical Immunology Translational Medicine Key Laboratory of Sichuan Province, School of Medicine, University of Electronic Science and Technology of China, Chengdu, PR China.,Chinese Academy of Sciences, Sichuan Translational Medicine Research Hospital, Chengdu, PR China.,Department of Palliative Medicine, Chongqing University Cancer Hospital, Chongqing, PR China
| | - Sipei Chen
- Department of Nephrology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, PR China.,Sichuan Clinical Research Center for Kidney Diseases, Clinical Immunology Translational Medicine Key Laboratory of Sichuan Province, School of Medicine, University of Electronic Science and Technology of China, Chengdu, PR China.,Chinese Academy of Sciences, Sichuan Translational Medicine Research Hospital, Chengdu, PR China
| | - Rong Chen
- Department of Nephrology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, PR China.,Sichuan Clinical Research Center for Kidney Diseases, Clinical Immunology Translational Medicine Key Laboratory of Sichuan Province, School of Medicine, University of Electronic Science and Technology of China, Chengdu, PR China.,Chinese Academy of Sciences, Sichuan Translational Medicine Research Hospital, Chengdu, PR China
| | - Zhe Yan
- College of Integration of Traditional Chinese and Western Medicine, Southwest Medical University, Luzhou, PR China
| | - Lei Pu
- Department of Nephrology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, PR China.,Sichuan Clinical Research Center for Kidney Diseases, Clinical Immunology Translational Medicine Key Laboratory of Sichuan Province, School of Medicine, University of Electronic Science and Technology of China, Chengdu, PR China.,Chinese Academy of Sciences, Sichuan Translational Medicine Research Hospital, Chengdu, PR China
| | - Li Wang
- Department of Nephrology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, PR China.,Sichuan Clinical Research Center for Kidney Diseases, Clinical Immunology Translational Medicine Key Laboratory of Sichuan Province, School of Medicine, University of Electronic Science and Technology of China, Chengdu, PR China.,Chinese Academy of Sciences, Sichuan Translational Medicine Research Hospital, Chengdu, PR China
| | - Guisen Li
- Department of Nephrology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, PR China.,Sichuan Clinical Research Center for Kidney Diseases, Clinical Immunology Translational Medicine Key Laboratory of Sichuan Province, School of Medicine, University of Electronic Science and Technology of China, Chengdu, PR China.,Chinese Academy of Sciences, Sichuan Translational Medicine Research Hospital, Chengdu, PR China
| | - Yi Li
- Department of Nephrology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, PR China.,Sichuan Clinical Research Center for Kidney Diseases, Clinical Immunology Translational Medicine Key Laboratory of Sichuan Province, School of Medicine, University of Electronic Science and Technology of China, Chengdu, PR China.,Chinese Academy of Sciences, Sichuan Translational Medicine Research Hospital, Chengdu, PR China
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High Risk Percutaneous Coronary Intervention of Left Main Bifurcation Stenosis in a Peritoneal Dialysis Patient. Pril (Makedon Akad Nauk Umet Odd Med Nauki) 2021; 42:71-78. [PMID: 34699707 DOI: 10.2478/prilozi-2021-0023] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/20/2022]
Abstract
Complex coronary artery disease is the leading cause of death in patients with end-stage renal disease. We report a case of a patient on peritoneal dialysis, preloaded with Prasugrel and acetylsalicylic acid as а potent dual antiplatelet therapy (DAPT). The patient underwent a high-risk percutaneous coronary intervention (PCI) due to bifurcation stenosis of the left main stem branch. A "double kiss crush" bifurcation stenting technique was performed. This case provides additional data about the treatment of this group of patients, a group that is often excluded from randomized control trials, but is frequently encountered in cardiovascular practice. Furthermore, it helps to advance PCI treatment along with exploring the safety of potent DAPT in a group that is susceptible to both ischemia and bleeding, thus presenting a great challenge in the decision for treatment.
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Schantl AE, Ivarsson ME, Leroux JC. Investigational Pharmacological Treatments for Vascular Calcification. ADVANCED THERAPEUTICS 2018. [DOI: 10.1002/adtp.201800094] [Citation(s) in RCA: 21] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/29/2022]
Affiliation(s)
- Antonia E. Schantl
- Institute of Pharmaceutical Sciences; ETH Zurich; Vladimir-Prelog-Weg 3 8093 Zurich Switzerland
| | | | - Jean-Christophe Leroux
- Institute of Pharmaceutical Sciences; ETH Zurich; Vladimir-Prelog-Weg 3 8093 Zurich Switzerland
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Mizuiri S, Nishizawa Y, Yamashita K, Mizuno K, Ishine M, Doi S, Masaki T, Shigemoto K. Coronary artery calcification score and common iliac artery calcification score in non-dialysis CKD patients. Nephrology (Carlton) 2018; 23:837-845. [PMID: 28703899 PMCID: PMC6120488 DOI: 10.1111/nep.13113] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 07/04/2017] [Indexed: 12/27/2022]
Abstract
AIM Many studies have validated Agatston's coronary artery calcification score (CACS) for assessing vascular calcification (VC) in chronic kidney disease (CKD) patients. This study aimed to evaluate the CACS and common iliac artery calcification score (IACS) and to examine the variables related to each score. METHODS The subjects were 145 non-dialysis CKD patients. The CACS and IACS were determined using the same thoracicoabdominal multi-detector computed tomography. Multiple regression analyses were performed to assess the factors associated with the CACS or IACS. The associations between progression to renal replacement therapy (RRT) and the CACS or IACS were studied using Cox hazards models. RESULTS The subjects' median age, estimated glomerular filtration rate (eGFR), and follow-up period were 72 (62-78) years, 32 (18-50) mL/min/1.73m2 , and 864 (550-1425) days, respectively. Age, diabetes, the serum phosphate level, and the eGFR were found to be significant factors of the CACS [β (95% CI): 0.38 (0.02-0.04), P < 0.0001, 0.28 (0.19-0.50), P < 0.0001, 0.16 (0.03-0.45), P < 0.05 and -0.15 (-0.02-0.00), P < 0.05, respectively]. Age and diabetes were shown to be significant factors of the IACS [β (95% CI): 0.53 (0.04-0.06), P < 0.0001, and 0.18 (0.07-0.40), P < 0.01, respectively]. Progression to RRT occurred in 31 patients and was significantly associated with the CACS (hazard ratio: 1.01, P < 0.01), urinary protein level and eGFR, but not the IACS. CONCLUSION Chronic kidney disease related risk factors for VC, such as the eGFR and hyperphosphataemia, are significantly associated with a high CACS, but not a high IACS, and the CACS is a significant predictor of progression to RRT.
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Affiliation(s)
- Sonoo Mizuiri
- Department of NephrologyIchiyokai Harada HospitalHiroshimaJapan
| | | | | | - Kenji Mizuno
- Department of RadiologyIchiyokai Harada HospitalHiroshimaJapan
| | - Masahiro Ishine
- Department of RadiologyIchiyokai Harada HospitalHiroshimaJapan
| | - Shigehiro Doi
- Department of NephrologyHiroshima University HospitalHiroshimaJapan
| | - Takao Masaki
- Department of NephrologyHiroshima University HospitalHiroshimaJapan
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Bover J, Górriz JL, Ureña-Torres P, Lloret MJ, Ruiz-García C, daSilva I, Chang P, Rodríguez M, Ballarín J. Detección de las calcificaciones cardiovasculares: ¿una herramienta útil para el nefrólogo? Nefrologia 2016; 36:587-596. [DOI: 10.1016/j.nefro.2016.05.021] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/10/2016] [Accepted: 05/19/2016] [Indexed: 12/12/2022] Open
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Sharaf El Din UAA, Salem MM, Abdulazim DO. Vascular calcification: When should we interfere in chronic kidney disease patients and how? World J Nephrol 2016; 5:398-417. [PMID: 27648404 PMCID: PMC5011247 DOI: 10.5527/wjn.v5.i5.398] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/17/2016] [Revised: 04/20/2016] [Accepted: 06/27/2016] [Indexed: 02/06/2023] Open
Abstract
Chronic kidney disease (CKD) patients are endangered with the highest mortality rate compared to other chronic diseases. Cardiovascular events account for up to 60% of the fatalities. Cardiovascular calcifications affect most of the CKD patients. Most of this calcification is related to disturbed renal phosphate handling. Fibroblast growth factor 23 and klotho deficiency were incriminated in the pathogenesis of vascular calcification through different mechanisms including their effects on endothelium and arterial wall smooth muscle cells. In addition, deficient klotho gene expression, a constant feature of CKD, promotes vascular pathology and shares in progression of the CKD. The role of gut in the etio-pathogenesis of systemic inflammation and vascular calcification is a newly discovered mechanism. This review will cover the medical history, prevalence, pathogenesis, clinical relevance, different tools used to diagnose, the ideal timing to prevent or to withhold the progression of vascular calcification and the different medications and medical procedures that can help to prolong the survival of CKD patients.
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