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

被引:38
|
作者
Izumaru, Kensuke [1 ]
Hata, Jun [2 ]
Nakano, Toshiaki [3 ]
Nakashima, Yutaka [4 ]
Nagata, Masaharu [5 ]
Fukuhara, Masayo [6 ]
Oda, Yoshinao [7 ]
Kitazono, Takanari [3 ]
Ninomiya, Toshiharu [2 ]
机构
[1] Gotanda Garden Clin, Tokyo, Japan
[2] Kyushu Univ, Grad Sch Med Sci, Dept Epidemiol & Publ Hlth, Fukuoka, Fukuoka, Japan
[3] Kyushu Univ, Grad Sch Med Sci, Dept Med & Clin Sci, Fukuoka, Fukuoka, Japan
[4] Japanese Red Cross Fukuoka Hosp, Fukuoka, Fukuoka, Japan
[5] Shin Eikai Hosp, Fukuoka, Fukuoka, Japan
[6] Kyushu Dent Univ, Div Gen Internal Med, Kitakyushu, Fukuoka, Japan
[7] Kyushu Univ, Grad Sch Med Sci, Dept Anat Pathol, Pathol Sci, Fukuoka, Fukuoka, Japan
关键词
CHRONIC KIDNEY-DISEASE; LEFT-VENTRICULAR HYPERTROPHY; RISK-FACTORS; MYOCARDIAL FIBROSIS; RENAL DYSFUNCTION; SECULAR TRENDS; ANEMIA; HEART; ANGIOGENESIS; OUTCOMES;
D O I
10.1053/j.ajkd.2019.02.013
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
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 m(2) 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 mu m for eGFRs >= 60, 45 to 59, 30 to 44, and <30 mL/min/1.73 m(2) (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 m(2) (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.
引用
收藏
页码:373 / 381
页数:9
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