Lipoprotein-associated phospholipase A2 predicts cardiovascular death in patients on maintenance hemodialysis: a 7-year prospective cohort study
Cardiovascular diseases (CVD) is the leading cause of death among maintenance hemodialysis patients, with dyslipidemia being a prevalent complication. The paradoxical relationship between cardiovascular outcomes and established lipid risk markers, such as low-density lipoprotein cholesterol (LDL-C),...
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Published in | Lipids in health and disease Vol. 23; no. 1; pp. 15 - 18 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
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England
BioMed Central Ltd
12.01.2024
BioMed Central BMC |
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Abstract | Cardiovascular diseases (CVD) is the leading cause of death among maintenance hemodialysis patients, with dyslipidemia being a prevalent complication. The paradoxical relationship between cardiovascular outcomes and established lipid risk markers, such as low-density lipoprotein cholesterol (LDL-C), complicates lipid management in this population. This study investigated Lipoprotein-associated phospholipase A2 (Lp-PLA2), an emerging biomarker known for its proinflammatory and proatherogenic properties, as a potential cardiovascular prognostic marker in this cohort. In this context, the association between Lp-PLA2 levels and cardiovascular outcomes was evaluated, with the aim to facilitate more accurate stratification and identification of high-risk individuals.
From August 2013 to January 2014, 361 hemodialysis patients were prospectively enrolled. Lp-PLA
activity and laboratory measures at baseline were quantified. Comorbidities and medications were recorded. All patients were followed until the end of April, 2022. The individual and combined effects of Lp-PLA
activity and LDL-C on patient outcomes were examined. The association between Lp-PLA
activity and all-cause mortality, cardiovascular mortality, and major adverse cardiovascular events (MACEs) was analyzed.
The median Lp-PLA
activity was 481.2 U/L. In subjects with Lp-PLA
activity over 481.2 U/L, significantly higher total cholesterol (4.89 vs. 3.98 mmol/L; P < 0.001), LDL-C (3.06 vs. 2.22 mmol/L; P < 0.001), and apolipoprotein B (0.95 vs. 0.75 mmol/L; P < 0.001) were observed. Over a median follow-up of 78.1 months, 182 patients died, with 77 cases identified as cardiovascular death, 88 MACEs happened. Cardiovascular mortality and MACEs, but not all-cause mortality, were significantly increased in the high Lp-PLA2 group. Cox regression analyses showed that high Lp-PLA
activity was associated with cardiovascular mortality and MACE occurrence. After comprehensive adjustment, high Lp-PLA
activity was independently associated with cardiovascular mortality(as a dichotomous variable: HR:2.57, 95%CI:1.58,4.18, P < 0.001; as a continuous variable: HR:1.25, 95%CI:1.10,1.41, P = 0.001) and MACEs(as a dichotomous variable: HR:2.17, 95%CI:1.39,3.40, P = 0.001; as a continuous variable: HR:1.20, 95%CI:1.07,1.36, P = 0.002). When participants were grouped by median Lp-PLA2 activity and LDL-C values, those with high Lp-PLA
and low LDL-C had the highest CV mortality. The addition of Lp-PLA2 significantly improved reclassification (as a dichotomous variable NRI = 42.51%, 95%CI: 5.0%,61.33%; as a continuous variable, NRI = 33.32%, 95% CI: 7.47%,56.21%).
High Lp-PLA
activity is an independent risk factor for cardiovascular mortality and MACEs occurrence in patients on hemodialysis. The combined measures of Lp-PLA
and LDL-C help to identify individuals with a higher risk of cardiovascular death. |
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AbstractList | Cardiovascular diseases (CVD) is the leading cause of death among maintenance hemodialysis patients, with dyslipidemia being a prevalent complication. The paradoxical relationship between cardiovascular outcomes and established lipid risk markers, such as low-density lipoprotein cholesterol (LDL-C), complicates lipid management in this population. This study investigated Lipoprotein-associated phospholipase A2 (Lp-PLA2), an emerging biomarker known for its proinflammatory and proatherogenic properties, as a potential cardiovascular prognostic marker in this cohort. In this context, the association between Lp-PLA2 levels and cardiovascular outcomes was evaluated, with the aim to facilitate more accurate stratification and identification of high-risk individuals.
From August 2013 to January 2014, 361 hemodialysis patients were prospectively enrolled. Lp-PLA
activity and laboratory measures at baseline were quantified. Comorbidities and medications were recorded. All patients were followed until the end of April, 2022. The individual and combined effects of Lp-PLA
activity and LDL-C on patient outcomes were examined. The association between Lp-PLA
activity and all-cause mortality, cardiovascular mortality, and major adverse cardiovascular events (MACEs) was analyzed.
The median Lp-PLA
activity was 481.2 U/L. In subjects with Lp-PLA
activity over 481.2 U/L, significantly higher total cholesterol (4.89 vs. 3.98 mmol/L; P < 0.001), LDL-C (3.06 vs. 2.22 mmol/L; P < 0.001), and apolipoprotein B (0.95 vs. 0.75 mmol/L; P < 0.001) were observed. Over a median follow-up of 78.1 months, 182 patients died, with 77 cases identified as cardiovascular death, 88 MACEs happened. Cardiovascular mortality and MACEs, but not all-cause mortality, were significantly increased in the high Lp-PLA2 group. Cox regression analyses showed that high Lp-PLA
activity was associated with cardiovascular mortality and MACE occurrence. After comprehensive adjustment, high Lp-PLA
activity was independently associated with cardiovascular mortality(as a dichotomous variable: HR:2.57, 95%CI:1.58,4.18, P < 0.001; as a continuous variable: HR:1.25, 95%CI:1.10,1.41, P = 0.001) and MACEs(as a dichotomous variable: HR:2.17, 95%CI:1.39,3.40, P = 0.001; as a continuous variable: HR:1.20, 95%CI:1.07,1.36, P = 0.002). When participants were grouped by median Lp-PLA2 activity and LDL-C values, those with high Lp-PLA
and low LDL-C had the highest CV mortality. The addition of Lp-PLA2 significantly improved reclassification (as a dichotomous variable NRI = 42.51%, 95%CI: 5.0%,61.33%; as a continuous variable, NRI = 33.32%, 95% CI: 7.47%,56.21%).
High Lp-PLA
activity is an independent risk factor for cardiovascular mortality and MACEs occurrence in patients on hemodialysis. The combined measures of Lp-PLA
and LDL-C help to identify individuals with a higher risk of cardiovascular death. Abstract Background Cardiovascular diseases (CVD) is the leading cause of death among maintenance hemodialysis patients, with dyslipidemia being a prevalent complication. The paradoxical relationship between cardiovascular outcomes and established lipid risk markers, such as low-density lipoprotein cholesterol (LDL-C), complicates lipid management in this population. This study investigated Lipoprotein-associated phospholipase A2 (Lp-PLA2), an emerging biomarker known for its proinflammatory and proatherogenic properties, as a potential cardiovascular prognostic marker in this cohort. In this context, the association between Lp-PLA2 levels and cardiovascular outcomes was evaluated, with the aim to facilitate more accurate stratification and identification of high-risk individuals. Methods From August 2013 to January 2014, 361 hemodialysis patients were prospectively enrolled. Lp-PLA2 activity and laboratory measures at baseline were quantified. Comorbidities and medications were recorded. All patients were followed until the end of April, 2022. The individual and combined effects of Lp-PLA2 activity and LDL-C on patient outcomes were examined. The association between Lp-PLA2 activity and all-cause mortality, cardiovascular mortality, and major adverse cardiovascular events (MACEs) was analyzed. Results The median Lp-PLA2 activity was 481.2 U/L. In subjects with Lp-PLA2 activity over 481.2 U/L, significantly higher total cholesterol (4.89 vs. 3.98 mmol/L; P < 0.001), LDL-C (3.06 vs. 2.22 mmol/L; P < 0.001), and apolipoprotein B (0.95 vs. 0.75 mmol/L; P < 0.001) were observed. Over a median follow-up of 78.1 months, 182 patients died, with 77 cases identified as cardiovascular death, 88 MACEs happened. Cardiovascular mortality and MACEs, but not all-cause mortality, were significantly increased in the high Lp-PLA2 group. Cox regression analyses showed that high Lp-PLA2 activity was associated with cardiovascular mortality and MACE occurrence. After comprehensive adjustment, high Lp-PLA2 activity was independently associated with cardiovascular mortality(as a dichotomous variable: HR:2.57, 95%CI:1.58,4.18, P < 0.001; as a continuous variable: HR:1.25, 95%CI:1.10,1.41, P = 0.001) and MACEs(as a dichotomous variable: HR:2.17, 95%CI:1.39,3.40, P = 0.001; as a continuous variable: HR:1.20, 95%CI:1.07,1.36, P = 0.002). When participants were grouped by median Lp-PLA2 activity and LDL-C values, those with high Lp-PLA2 and low LDL-C had the highest CV mortality. The addition of Lp-PLA2 significantly improved reclassification (as a dichotomous variable NRI = 42.51%, 95%CI: 5.0%,61.33%; as a continuous variable, NRI = 33.32%, 95% CI: 7.47%,56.21%). Conclusions High Lp-PLA2 activity is an independent risk factor for cardiovascular mortality and MACEs occurrence in patients on hemodialysis. The combined measures of Lp-PLA2 and LDL-C help to identify individuals with a higher risk of cardiovascular death. Background Cardiovascular diseases (CVD) is the leading cause of death among maintenance hemodialysis patients, with dyslipidemia being a prevalent complication. The paradoxical relationship between cardiovascular outcomes and established lipid risk markers, such as low-density lipoprotein cholesterol (LDL-C), complicates lipid management in this population. This study investigated Lipoprotein-associated phospholipase A2 (Lp-PLA2), an emerging biomarker known for its proinflammatory and proatherogenic properties, as a potential cardiovascular prognostic marker in this cohort. In this context, the association between Lp-PLA2 levels and cardiovascular outcomes was evaluated, with the aim to facilitate more accurate stratification and identification of high-risk individuals. Methods From August 2013 to January 2014, 361 hemodialysis patients were prospectively enrolled. Lp-PLA.sub.2 activity and laboratory measures at baseline were quantified. Comorbidities and medications were recorded. All patients were followed until the end of April, 2022. The individual and combined effects of Lp-PLA.sub.2 activity and LDL-C on patient outcomes were examined. The association between Lp-PLA.sub.2 activity and all-cause mortality, cardiovascular mortality, and major adverse cardiovascular events (MACEs) was analyzed. Results The median Lp-PLA.sub.2 activity was 481.2 U/L. In subjects with Lp-PLA.sub.2 activity over 481.2 U/L, significantly higher total cholesterol (4.89 vs. 3.98 mmol/L; P < 0.001), LDL-C (3.06 vs. 2.22 mmol/L; P < 0.001), and apolipoprotein B (0.95 vs. 0.75 mmol/L; P < 0.001) were observed. Over a median follow-up of 78.1 months, 182 patients died, with 77 cases identified as cardiovascular death, 88 MACEs happened. Cardiovascular mortality and MACEs, but not all-cause mortality, were significantly increased in the high Lp-PLA2 group. Cox regression analyses showed that high Lp-PLA.sub.2 activity was associated with cardiovascular mortality and MACE occurrence. After comprehensive adjustment, high Lp-PLA.sub.2 activity was independently associated with cardiovascular mortality(as a dichotomous variable: HR:2.57, 95%CI:1.58,4.18, P < 0.001; as a continuous variable: HR:1.25, 95%CI:1.10,1.41, P = 0.001) and MACEs(as a dichotomous variable: HR:2.17, 95%CI:1.39,3.40, P = 0.001; as a continuous variable: HR:1.20, 95%CI:1.07,1.36, P = 0.002). When participants were grouped by median Lp-PLA2 activity and LDL-C values, those with high Lp-PLA.sub.2 and low LDL-C had the highest CV mortality. The addition of Lp-PLA2 significantly improved reclassification (as a dichotomous variable NRI = 42.51%, 95%CI: 5.0%,61.33%; as a continuous variable, NRI = 33.32%, 95% CI: 7.47%,56.21%). Conclusions High Lp-PLA.sub.2 activity is an independent risk factor for cardiovascular mortality and MACEs occurrence in patients on hemodialysis. The combined measures of Lp-PLA.sub.2 and LDL-C help to identify individuals with a higher risk of cardiovascular death. Keywords: Hemodialysis, Lipoprotein-associated phospholipase A2, Dyslipidemia, Cardiovascular disease Cardiovascular diseases (CVD) is the leading cause of death among maintenance hemodialysis patients, with dyslipidemia being a prevalent complication. The paradoxical relationship between cardiovascular outcomes and established lipid risk markers, such as low-density lipoprotein cholesterol (LDL-C), complicates lipid management in this population. This study investigated Lipoprotein-associated phospholipase A2 (Lp-PLA2), an emerging biomarker known for its proinflammatory and proatherogenic properties, as a potential cardiovascular prognostic marker in this cohort. In this context, the association between Lp-PLA2 levels and cardiovascular outcomes was evaluated, with the aim to facilitate more accurate stratification and identification of high-risk individuals. From August 2013 to January 2014, 361 hemodialysis patients were prospectively enrolled. Lp-PLA.sub.2 activity and laboratory measures at baseline were quantified. Comorbidities and medications were recorded. All patients were followed until the end of April, 2022. The individual and combined effects of Lp-PLA.sub.2 activity and LDL-C on patient outcomes were examined. The association between Lp-PLA.sub.2 activity and all-cause mortality, cardiovascular mortality, and major adverse cardiovascular events (MACEs) was analyzed. The median Lp-PLA.sub.2 activity was 481.2 U/L. In subjects with Lp-PLA.sub.2 activity over 481.2 U/L, significantly higher total cholesterol (4.89 vs. 3.98 mmol/L; P < 0.001), LDL-C (3.06 vs. 2.22 mmol/L; P < 0.001), and apolipoprotein B (0.95 vs. 0.75 mmol/L; P < 0.001) were observed. Over a median follow-up of 78.1 months, 182 patients died, with 77 cases identified as cardiovascular death, 88 MACEs happened. Cardiovascular mortality and MACEs, but not all-cause mortality, were significantly increased in the high Lp-PLA2 group. Cox regression analyses showed that high Lp-PLA.sub.2 activity was associated with cardiovascular mortality and MACE occurrence. After comprehensive adjustment, high Lp-PLA.sub.2 activity was independently associated with cardiovascular mortality(as a dichotomous variable: HR:2.57, 95%CI:1.58,4.18, P < 0.001; as a continuous variable: HR:1.25, 95%CI:1.10,1.41, P = 0.001) and MACEs(as a dichotomous variable: HR:2.17, 95%CI:1.39,3.40, P = 0.001; as a continuous variable: HR:1.20, 95%CI:1.07,1.36, P = 0.002). When participants were grouped by median Lp-PLA2 activity and LDL-C values, those with high Lp-PLA.sub.2 and low LDL-C had the highest CV mortality. The addition of Lp-PLA2 significantly improved reclassification (as a dichotomous variable NRI = 42.51%, 95%CI: 5.0%,61.33%; as a continuous variable, NRI = 33.32%, 95% CI: 7.47%,56.21%). High Lp-PLA.sub.2 activity is an independent risk factor for cardiovascular mortality and MACEs occurrence in patients on hemodialysis. The combined measures of Lp-PLA.sub.2 and LDL-C help to identify individuals with a higher risk of cardiovascular death. Cardiovascular diseases (CVD) is the leading cause of death among maintenance hemodialysis patients, with dyslipidemia being a prevalent complication. The paradoxical relationship between cardiovascular outcomes and established lipid risk markers, such as low-density lipoprotein cholesterol (LDL-C), complicates lipid management in this population. This study investigated Lipoprotein-associated phospholipase A2 (Lp-PLA2), an emerging biomarker known for its proinflammatory and proatherogenic properties, as a potential cardiovascular prognostic marker in this cohort. In this context, the association between Lp-PLA2 levels and cardiovascular outcomes was evaluated, with the aim to facilitate more accurate stratification and identification of high-risk individuals.BACKGROUNDCardiovascular diseases (CVD) is the leading cause of death among maintenance hemodialysis patients, with dyslipidemia being a prevalent complication. The paradoxical relationship between cardiovascular outcomes and established lipid risk markers, such as low-density lipoprotein cholesterol (LDL-C), complicates lipid management in this population. This study investigated Lipoprotein-associated phospholipase A2 (Lp-PLA2), an emerging biomarker known for its proinflammatory and proatherogenic properties, as a potential cardiovascular prognostic marker in this cohort. In this context, the association between Lp-PLA2 levels and cardiovascular outcomes was evaluated, with the aim to facilitate more accurate stratification and identification of high-risk individuals.From August 2013 to January 2014, 361 hemodialysis patients were prospectively enrolled. Lp-PLA2 activity and laboratory measures at baseline were quantified. Comorbidities and medications were recorded. All patients were followed until the end of April, 2022. The individual and combined effects of Lp-PLA2 activity and LDL-C on patient outcomes were examined. The association between Lp-PLA2 activity and all-cause mortality, cardiovascular mortality, and major adverse cardiovascular events (MACEs) was analyzed.METHODSFrom August 2013 to January 2014, 361 hemodialysis patients were prospectively enrolled. Lp-PLA2 activity and laboratory measures at baseline were quantified. Comorbidities and medications were recorded. All patients were followed until the end of April, 2022. The individual and combined effects of Lp-PLA2 activity and LDL-C on patient outcomes were examined. The association between Lp-PLA2 activity and all-cause mortality, cardiovascular mortality, and major adverse cardiovascular events (MACEs) was analyzed.The median Lp-PLA2 activity was 481.2 U/L. In subjects with Lp-PLA2 activity over 481.2 U/L, significantly higher total cholesterol (4.89 vs. 3.98 mmol/L; P < 0.001), LDL-C (3.06 vs. 2.22 mmol/L; P < 0.001), and apolipoprotein B (0.95 vs. 0.75 mmol/L; P < 0.001) were observed. Over a median follow-up of 78.1 months, 182 patients died, with 77 cases identified as cardiovascular death, 88 MACEs happened. Cardiovascular mortality and MACEs, but not all-cause mortality, were significantly increased in the high Lp-PLA2 group. Cox regression analyses showed that high Lp-PLA2 activity was associated with cardiovascular mortality and MACE occurrence. After comprehensive adjustment, high Lp-PLA2 activity was independently associated with cardiovascular mortality(as a dichotomous variable: HR:2.57, 95%CI:1.58,4.18, P < 0.001; as a continuous variable: HR:1.25, 95%CI:1.10,1.41, P = 0.001) and MACEs(as a dichotomous variable: HR:2.17, 95%CI:1.39,3.40, P = 0.001; as a continuous variable: HR:1.20, 95%CI:1.07,1.36, P = 0.002). When participants were grouped by median Lp-PLA2 activity and LDL-C values, those with high Lp-PLA2 and low LDL-C had the highest CV mortality. The addition of Lp-PLA2 significantly improved reclassification (as a dichotomous variable NRI = 42.51%, 95%CI: 5.0%,61.33%; as a continuous variable, NRI = 33.32%, 95% CI: 7.47%,56.21%).RESULTSThe median Lp-PLA2 activity was 481.2 U/L. In subjects with Lp-PLA2 activity over 481.2 U/L, significantly higher total cholesterol (4.89 vs. 3.98 mmol/L; P < 0.001), LDL-C (3.06 vs. 2.22 mmol/L; P < 0.001), and apolipoprotein B (0.95 vs. 0.75 mmol/L; P < 0.001) were observed. Over a median follow-up of 78.1 months, 182 patients died, with 77 cases identified as cardiovascular death, 88 MACEs happened. Cardiovascular mortality and MACEs, but not all-cause mortality, were significantly increased in the high Lp-PLA2 group. Cox regression analyses showed that high Lp-PLA2 activity was associated with cardiovascular mortality and MACE occurrence. After comprehensive adjustment, high Lp-PLA2 activity was independently associated with cardiovascular mortality(as a dichotomous variable: HR:2.57, 95%CI:1.58,4.18, P < 0.001; as a continuous variable: HR:1.25, 95%CI:1.10,1.41, P = 0.001) and MACEs(as a dichotomous variable: HR:2.17, 95%CI:1.39,3.40, P = 0.001; as a continuous variable: HR:1.20, 95%CI:1.07,1.36, P = 0.002). When participants were grouped by median Lp-PLA2 activity and LDL-C values, those with high Lp-PLA2 and low LDL-C had the highest CV mortality. The addition of Lp-PLA2 significantly improved reclassification (as a dichotomous variable NRI = 42.51%, 95%CI: 5.0%,61.33%; as a continuous variable, NRI = 33.32%, 95% CI: 7.47%,56.21%).High Lp-PLA2 activity is an independent risk factor for cardiovascular mortality and MACEs occurrence in patients on hemodialysis. The combined measures of Lp-PLA2 and LDL-C help to identify individuals with a higher risk of cardiovascular death.CONCLUSIONSHigh Lp-PLA2 activity is an independent risk factor for cardiovascular mortality and MACEs occurrence in patients on hemodialysis. The combined measures of Lp-PLA2 and LDL-C help to identify individuals with a higher risk of cardiovascular death. BackgroundCardiovascular diseases (CVD) is the leading cause of death among maintenance hemodialysis patients, with dyslipidemia being a prevalent complication. The paradoxical relationship between cardiovascular outcomes and established lipid risk markers, such as low-density lipoprotein cholesterol (LDL-C), complicates lipid management in this population. This study investigated Lipoprotein-associated phospholipase A2 (Lp-PLA2), an emerging biomarker known for its proinflammatory and proatherogenic properties, as a potential cardiovascular prognostic marker in this cohort. In this context, the association between Lp-PLA2 levels and cardiovascular outcomes was evaluated, with the aim to facilitate more accurate stratification and identification of high-risk individuals.MethodsFrom August 2013 to January 2014, 361 hemodialysis patients were prospectively enrolled. Lp-PLA2 activity and laboratory measures at baseline were quantified. Comorbidities and medications were recorded. All patients were followed until the end of April, 2022. The individual and combined effects of Lp-PLA2 activity and LDL-C on patient outcomes were examined. The association between Lp-PLA2 activity and all-cause mortality, cardiovascular mortality, and major adverse cardiovascular events (MACEs) was analyzed.ResultsThe median Lp-PLA2 activity was 481.2 U/L. In subjects with Lp-PLA2 activity over 481.2 U/L, significantly higher total cholesterol (4.89 vs. 3.98 mmol/L; P < 0.001), LDL-C (3.06 vs. 2.22 mmol/L; P < 0.001), and apolipoprotein B (0.95 vs. 0.75 mmol/L; P < 0.001) were observed. Over a median follow-up of 78.1 months, 182 patients died, with 77 cases identified as cardiovascular death, 88 MACEs happened. Cardiovascular mortality and MACEs, but not all-cause mortality, were significantly increased in the high Lp-PLA2 group. Cox regression analyses showed that high Lp-PLA2 activity was associated with cardiovascular mortality and MACE occurrence. After comprehensive adjustment, high Lp-PLA2 activity was independently associated with cardiovascular mortality(as a dichotomous variable: HR:2.57, 95%CI:1.58,4.18, P < 0.001; as a continuous variable: HR:1.25, 95%CI:1.10,1.41, P = 0.001) and MACEs(as a dichotomous variable: HR:2.17, 95%CI:1.39,3.40, P = 0.001; as a continuous variable: HR:1.20, 95%CI:1.07,1.36, P = 0.002). When participants were grouped by median Lp-PLA2 activity and LDL-C values, those with high Lp-PLA2 and low LDL-C had the highest CV mortality. The addition of Lp-PLA2 significantly improved reclassification (as a dichotomous variable NRI = 42.51%, 95%CI: 5.0%,61.33%; as a continuous variable, NRI = 33.32%, 95% CI: 7.47%,56.21%).ConclusionsHigh Lp-PLA2 activity is an independent risk factor for cardiovascular mortality and MACEs occurrence in patients on hemodialysis. The combined measures of Lp-PLA2 and LDL-C help to identify individuals with a higher risk of cardiovascular death. |
ArticleNumber | 15 |
Audience | Academic |
Author | Shi, Yiqin Lin, Lin Ding, Xiaoqiang Zhang, Zhen Xu, Xialian Cao, Xuesen Shen, Bo Xiang, Fangfang Xie, Qiwen Teng, Jie |
Author_xml | – sequence: 1 givenname: Lin surname: Lin fullname: Lin, Lin – sequence: 2 givenname: Jie surname: Teng fullname: Teng, Jie – sequence: 3 givenname: Yiqin surname: Shi fullname: Shi, Yiqin – sequence: 4 givenname: Qiwen surname: Xie fullname: Xie, Qiwen – sequence: 5 givenname: Bo surname: Shen fullname: Shen, Bo – sequence: 6 givenname: Fangfang surname: Xiang fullname: Xiang, Fangfang – sequence: 7 givenname: Xuesen surname: Cao fullname: Cao, Xuesen – sequence: 8 givenname: Xiaoqiang surname: Ding fullname: Ding, Xiaoqiang – sequence: 9 givenname: Xialian surname: Xu fullname: Xu, Xialian – sequence: 10 givenname: Zhen surname: Zhang fullname: Zhang, Zhen |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/38216940$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1186_s40001_024_02117_7 |
Cites_doi | 10.1016/S0140-6736(10)60319-4 10.1007/s40620-018-0521-3 10.1111/j.1365-2362.2011.02634.x 10.1016/j.kint.2015.12.033 10.1016/j.coph.2005.11.008 10.1161/01.ATV.0000222983.73369.c8 10.1038/ki.2014.31 10.1016/S0140-6736(10)61350-5 10.1046/j.1523-1755.2002.00324.x 10.1007/s11883-009-0074-y 10.4330/wjc.v7.i10.609 10.1016/S0140-6736(11)60739-3 10.1056/NEJMoa043545 10.1016/S0021-9150(00)00710-3 10.1002/med.21597 10.1001/jama.2009.1488 10.1056/NEJMoa1315878 10.1038/s41586-021-03392-8 10.31083/j.rcm2401010 10.1155/2013/432136 10.1186/1476-511X-13-6 10.1056/NEJM200010193431603 10.1097/01.ASN.0000100127.54107.57 10.1038/ki.1996.403 10.1681/ASN.2005121320 10.1159/000083529 10.1001/jama.2014.11061 10.1093/ndt/gfq471 10.1093/eurheartj/ehp311 10.1056/NEJMoa0810177 10.1161/ATVBAHA.119.312705 10.1111/1744-9987.13465 10.1186/s12944-023-01833-z 10.1532/hsf.3833 10.31083/j.rcm2306212 10.1007/s10557-020-07020-x 10.1021/cr200085w 10.1007/s11154-016-9402-z 10.31083/j.rcm2407185 10.1007/s40265-017-0858-2 10.1053/j.ajkd.2018.01.002 10.1161/01.CIR.0000116763.91992.F1 10.1016/j.jacc.2018.11.003 10.1056/NEJMoa041031 |
ContentType | Journal Article |
Copyright | 2024. The Author(s). COPYRIGHT 2024 BioMed Central Ltd. 2024. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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References | C Wanner (1991_CR34) 2014; 85 EA Dennis (1991_CR15) 2011; 111 L Visconti (1991_CR26) 2016; 6 A Upadhyay (1991_CR2) 2011; 26 DJ De Jager (1991_CR4) 2009; 302 F Huang (1991_CR37) 2020; 40 Z Zhang (1991_CR6) 2023; 24 C Baigent (1991_CR13) 2011; 377 Lp-PLA(2) Studies Collaboration (1991_CR18) 2010; 375 P Libby (1991_CR8) 2021; 592 A Cai (1991_CR16) 2013; 34 R Trevisan (1991_CR10) 2006; 17 L-M Feng (1991_CR23) 2014; 13 K Prasad (1991_CR7) 2022; 23 D Marcelli (1991_CR5) 1996; 50 DA Goodkin (1991_CR3) 2003; 14 K Winkler (1991_CR22) 2012; 42 RO Mathew (1991_CR28) 2021; 35 J Rakocevic (1991_CR42) 2023; 24 C-K Chiang (1991_CR31) 2005; 23 The STABILITY Investigators (1991_CR45) 2014; 370 AS Go (1991_CR1) 2004; 351 A De Mauri (1991_CR21) 2019; 32 V Calice-Silva (1991_CR24) 2023; 22 T Munzel (1991_CR39) 2009; 30 1991_CR29 BC Fellström (1991_CR14) 2009; 360 G Maiolino (1991_CR17) 2015; 7 V Krane (1991_CR35) 2016; 89 C Wanner (1991_CR12) 2005; 353 CJ Packard (1991_CR19) 2000; 343 C Deighan (1991_CR25) 2001; 157 JM Valdivielso (1991_CR9) 2019; 39 CM Ballantyne (1991_CR41) 2004; 109 W Koenig (1991_CR20) 2006; 26 B Zheng-Lin (1991_CR27) 2018; 78 X Zhang (1991_CR40) 2021; 24 R Saran (1991_CR32) 2018; 71 A De Mauri (1991_CR46) 2020; 24 SM Grundy (1991_CR36) 2019; 73 Alteration of lipid metabolism in chronic kidney disease (1991_CR11) 2019; 19 LT Braun (1991_CR43) 2010; 12 Cholesterol Treatment Trialists’ (CTT) Collaboration (1991_CR33) 2010; 376 C Macphee (1991_CR38) 2006; 6 ML O’Donoghue (1991_CR44) 2014; 312 K Iseki (1991_CR30) 2002; 61 |
References_xml | – volume: 375 start-page: 1536 year: 2010 ident: 1991_CR18 publication-title: Lancet doi: 10.1016/S0140-6736(10)60319-4 – volume: 32 start-page: 283 year: 2019 ident: 1991_CR21 publication-title: J Nephrol doi: 10.1007/s40620-018-0521-3 – volume: 42 start-page: 693 year: 2012 ident: 1991_CR22 publication-title: Eur J Clin Invest doi: 10.1111/j.1365-2362.2011.02634.x – volume: 89 start-page: 1380 year: 2016 ident: 1991_CR35 publication-title: Kidney Int doi: 10.1016/j.kint.2015.12.033 – volume: 6 start-page: 154 year: 2006 ident: 1991_CR38 publication-title: Curr Opin Pharmacol doi: 10.1016/j.coph.2005.11.008 – volume: 26 start-page: 1586 year: 2006 ident: 1991_CR20 publication-title: ATVB doi: 10.1161/01.ATV.0000222983.73369.c8 – volume: 85 start-page: 1303 year: 2014 ident: 1991_CR34 publication-title: Kidney Int doi: 10.1038/ki.2014.31 – volume: 376 start-page: 1670 year: 2010 ident: 1991_CR33 publication-title: Lancet doi: 10.1016/S0140-6736(10)61350-5 – volume: 61 start-page: 1887 year: 2002 ident: 1991_CR30 publication-title: Kidney Int doi: 10.1046/j.1523-1755.2002.00324.x – volume: 12 start-page: 29 year: 2010 ident: 1991_CR43 publication-title: Curr Atheroscler Rep doi: 10.1007/s11883-009-0074-y – volume: 7 start-page: 609 year: 2015 ident: 1991_CR17 publication-title: WJC doi: 10.4330/wjc.v7.i10.609 – volume: 377 start-page: 2181 year: 2011 ident: 1991_CR13 publication-title: The Lancet doi: 10.1016/S0140-6736(11)60739-3 – volume: 353 start-page: 238 year: 2005 ident: 1991_CR12 publication-title: N Engl J Med doi: 10.1056/NEJMoa043545 – volume: 157 start-page: 211 year: 2001 ident: 1991_CR25 publication-title: Atherosclerosis doi: 10.1016/S0021-9150(00)00710-3 – volume: 6 start-page: 8 year: 2016 ident: 1991_CR26 publication-title: J Clin Transl Endocrinol – volume: 40 start-page: 79 year: 2020 ident: 1991_CR37 publication-title: Med Res Rev doi: 10.1002/med.21597 – volume: 302 start-page: 1782 year: 2009 ident: 1991_CR4 publication-title: JAMA doi: 10.1001/jama.2009.1488 – volume: 370 start-page: 1702 year: 2014 ident: 1991_CR45 publication-title: N Engl J Med doi: 10.1056/NEJMoa1315878 – volume: 592 start-page: 524 year: 2021 ident: 1991_CR8 publication-title: Nature doi: 10.1038/s41586-021-03392-8 – volume: 24 start-page: 10 year: 2023 ident: 1991_CR42 publication-title: Rev Cardiovasc Med doi: 10.31083/j.rcm2401010 – volume: 19 start-page: 77 year: 2019 ident: 1991_CR11 publication-title: Rev Cardiovasc Med – volume: 34 start-page: 323 year: 2013 ident: 1991_CR16 publication-title: Dis Markers doi: 10.1155/2013/432136 – volume: 13 start-page: 6 year: 2014 ident: 1991_CR23 publication-title: Lipids Health Dis doi: 10.1186/1476-511X-13-6 – volume: 343 start-page: 1148 year: 2000 ident: 1991_CR19 publication-title: N Engl J Med doi: 10.1056/NEJM200010193431603 – volume: 14 start-page: 3270 year: 2003 ident: 1991_CR3 publication-title: J Am Soc Nephrol doi: 10.1097/01.ASN.0000100127.54107.57 – volume: 50 start-page: 1013 year: 1996 ident: 1991_CR5 publication-title: Kidney Int doi: 10.1038/ki.1996.403 – volume: 17 start-page: S145 year: 2006 ident: 1991_CR10 publication-title: J Am Soc Nephrol doi: 10.1681/ASN.2005121320 – volume: 23 start-page: 134 year: 2005 ident: 1991_CR31 publication-title: Blood Purif doi: 10.1159/000083529 – volume: 312 start-page: 1006 year: 2014 ident: 1991_CR44 publication-title: JAMA doi: 10.1001/jama.2014.11061 – volume: 26 start-page: 920 year: 2011 ident: 1991_CR2 publication-title: Nephrol Dial Transplant doi: 10.1093/ndt/gfq471 – volume: 30 start-page: 2829 year: 2009 ident: 1991_CR39 publication-title: Eur Heart J doi: 10.1093/eurheartj/ehp311 – volume: 360 start-page: 1395 year: 2009 ident: 1991_CR14 publication-title: N Engl J Med doi: 10.1056/NEJMoa0810177 – volume: 39 start-page: 1938 year: 2019 ident: 1991_CR9 publication-title: ATVB doi: 10.1161/ATVBAHA.119.312705 – volume: 24 start-page: 548 year: 2020 ident: 1991_CR46 publication-title: Ther Apher Dial doi: 10.1111/1744-9987.13465 – volume: 22 start-page: 67 year: 2023 ident: 1991_CR24 publication-title: Lipids Health Dis doi: 10.1186/s12944-023-01833-z – volume: 24 start-page: 611 year: 2021 ident: 1991_CR40 publication-title: HSF doi: 10.1532/hsf.3833 – volume: 23 start-page: 212 year: 2022 ident: 1991_CR7 publication-title: Rev Cardiovasc Med doi: 10.31083/j.rcm2306212 – volume: 35 start-page: 479 year: 2021 ident: 1991_CR28 publication-title: Cardiovasc Drugs Ther doi: 10.1007/s10557-020-07020-x – volume: 111 start-page: 6130 year: 2011 ident: 1991_CR15 publication-title: Chem Rev doi: 10.1021/cr200085w – ident: 1991_CR29 doi: 10.1007/s11154-016-9402-z – volume: 24 start-page: 185 year: 2023 ident: 1991_CR6 publication-title: Rev Cardiovasc Med doi: 10.31083/j.rcm2407185 – volume: 78 start-page: 215 year: 2018 ident: 1991_CR27 publication-title: Drugs doi: 10.1007/s40265-017-0858-2 – volume: 71 start-page: A7 year: 2018 ident: 1991_CR32 publication-title: Am J Kidney Dis doi: 10.1053/j.ajkd.2018.01.002 – volume: 109 start-page: 837 year: 2004 ident: 1991_CR41 publication-title: Circulation doi: 10.1161/01.CIR.0000116763.91992.F1 – volume: 73 start-page: e285 year: 2019 ident: 1991_CR36 publication-title: J Am Coll Cardiol doi: 10.1016/j.jacc.2018.11.003 – volume: 351 start-page: 1296 year: 2004 ident: 1991_CR1 publication-title: N Engl J Med doi: 10.1056/NEJMoa041031 |
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Snippet | Cardiovascular diseases (CVD) is the leading cause of death among maintenance hemodialysis patients, with dyslipidemia being a prevalent complication. The... Background Cardiovascular diseases (CVD) is the leading cause of death among maintenance hemodialysis patients, with dyslipidemia being a prevalent... BackgroundCardiovascular diseases (CVD) is the leading cause of death among maintenance hemodialysis patients, with dyslipidemia being a prevalent... Abstract Background Cardiovascular diseases (CVD) is the leading cause of death among maintenance hemodialysis patients, with dyslipidemia being a prevalent... |
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SubjectTerms | 1-Alkyl-2-acetylglycerophosphocholine Esterase Acute coronary syndromes Apolipoprotein B Atherosclerosis Biomarkers Cardiac arrhythmia Cardiovascular disease Cardiovascular Diseases Care and treatment Cholesterol Cholesterol, LDL Chronic kidney failure Comorbidity Complications and side effects Death Diabetes Dyslipidemia Health aspects Heart failure Hemodialysis Hemodialysis patients High density lipoprotein Humans Inflammation Kidney diseases Kidney transplants Lipids Lipoprotein-associated phospholipase A2 Lipoproteins Low density lipoprotein Medical imaging Metabolic disorders Mortality Patient outcomes Patients Peritoneal dialysis Phospholipase Phospholipase A2 Phospholipases Physiological aspects Population Population studies Prognosis Prospective Studies Reclassification Renal Dialysis Risk Factors Statins Stroke Variables |
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Title | Lipoprotein-associated phospholipase A2 predicts cardiovascular death in patients on maintenance hemodialysis: a 7-year prospective cohort study |
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