TY - JOUR
T1 - Cardiac Structure and Function and Subsequent Kidney Disease Progression in Adults With CKD
T2 - The Chronic Renal Insufficiency Cohort (CRIC) Study
AU - CRIC Study Investigators
AU - Ishigami, Junichi
AU - Kansal, Mayank
AU - Mehta, Rupal
AU - Srivastava, Anand
AU - Rahman, Mahboob
AU - Dobre, Mirela
AU - Al-Kindi, Sadeer G.
AU - Go, Alan S.
AU - Navaneethan, Sankar D.
AU - Chen, Jing
AU - He, Jiang
AU - Bhat, Zeenat Yousuf
AU - Jaar, Bernard G.
AU - Appel, Lawrence J.
AU - Matsushita, Kunihiro
AU - Cohen, Debbie L.
AU - Feldman, Harold I.
AU - Lash, James P.
AU - Nelson, Robert G.
AU - Rao, Panduranga S.
AU - Shah, Vallabh O.
AU - Unruh, Mark L.
N1 - Funding Information:
Funding for the CRIC Study was obtained under a cooperative agreement from the National Institute of Diabetes and Digestive and Kidney Diseases (U01DK060990, U01DK060984, U01DK061022, U01DK061021, U01DK061028, U01DK060980, U01DK060963, U01DK060902, and U24DK060990). In addition, this work was supported in part by the Perelman School of Medicine at the University of Pennsylvania Clinical and Translational Science Award NIH/ NCATS UL1TR000003 , Johns Hopkins University UL1 TR-000424 , University of Maryland GCRC M01 RR-16500, Clinical and Translational Science Collaborative of Cleveland, UL1TR000439 from the National Center for Advancing Translational Sciences (NCATS) component of the National Institutes of Health and NIH roadmap for Medical Research, Michigan Institute for Clinical and Health Research (MICHR) UL1TR000433 , University of Illinois at Chicago CTSA UL1RR029879, Tulane COBRE for Clinical and Translational Research in Cardiometabolic Diseases P20 GM109036 , Kaiser Permanente NIH/ NCRR UCSF-CTSI UL1 RR-024131, Department of Internal Medicine , University of New Mexico School of Medicine Albuquerque , NM R01DK119199 . Dr Ishigami is supported by K01DK125616. Dr Mehta is supported by K23HL150236. Dr Srivastava is supported by K23DK120811 and U01AI163081. Dr Dobre is supported by R01HL141846. The funders did not have any role in study design, data collection, analysis, reporting, or the decision to submit for publication.
Funding Information:
In addition to authors Authors Rahman, Go, Chen, and Appel, the CRIC Study Investigators are Debbie L. Cohen, MD, Harold I. Feldman, MD, MSCE, James P. Lash, MD, Robert G. Nelson, MD, PhD, MS, Panduranga S. Rao, MD, Vallabh O. Shah, PhD, MS, and Mark L. Unruh, MD, MS. Junichi Ishigami, MD, MPH, Mayank Kansal, MD, Rupal Mehta, MD, Anand Srivastava, MD, Mahboob Rahman, MD, Mirela Dobre, MD, Sadeer G. Al-Kindi, MD, Alan S. Go, MD, Sankar D. Navaneethan, MD, Jing Chen, MD, Jiang He, MD, Zeenat Yousuf Bhat, MD, Bernard G. Jaar, MD, MPH, Lawrence J. Appel, MD, MPH, and Kunihiro Matsushita, MD, PhD. Research idea and study design: JI, KM; data acquisition: JI, LJA; data analysis/interpretation: all authors; statistical analysis: JI; supervision or mentorship: LJA, KM. Each author contributed important intellectual content during manuscript drafting or revision and agrees to be personally accountable for the individual's own contributions and to ensure that questions pertaining to the accuracy or integrity of any portion of the work, even one in which the author was not directly involved, are appropriately investigated and resolved, including with documentation in the literature if appropriate. Funding for the CRIC Study was obtained under a cooperative agreement from the National Institute of Diabetes and Digestive and Kidney Diseases (U01DK060990, U01DK060984, U01DK061022, U01DK061021, U01DK061028, U01DK060980, U01DK060963, U01DK060902, and U24DK060990). In addition, this work was supported in part by the Perelman School of Medicine at the University of Pennsylvania Clinical and Translational Science Award NIH/NCATS UL1TR000003, Johns Hopkins University UL1 TR-000424, University of Maryland GCRC M01 RR-16500, Clinical and Translational Science Collaborative of Cleveland, UL1TR000439 from the National Center for Advancing Translational Sciences (NCATS) component of the National Institutes of Health and NIH roadmap for Medical Research, Michigan Institute for Clinical and Health Research (MICHR) UL1TR000433, University of Illinois at Chicago CTSA UL1RR029879, Tulane COBRE for Clinical and Translational Research in Cardiometabolic Diseases P20 GM109036, Kaiser Permanente NIH/NCRR UCSF-CTSI UL1 RR-024131, Department of Internal Medicine, University of New Mexico School of Medicine Albuquerque, NM R01DK119199. Dr Ishigami is supported by K01DK125616. Dr Mehta is supported by K23HL150236. Dr Srivastava is supported by K23DK120811 and U01AI163081. Dr Dobre is supported by R01HL141846. The funders did not have any role in study design, data collection, analysis, reporting, or the decision to submit for publication. Dr Mehta has stock interest in AbbVie and is on the speakers’ bureau for AstraZeneca. The other authors declare that they have no relevant financial interests. The authors thank the other investigators, staff, and participants of the CRIC Study for their valuable contribution. The views expressed in this article are those of the authors and do not necessarily reflect the position or policy of the Department of Veterans Affairs or the United States government. Received September 8, 2022. Evaluated by 3 external peer reviewers and a statistician, with editorial input from an Acting Editor-in-Chief (Editorial Board Member Eduardo Lacson Jr, MD, MPH). Accepted in revised form December 5, 2022. The involvement of an Acting Editor-in-Chief to handle the peer-review and decision-making processes was to comply with AJKD's procedures for potential conflicts of interest for editors, described in the Information for Authors & Journal Policies.
Publisher Copyright:
© 2023 National Kidney Foundation, Inc.
PY - 2023/8
Y1 - 2023/8
N2 - Rationale & Objective: Heart-kidney crosstalk is recognized as the cardiorenal syndrome. We examined the association of cardiac function and structure with the risk of kidney failure with replacement therapy (KFRT) in a chronic kidney disease (CKD) population. Study Design: Prospective observational cohort study. Setting & Participants: 3,027 participants from the Chronic Renal Insufficiency Cohort Study. Exposure: Five preselected variables that assess different aspects of cardiac structure and function: left ventricular mass index (LVMI), LV volume, left atrial (LA) area, peak tricuspid regurgitation (TR) velocity, and left ventricular ejection fraction (EF) as assessed by echocardiography. Outcome: Incident KFRT (primary outcome), and annual estimated glomerular filtration rate (eGFR) slope (secondary outcome). Analytical Approach: Multivariable Cox models and mixed-effects models. Results: The mean age of the participants was 59 ± 11 SD years, 54% were men, and mean eGFR was 43 ± 17 mL/min/1.73 m2. Between 2003 and 2018 (median follow-up, 9.9 years), 883 participants developed KFRT. Higher LVMI, LV volume, LA area, peak TR velocity, and lower EF were each statistically significantly associated with an increased risk of KFRT, with corresponding HRs for the highest versus lowest quartiles (lowest vs highest for EF) of 1.70 (95% CI, 1.27-2.26), 1.50 (95% CI, 1.19-1.90), 1.43 (95% CI, 1.11-1.84), 1.45 (95% CI, 1.06-1.96), and 1.26 (95% CI, 1.03-1.56), respectively. For the secondary outcome, participants in the highest versus lowest quartiles (lowest vs highest for EF) had a statistically significantly faster eGFR decline, except for LA area (ΔeGFR slope per year, −0.57 [95% CI, −0.68 to −0.46] mL/min/1.73 m2 for LVMI, −0.25 [95% CI, −0.35 to −0.15] mL/min/1.73 m2 for LV volume, −0.01 [95% CI, −0.12 to −0.01] mL/min/1.73 m2 for LA area, −0.42 [95% CI, −0.56 to −0.28] mL/min/1.73 m2 for peak TR velocity, and −0.11 [95% CI, −0.20 to −0.01] mL/min/1.73 m2 for EF, respectively). Limitations: The possibility of residual confounding. Conclusions: Multiple aspects of cardiac structure and function were statistically significantly associated with the risk of KFRT. These findings suggest that cardiac abnormalities and incidence of KFRT are potentially on the same causal pathway related to the interaction between hypertension, heart failure, and coronary artery diseases. Plain-Language Summary: Heart disease and kidney disease are known to interact with each other. In this study, we examined whether cardiac abnormalities, as assessed by echocardiography, were linked to the subsequent progression of kidney disease among people living with chronic kidney disease (CKD). We found that people with abnormalities in heart structure and function had a greater risk of progression to advanced CKD that required kidney replacement therapy and had a faster rate of decline in kidney function. Our study indicates the potential role of abnormal heart structure and function in the progression of kidney disease among people living with CKD.
AB - Rationale & Objective: Heart-kidney crosstalk is recognized as the cardiorenal syndrome. We examined the association of cardiac function and structure with the risk of kidney failure with replacement therapy (KFRT) in a chronic kidney disease (CKD) population. Study Design: Prospective observational cohort study. Setting & Participants: 3,027 participants from the Chronic Renal Insufficiency Cohort Study. Exposure: Five preselected variables that assess different aspects of cardiac structure and function: left ventricular mass index (LVMI), LV volume, left atrial (LA) area, peak tricuspid regurgitation (TR) velocity, and left ventricular ejection fraction (EF) as assessed by echocardiography. Outcome: Incident KFRT (primary outcome), and annual estimated glomerular filtration rate (eGFR) slope (secondary outcome). Analytical Approach: Multivariable Cox models and mixed-effects models. Results: The mean age of the participants was 59 ± 11 SD years, 54% were men, and mean eGFR was 43 ± 17 mL/min/1.73 m2. Between 2003 and 2018 (median follow-up, 9.9 years), 883 participants developed KFRT. Higher LVMI, LV volume, LA area, peak TR velocity, and lower EF were each statistically significantly associated with an increased risk of KFRT, with corresponding HRs for the highest versus lowest quartiles (lowest vs highest for EF) of 1.70 (95% CI, 1.27-2.26), 1.50 (95% CI, 1.19-1.90), 1.43 (95% CI, 1.11-1.84), 1.45 (95% CI, 1.06-1.96), and 1.26 (95% CI, 1.03-1.56), respectively. For the secondary outcome, participants in the highest versus lowest quartiles (lowest vs highest for EF) had a statistically significantly faster eGFR decline, except for LA area (ΔeGFR slope per year, −0.57 [95% CI, −0.68 to −0.46] mL/min/1.73 m2 for LVMI, −0.25 [95% CI, −0.35 to −0.15] mL/min/1.73 m2 for LV volume, −0.01 [95% CI, −0.12 to −0.01] mL/min/1.73 m2 for LA area, −0.42 [95% CI, −0.56 to −0.28] mL/min/1.73 m2 for peak TR velocity, and −0.11 [95% CI, −0.20 to −0.01] mL/min/1.73 m2 for EF, respectively). Limitations: The possibility of residual confounding. Conclusions: Multiple aspects of cardiac structure and function were statistically significantly associated with the risk of KFRT. These findings suggest that cardiac abnormalities and incidence of KFRT are potentially on the same causal pathway related to the interaction between hypertension, heart failure, and coronary artery diseases. Plain-Language Summary: Heart disease and kidney disease are known to interact with each other. In this study, we examined whether cardiac abnormalities, as assessed by echocardiography, were linked to the subsequent progression of kidney disease among people living with chronic kidney disease (CKD). We found that people with abnormalities in heart structure and function had a greater risk of progression to advanced CKD that required kidney replacement therapy and had a faster rate of decline in kidney function. Our study indicates the potential role of abnormal heart structure and function in the progression of kidney disease among people living with CKD.
KW - Cardiorenal
KW - cardiovascular disease
KW - chronic kidney disease
KW - echocardiography
KW - end-stage kidney disease
KW - kidney failure with replacement therapy
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U2 - 10.1053/j.ajkd.2023.01.442
DO - 10.1053/j.ajkd.2023.01.442
M3 - Article
C2 - 36935072
AN - SCOPUS:85153601082
SN - 0272-6386
VL - 82
SP - 225
EP - 236
JO - American Journal of Kidney Diseases
JF - American Journal of Kidney Diseases
IS - 2
ER -
