Cardiac Structure and Function and Subsequent Kidney Disease Progression in Adults With CKD: The Chronic Renal Insufficiency Cohort (CRIC) Study

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. 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. Prospective observational cohort study. 3,027 participants from the Chronic Renal Insufficiency Cohort Study. 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. Incident KFRT (primary outcome), and annual estimated glomerular filtration rate (eGFR) slope (secondary outcome). Multivariable Cox models and mixed-effects models. 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). The possibility of residual confounding. 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.