Reduced Estimated GFR and Cardiac Remodeling: A Population-Based Autopsy Study

Kensuke Izumaru, Jun Hata, Toshiaki Nakano, Yutaka Nakashima, Masaharu Nagata, Masayo Fukuhara, Yoshinao Oda, Takanari Kitazono, Toshiharu Ninomiya

研究成果: ジャーナルへの寄稿記事

抄録

Rationale & Objective: Evidence suggests that cardiac remodeling, including left ventricular hypertrophy and myocardial fibrosis, develops with progression of kidney disease. Few studies have examined cardiac pathology across a range of estimated glomerular filtration rates (eGFRs), which was the objective of this investigation. Study Design: Population-based cross-sectional study of deceased patients undergoing autopsy. Setting & Participants: 334 of 694 consecutive deceased patients undergoing autopsy with available cardiac tissue, with a prior health examination within 6 years and without a prior diagnosis of heart disease. Exposure: eGFR. Outcomes: The thickness of the left ventricular wall, sizes of cardiac cells, and percentages of fibrosis, estimated from pathology examination of autopsy samples. Analytical Approach: Generalized estimating equations. Results: Lower eGFRs were associated with greater left ventricular wall thickness. Deceased patients with eGFRs ≥ 60, 45 to 59, 30 to 44, and <30 mL/min/1.73 m2 had left ventricular wall thicknesses of 9.1, 9.5, 9.8, and 10.3 mm, respectively (P for trend < 0.05). Lower eGFRs were also significantly associated with greater mean values of cardiac cell size in the left ventricular wall after adjusting for confounders: 15.3, 16.1, 16.4, and 17.4 μm for eGFRs ≥ 60, 45 to 59, 30 to 44, and <30 mL/min/1.73 m2 (P for trend < 0.01). Patients with lower eGFRs had significantly higher multivariable-adjusted geometric mean values for fibrosis percentage in the left ventricular wall: 3.22%, 4.33%, 3.83%, and 6.14% for eGFRs ≥ 60, 45 to 59, 30 to 44, and <30 mL/min/1.73 m2 (P for trend < 0.001). The negative association of eGFR with multivariable-adjusted mean values of cardiac cell width was stronger among patients with than those without anemia. Limitations: Cross-sectional study with a high proportion of elderly patients, no available information for severity or duration of hypertension and other cardiovascular risk factors, no information for medication use. Conclusions: These findings suggest that reduced eGFR is associated with cardiac hypertrophy and fibrosis of the left ventricle, cardiac cell enlargement, and cardiac fibrosis.

元の言語英語
ページ(範囲)373-381
ページ数9
ジャーナルAmerican Journal of Kidney Diseases
74
発行部数3
DOI
出版物ステータス出版済み - 9 2019

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Glomerular Filtration Rate
Autopsy
Population
Fibrosis
Cell Size
Cross-Sectional Studies
Cell Enlargement
Pathology
Kidney Diseases
Cardiomegaly
Left Ventricular Hypertrophy
Heart Ventricles
Anemia
Heart Diseases
Hypertension
Health

All Science Journal Classification (ASJC) codes

  • Nephrology

これを引用

Reduced Estimated GFR and Cardiac Remodeling : A Population-Based Autopsy Study. / Izumaru, Kensuke; Hata, Jun; Nakano, Toshiaki; Nakashima, Yutaka; Nagata, Masaharu; Fukuhara, Masayo; Oda, Yoshinao; Kitazono, Takanari; Ninomiya, Toshiharu.

:: American Journal of Kidney Diseases, 巻 74, 番号 3, 09.2019, p. 373-381.

研究成果: ジャーナルへの寄稿記事

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title = "Reduced Estimated GFR and Cardiac Remodeling: A Population-Based Autopsy Study",
abstract = "Rationale & Objective: Evidence suggests that cardiac remodeling, including left ventricular hypertrophy and myocardial fibrosis, develops with progression of kidney disease. Few studies have examined cardiac pathology across a range of estimated glomerular filtration rates (eGFRs), which was the objective of this investigation. Study Design: Population-based cross-sectional study of deceased patients undergoing autopsy. Setting & Participants: 334 of 694 consecutive deceased patients undergoing autopsy with available cardiac tissue, with a prior health examination within 6 years and without a prior diagnosis of heart disease. Exposure: eGFR. Outcomes: The thickness of the left ventricular wall, sizes of cardiac cells, and percentages of fibrosis, estimated from pathology examination of autopsy samples. Analytical Approach: Generalized estimating equations. Results: Lower eGFRs were associated with greater left ventricular wall thickness. Deceased patients with eGFRs ≥ 60, 45 to 59, 30 to 44, and <30 mL/min/1.73 m2 had left ventricular wall thicknesses of 9.1, 9.5, 9.8, and 10.3 mm, respectively (P for trend < 0.05). Lower eGFRs were also significantly associated with greater mean values of cardiac cell size in the left ventricular wall after adjusting for confounders: 15.3, 16.1, 16.4, and 17.4 μm for eGFRs ≥ 60, 45 to 59, 30 to 44, and <30 mL/min/1.73 m2 (P for trend < 0.01). Patients with lower eGFRs had significantly higher multivariable-adjusted geometric mean values for fibrosis percentage in the left ventricular wall: 3.22{\%}, 4.33{\%}, 3.83{\%}, and 6.14{\%} for eGFRs ≥ 60, 45 to 59, 30 to 44, and <30 mL/min/1.73 m2 (P for trend < 0.001). The negative association of eGFR with multivariable-adjusted mean values of cardiac cell width was stronger among patients with than those without anemia. Limitations: Cross-sectional study with a high proportion of elderly patients, no available information for severity or duration of hypertension and other cardiovascular risk factors, no information for medication use. Conclusions: These findings suggest that reduced eGFR is associated with cardiac hypertrophy and fibrosis of the left ventricle, cardiac cell enlargement, and cardiac fibrosis.",
author = "Kensuke Izumaru and Jun Hata and Toshiaki Nakano and Yutaka Nakashima and Masaharu Nagata and Masayo Fukuhara and Yoshinao Oda and Takanari Kitazono and Toshiharu Ninomiya",
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T1 - Reduced Estimated GFR and Cardiac Remodeling

T2 - A Population-Based Autopsy Study

AU - Izumaru, Kensuke

AU - Hata, Jun

AU - Nakano, Toshiaki

AU - Nakashima, Yutaka

AU - Nagata, Masaharu

AU - Fukuhara, Masayo

AU - Oda, Yoshinao

AU - Kitazono, Takanari

AU - Ninomiya, Toshiharu

PY - 2019/9

Y1 - 2019/9

N2 - Rationale & Objective: Evidence suggests that cardiac remodeling, including left ventricular hypertrophy and myocardial fibrosis, develops with progression of kidney disease. Few studies have examined cardiac pathology across a range of estimated glomerular filtration rates (eGFRs), which was the objective of this investigation. Study Design: Population-based cross-sectional study of deceased patients undergoing autopsy. Setting & Participants: 334 of 694 consecutive deceased patients undergoing autopsy with available cardiac tissue, with a prior health examination within 6 years and without a prior diagnosis of heart disease. Exposure: eGFR. Outcomes: The thickness of the left ventricular wall, sizes of cardiac cells, and percentages of fibrosis, estimated from pathology examination of autopsy samples. Analytical Approach: Generalized estimating equations. Results: Lower eGFRs were associated with greater left ventricular wall thickness. Deceased patients with eGFRs ≥ 60, 45 to 59, 30 to 44, and <30 mL/min/1.73 m2 had left ventricular wall thicknesses of 9.1, 9.5, 9.8, and 10.3 mm, respectively (P for trend < 0.05). Lower eGFRs were also significantly associated with greater mean values of cardiac cell size in the left ventricular wall after adjusting for confounders: 15.3, 16.1, 16.4, and 17.4 μm for eGFRs ≥ 60, 45 to 59, 30 to 44, and <30 mL/min/1.73 m2 (P for trend < 0.01). Patients with lower eGFRs had significantly higher multivariable-adjusted geometric mean values for fibrosis percentage in the left ventricular wall: 3.22%, 4.33%, 3.83%, and 6.14% for eGFRs ≥ 60, 45 to 59, 30 to 44, and <30 mL/min/1.73 m2 (P for trend < 0.001). The negative association of eGFR with multivariable-adjusted mean values of cardiac cell width was stronger among patients with than those without anemia. Limitations: Cross-sectional study with a high proportion of elderly patients, no available information for severity or duration of hypertension and other cardiovascular risk factors, no information for medication use. Conclusions: These findings suggest that reduced eGFR is associated with cardiac hypertrophy and fibrosis of the left ventricle, cardiac cell enlargement, and cardiac fibrosis.

AB - Rationale & Objective: Evidence suggests that cardiac remodeling, including left ventricular hypertrophy and myocardial fibrosis, develops with progression of kidney disease. Few studies have examined cardiac pathology across a range of estimated glomerular filtration rates (eGFRs), which was the objective of this investigation. Study Design: Population-based cross-sectional study of deceased patients undergoing autopsy. Setting & Participants: 334 of 694 consecutive deceased patients undergoing autopsy with available cardiac tissue, with a prior health examination within 6 years and without a prior diagnosis of heart disease. Exposure: eGFR. Outcomes: The thickness of the left ventricular wall, sizes of cardiac cells, and percentages of fibrosis, estimated from pathology examination of autopsy samples. Analytical Approach: Generalized estimating equations. Results: Lower eGFRs were associated with greater left ventricular wall thickness. Deceased patients with eGFRs ≥ 60, 45 to 59, 30 to 44, and <30 mL/min/1.73 m2 had left ventricular wall thicknesses of 9.1, 9.5, 9.8, and 10.3 mm, respectively (P for trend < 0.05). Lower eGFRs were also significantly associated with greater mean values of cardiac cell size in the left ventricular wall after adjusting for confounders: 15.3, 16.1, 16.4, and 17.4 μm for eGFRs ≥ 60, 45 to 59, 30 to 44, and <30 mL/min/1.73 m2 (P for trend < 0.01). Patients with lower eGFRs had significantly higher multivariable-adjusted geometric mean values for fibrosis percentage in the left ventricular wall: 3.22%, 4.33%, 3.83%, and 6.14% for eGFRs ≥ 60, 45 to 59, 30 to 44, and <30 mL/min/1.73 m2 (P for trend < 0.001). The negative association of eGFR with multivariable-adjusted mean values of cardiac cell width was stronger among patients with than those without anemia. Limitations: Cross-sectional study with a high proportion of elderly patients, no available information for severity or duration of hypertension and other cardiovascular risk factors, no information for medication use. Conclusions: These findings suggest that reduced eGFR is associated with cardiac hypertrophy and fibrosis of the left ventricle, cardiac cell enlargement, and cardiac fibrosis.

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