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),...

Full description

Saved in:
Bibliographic Details
Published inLipids in health and disease Vol. 23; no. 1; pp. 15 - 18
Main Authors Lin, Lin, Teng, Jie, Shi, Yiqin, Xie, Qiwen, Shen, Bo, Xiang, Fangfang, Cao, Xuesen, Ding, Xiaoqiang, Xu, Xialian, Zhang, Zhen
Format Journal Article
LanguageEnglish
Published England BioMed Central Ltd 12.01.2024
BioMed Central
BMC
Subjects
Online AccessGet full text

Cover

Loading…
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.
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
BookMark eNp9ktuKFDEQhhtZcQ_6Al5IwBtves2hk-54tyweFga8UfAuVCfVOxl6kraTXpi38JHNzKyrLiIhJBTfX5VK_efVSYgBq-olo5eMdeptYlw3TU25qCnTmtX0SXXGmlbVkrFvJ3_cT6vzlDaUctoq9aw6FR1nSjf0rPqx8lOc5pjRhxpSitZDRkemdUxlj36ChOSKk2lG521OxMLsfLyDZJcRZuIQ8pr4QCbIHkMBYiBb8CFjgGCRrHEbnYdxl3x6R4C09Q6LrtRME9rs75DYuI5zJikvbve8ejrAmPDF_XlRff3w_sv1p3r1-ePN9dWqtpJ2udaou6btpeqVY42gg7JiUK5nfauE4xpb11tefoX3TDluKUgmRQ9WCueE7MVFdXPM6yJszDT7Lcw7E8GbQyDOtwbm7O2IRkgLVEuggNgMTHUOG9vJ1up-4IPCkuvNMVdp6vuCKZutTxbHEQLGJRmuWcMlp0IW9PUjdBOXOZROD5QojBK_qVso9X0YYp7B7pOaq7bMTjdM6EJd_oMqy-HW2-KVwZf4X4JX98WXfovuoetfdigAPwK2TCfNODwgjJq958zRc6Z4zhw8Z_ai7pHI-lzMEEN5jh__J_0JlzbcCg
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.
Copyright_xml – notice: 2024. The Author(s).
– notice: COPYRIGHT 2024 BioMed Central Ltd.
– notice: 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.
DBID AAYXX
CITATION
CGR
CUY
CVF
ECM
EIF
NPM
3V.
7X7
7XB
88E
8FD
8FE
8FH
8FI
8FJ
8FK
ABUWG
AFKRA
AZQEC
BBNVY
BENPR
BHPHI
CCPQU
DWQXO
FR3
FYUFA
GHDGH
GNUQQ
HCIFZ
K9.
LK8
M0S
M1P
M7P
P64
PHGZM
PHGZT
PIMPY
PJZUB
PKEHL
PPXIY
PQEST
PQGLB
PQQKQ
PQUKI
PRINS
RC3
7X8
DOA
DOI 10.1186/s12944-023-01991-0
DatabaseName CrossRef
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
ProQuest Central (Corporate)
Health & Medical Collection
ProQuest Central (purchase pre-March 2016)
Medical Database (Alumni Edition)
Technology Research Database
ProQuest SciTech Collection
ProQuest Natural Science Journals
ProQuest Hospital Collection
Hospital Premium Collection (Alumni Edition)
ProQuest Central (Alumni) (purchase pre-March 2016)
ProQuest Central (Alumni)
ProQuest Central UK/Ireland
ProQuest Central Essentials
Biological Science Database
ProQuest Central
Natural Science Collection
ProQuest One Community College
ProQuest Central
Engineering Research Database
Health Research Premium Collection
Health Research Premium Collection (Alumni)
ProQuest Central Student
ProQuest SciTech Premium Collection
ProQuest Health & Medical Complete (Alumni)
Biological Sciences
ProQuest Health & Medical Collection
Proquest Medical Database
Biological Science Database
Biotechnology and BioEngineering Abstracts
ProQuest Central Premium
ProQuest One Academic
Publicly Available Content Database
ProQuest Health & Medical Research Collection
ProQuest One Academic Middle East (New)
ProQuest One Health & Nursing
ProQuest One Academic Eastern Edition (DO NOT USE)
ProQuest One Applied & Life Sciences
ProQuest One Academic
ProQuest One Academic UKI Edition
ProQuest Central China
Genetics Abstracts
MEDLINE - Academic
DOAJ Directory of Open Access Journals
DatabaseTitle CrossRef
MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
Publicly Available Content Database
ProQuest Central Student
Technology Research Database
ProQuest One Academic Middle East (New)
ProQuest Central Essentials
ProQuest Health & Medical Complete (Alumni)
ProQuest Central (Alumni Edition)
SciTech Premium Collection
ProQuest One Community College
ProQuest One Health & Nursing
ProQuest Natural Science Collection
ProQuest Central China
ProQuest Central
ProQuest One Applied & Life Sciences
ProQuest Health & Medical Research Collection
Genetics Abstracts
Health Research Premium Collection
Health and Medicine Complete (Alumni Edition)
Natural Science Collection
ProQuest Central Korea
Health & Medical Research Collection
Biological Science Collection
ProQuest Central (New)
ProQuest Medical Library (Alumni)
ProQuest Biological Science Collection
ProQuest One Academic Eastern Edition
ProQuest Hospital Collection
Health Research Premium Collection (Alumni)
Biological Science Database
ProQuest SciTech Collection
ProQuest Hospital Collection (Alumni)
Biotechnology and BioEngineering Abstracts
ProQuest Health & Medical Complete
ProQuest Medical Library
ProQuest One Academic UKI Edition
Engineering Research Database
ProQuest One Academic
ProQuest One Academic (New)
ProQuest Central (Alumni)
MEDLINE - Academic
DatabaseTitleList MEDLINE



MEDLINE - Academic
Publicly Available Content Database
Database_xml – sequence: 1
  dbid: DOA
  name: DOAJ Directory of Open Access Journals
  url: https://www.doaj.org/
  sourceTypes: Open Website
– sequence: 2
  dbid: NPM
  name: PubMed
  url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 3
  dbid: EIF
  name: MEDLINE
  url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search
  sourceTypes: Index Database
– sequence: 4
  dbid: BENPR
  name: ProQuest Central
  url: https://www.proquest.com/central
  sourceTypes: Aggregation Database
DeliveryMethod fulltext_linktorsrc
Discipline Medicine
Anatomy & Physiology
EISSN 1476-511X
EndPage 18
ExternalDocumentID oai_doaj_org_article_35ca095a0aee4f168de4c857c9bf2f6e
A782194139
38216940
10_1186_s12944_023_01991_0
Genre Journal Article
GeographicLocations China
GeographicLocations_xml – name: China
GrantInformation_xml – fundername: National Natural Science Foundation of China
  grantid: 82104617
– fundername: Guiding Project of Xiamen Medical and Health Department
  grantid: 3502Z20214ZD1068
– fundername: Shanghai Federation of Nephrology Project supported by Shanghai ShenKang Hospital Development Center
  grantid: SHDC2202230
GroupedDBID ---
0R~
29L
2WC
53G
5GY
5VS
7X7
88E
8FE
8FH
8FI
8FJ
A8Z
AAFWJ
AAHBH
AAJSJ
AASML
AAYXX
ABDBF
ABUWG
ACGFO
ACGFS
ACPRK
ACUHS
ADBBV
ADRAZ
ADUKV
AENEX
AFKRA
AFPKN
AHBYD
AHMBA
AHYZX
ALIPV
ALMA_UNASSIGNED_HOLDINGS
AMKLP
AMTXH
AOIJS
BAPOH
BAWUL
BBNVY
BCNDV
BENPR
BFQNJ
BHPHI
BMC
BPHCQ
BVXVI
C6C
CCPQU
CITATION
CS3
DIK
E3Z
EAD
EAP
EAS
EBD
EBLON
EBS
EMB
EMK
EMOBN
ESX
F5P
FYUFA
GROUPED_DOAJ
GX1
HCIFZ
HH5
HMCUK
HYE
IAO
IGS
IHR
INH
INR
ITC
KQ8
LK8
M1P
M48
M7P
M~E
O5R
O5S
OK1
OVT
P2P
P6G
PGMZT
PHGZM
PHGZT
PIMPY
PQQKQ
PROAC
PSQYO
RBZ
RNS
ROL
RPM
RSV
SBL
SOJ
SV3
TR2
TUS
U2A
UKHRP
W2D
WOQ
WOW
XSB
CGR
CUY
CVF
ECM
EIF
NPM
PJZUB
PPXIY
PQGLB
PMFND
3V.
7XB
8FD
8FK
AZQEC
DWQXO
FR3
GNUQQ
K9.
P64
PKEHL
PQEST
PQUKI
PRINS
RC3
7X8
PUEGO
ID FETCH-LOGICAL-c508t-9e9847b56b6d1430f6c3f6db1b763d29e7dbc21992b16d2c0a5153bac53dd35b3
IEDL.DBID M48
ISSN 1476-511X
IngestDate Wed Aug 27 01:22:30 EDT 2025
Fri Jul 11 03:59:30 EDT 2025
Fri Jul 25 10:44:28 EDT 2025
Tue Jun 17 22:14:49 EDT 2025
Tue Jun 10 21:13:16 EDT 2025
Mon Jul 21 05:58:56 EDT 2025
Tue Jul 01 00:23:20 EDT 2025
Thu Apr 24 23:08:47 EDT 2025
IsDoiOpenAccess true
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 1
Keywords Cardiovascular disease
Lipoprotein-associated phospholipase A2
Hemodialysis
Dyslipidemia
Language English
License 2024. The Author(s).
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c508t-9e9847b56b6d1430f6c3f6db1b763d29e7dbc21992b16d2c0a5153bac53dd35b3
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
OpenAccessLink https://doaj.org/article/35ca095a0aee4f168de4c857c9bf2f6e
PMID 38216940
PQID 2914303563
PQPubID 42587
PageCount 18
ParticipantIDs doaj_primary_oai_doaj_org_article_35ca095a0aee4f168de4c857c9bf2f6e
proquest_miscellaneous_2914252035
proquest_journals_2914303563
gale_infotracmisc_A782194139
gale_infotracacademiconefile_A782194139
pubmed_primary_38216940
crossref_primary_10_1186_s12944_023_01991_0
crossref_citationtrail_10_1186_s12944_023_01991_0
ProviderPackageCode CITATION
AAYXX
PublicationCentury 2000
PublicationDate 2024-01-12
PublicationDateYYYYMMDD 2024-01-12
PublicationDate_xml – month: 01
  year: 2024
  text: 2024-01-12
  day: 12
PublicationDecade 2020
PublicationPlace England
PublicationPlace_xml – name: England
– name: London
PublicationTitle Lipids in health and disease
PublicationTitleAlternate Lipids Health Dis
PublicationYear 2024
Publisher BioMed Central Ltd
BioMed Central
BMC
Publisher_xml – name: BioMed Central Ltd
– name: BioMed Central
– name: BMC
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
SSID ssj0020766
Score 2.3491642
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...
SourceID doaj
proquest
gale
pubmed
crossref
SourceType Open Website
Aggregation Database
Index Database
Enrichment Source
StartPage 15
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
SummonAdditionalLinks – databaseName: DOAJ Directory of Open Access Journals
  dbid: DOA
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Lb9QwELZQD4gLgpZHSkFGQnBAURPbcWJuC6KqEOVEpd4sv6Ku1E2iTXrov-AnM-M4KxYkuHDYy2YcxZ4ZzzfJzGdC3pRtG1QjHDiSK3LhyiY31pgcokkBY0rLKmwUvvgmzy_Fl6vq6pejvrAmbKYHnhfulFfOAAwwhQlBtKVsfBCuqWqnbMtaGXD3hZi3JFMp1YLsXC4tMo08HSGqCZFDfILUOdb67IWhyNb_5578G9KMEefsEXmYoCJdzY_4mNwL3SE5WnWQJm_u6FsaizfjW_FDcv8ifSM_Ij--roc-0i-su9yk1Q-eDtf9CL-b9QCBi64YHbY4Zhqp26tJpR5RIV13NHGujrTv6MYgsQSycwR6HTY99psgmckHamid34G_wP36pW-T4rm724lG8ton5PLs8_dP53k6dyF3ANemXKH2altJKz3AqaKVjrfS29LCZuSZCrW3jmHdqi2lZ64wAIq4Na7i3vPK8qfkoOu78JzQWjgFoLAGpUGeVzgLeElI50GRrQKNZqRc1KBdIiXHszFudExOGqln1WlQnY6q00VG3u_GDDMlx1-lP6J2d5JIpx3_ACPTycj0v4wsI-_QNjQ6PTyeM6l3ASaJ9Fl6BTirVIAHVEZO9iTBWd3-5cW6dNosRs0UrjKvJM_I691lHIkFcF3ob2cZVjGQysiz2Sp3U-Jwd6lEcfw_pvqCPGCA2_AtU8lOyMG0vQ0vAXdN9lV0sZ9_kCvo
  priority: 102
  providerName: Directory of Open Access Journals
– databaseName: Health & Medical Collection
  dbid: 7X7
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV1Lb9QwELagSIgLgpZHoCAjITigqInjODEXtCCqClFOVNqb5VfoSt0kbNJD_0V_cmccZ6sFqYdckrHlZDwz3zjjz4S8z5vGy5pbMCSbpdzmdaqN1ilEkwza5IaVuFH49Jc4OeM_luUyLrgNsaxy9onBUbvO4hr5EZMQ2bOiFMWX_m-Kp0bh39V4hMZ98gCpy7Ckq1reJlyQo4t5o0wtjgaIbZynEKUggQ4VPzvBKHD2_--Z_8GbIe4cPyGPI2Cki0nDT8k93-6Tg0ULyfL6in6goYQzrI3vk4en8U_5Abn-ueq7QMKwalMddeAd7c-7Aa6LVQ_hiy4Y7TfYZhyo3alMpQ6xIV21NDKvDrRr6VojvQRydHh67tcd7jpBSpPPVNMqvQKrgf66efcmxdN3NyMNFLbPyNnx99_fTtJ4-kJqAbSNqUQdVqYURjj89I2wRSOcyQ24JMekr5yxDKtXTS4cs5kGaFQYbcvCuaI0xXOy13atf0loxa0EaFg5zyHby6wB1MSFdU0uGqm9T0g-q0HZSE2OJ2RcqJCi1EJNqlOgOhVUp7KEfNq26Sdijjulv6J2t5JIqh1udJs_KtqoKkqrAXHqDIbEYWw1jNfWZWWlaVgjYJgfcW4oNH0YntVxBwO8JJJoqQWgrVwCKpAJOdyRBJO1u4_n2aWiyxjU7QRPyLvtY2yJZXCt7y4nGVYykErIi2lWbl-pgN6F5Nmruzt_TR4xwGW4ipSzQ7I3bi79G8BVo3kbjOcGzvIiFw
  priority: 102
  providerName: ProQuest
Title Lipoprotein-associated phospholipase A2 predicts cardiovascular death in patients on maintenance hemodialysis: a 7-year prospective cohort study
URI https://www.ncbi.nlm.nih.gov/pubmed/38216940
https://www.proquest.com/docview/2914303563
https://www.proquest.com/docview/2914252035
https://doaj.org/article/35ca095a0aee4f168de4c857c9bf2f6e
Volume 23
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV1ti9NAEF7uBcQvonfqRc-ygugHiSabzSYRRHJyx1HsIWqh35Z9i1dok9r2wP4Lf7Izm6RQPcQPIZDMLpPMTuaZzc6zhLyIq8oVOTfgSCYKuYnzUGmlQogmEbSJNUuxUHh0JS7HfDhJJ3uk3-6oe4GrW1M73E9qvJy9-flj8wEc_r13-Fy8XUHM4jyE6AOJsV_Js08OITJl6Kgjvv2rwCBnb6uNMhEC0Jj0RTS39rETqDyf_99f7T-wqI9JF_fJvQ5M0rK1_gOy5-ojclzWkEjPN_Ql9cs7_bz5Ebkz6v6iH5Nfn6aLxhM0TOtQdfZxli6umxUcs-kCQhstGV0ssc16Rc3OqlVqETfSaU07VtYVbWo6V0g9gfwdjl67eYMVKUh38o4qmoUb8Cjor-krOynuzLtcU09v-5CML86_fbwMu50ZQgOAbh0WaN9Mp0ILC4ArqoRJKmF1rOFzZVnhMqsNw5WtOhaWmUgBbEq0MmlibZLq5BE5qJvanRCacVMAbMys45AJRkYDouLC2CoWVaGcC0jcm0GajrYcd8-YSZ--5EK2ppNgOulNJ6OAvN62WbSkHf-UPkPrbiWRcNtfaJbfZee_MkmNAjSqIlCJg2456GvyNDOFrlglQM1XODYkDlRQz6iuugEeEgm2ZAlILC4AMRQBOd2RBHc2u7f70SV7b5CswLecpCIJyPPtbWyJS-Rq19y0MixlIBWQx-2o3D5SAr2LgkdP_lvLp-QuA_iGk00xOyUH6-WNewbwa60HZD-bZANyWJbDr0M4n51fff4y8JMZA-9vvwF7JjBu
linkProvider Scholars Portal
linkToHtml http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1Lb9NAEF6VVAIuCFoeKQUWiccBWbXX67WNhFAKrVKaRAi1Um_LvtxGamwTp0L5F_wSfiMzfgQFpN56yCXeHY01OzPfrOdByKsgy1yacAOKZHyPmyDxlFbKA2_iw55AswgLhccTMTzlX86isw3yu6uFwbTKzibWhtoWBu_I91gKnt0PIxF-LH94ODUKv652IzSaY3Hslj8hZKs-HH0G-b5m7PDg5NPQa6cKeAbAyMJLkbdYR0ILiyQzYcJMWB1oUDXLUhdbbRhmZepAWGZ8BS4_1MpEobVhpEOge4ts8hBCmR7Z3D-YfP22CvH8WIiuNCcRexV4U8498IsQstc5Rmvur54S8L8v-Afh1p7u8D6510JUOmjO1AOy4fItsj3IITyfLekbWieN1rfxW-T2uP02v01-jaZlUbd9mOaeaqXuLC0vigp-l9MSHCYdMFrOcc-iomYtF5ZaRKN0mtO212tFi5zOFDa0wK4gjl64WYF1LthE5T1VNPaWIBCgV3T1ohTn_c4XtG6a-5Cc3ohkHpFeXuTuCaExNymA0dg6DvGlbzTgNC6MzQKRpcq5Pgk6MUjTNkPHmRyXsg6KEiEb0UkQnaxFJ_0-ebfaUzatQK5dvY_SXa3ENt71H8X8XLZWQYaRUYBxlQ8sceAtAX5NEsUm1RnLBLD5Fs-GRGMD7BnV1kzAS2LbLjkAfBekgEPSPtldWwlGwqw_7k6XbI1UJf-qVJ-8XD3GnZh4l7viqlnDIgar-uRxcypXrxQCdZFyf-d64i_IneHJeCRHR5Pjp-QuA1SId1gB2yW9xfzKPQNUt9DPW1Wi5PtNa-8fUppgcA
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Lipoprotein-associated+phospholipase+A2+predicts+cardiovascular+death+in+patients+on+maintenance+hemodialysis%3A+a+7-year+prospective+cohort+study&rft.jtitle=Lipids+in+health+and+disease&rft.au=Lin%2C+Lin&rft.au=Teng%2C+Jie&rft.au=Shi%2C+Yiqin&rft.au=Xie%2C+Qiwen&rft.date=2024-01-12&rft.pub=BioMed+Central+Ltd&rft.issn=1476-511X&rft.eissn=1476-511X&rft.volume=23&rft.issue=1&rft_id=info:doi/10.1186%2Fs12944-023-01991-0&rft.externalDocID=A782194139
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1476-511X&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1476-511X&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1476-511X&client=summon