TY - JOUR
T1 - Acceleration of kidney function decline after incident hospitalization with cardiovascular disease
T2 - the Stockholm CREAtinine Measurements (SCREAM) project
AU - Ishigami, Junichi
AU - Trevisan, Marco
AU - Lund, Lars H.
AU - Jernberg, Tomas
AU - Coresh, Josef
AU - Matsushita, Kunihiro
AU - Carrero, Juan Jesus
N1 - Funding Information:
The SCREAM project obtained financial support from the Swedish Research Council (2019-01059). The funders did not have a role in study design; collection, analysis, and interpretation of data; writing the report; or the decision to submit the report for publication. Conflict of interest: K.M. received research funding and personal fee from Kyowa Kirin and personal fee from Akebia outside the submitted work. All other authors have nothing to disclose.
Funding Information:
The SCREAM project obtained financial support from the Swedish Research Council (2019‐01059). The funders did not have a role in study design; collection, analysis, and interpretation of data; writing the report; or the decision to submit the report for publication.
Publisher Copyright:
© 2020 European Society of Cardiology
PY - 2020/10/1
Y1 - 2020/10/1
N2 - Aims: The cardiorenal syndrome refers to a bidirectional relationship between the kidney and the heart. However, epidemiological evidence of cardiovascular disease (CVD) as a risk factor for chronic kidney disease (CKD) progression is actually scarce. Methods and results: We examined the slopes of estimated glomerular filtration rate (eGFR) decline in the 2 years before vs. after an incident hospitalization with heart failure (HF) (n = 20 420), coronary heart disease (CHD) (n = 18 152), or stroke (n = 1808) using data from a complete laboratory data collection in Stockholm, Sweden between 2006 and 2011. eGFR slopes were estimated using mixed-effect models with unstructured residual correlation. Overall, incident hospitalization with HF and CHD, but not stroke, was significantly associated with a subsequent accelerated decline in eGFR, with a faster eGFR decline and greater slope change after HF than CHD. The pre-event vs. post-event eGFR slopes (mL/min/1.73 m2 per year) were −1.67 (−1.77 to −1.57) vs. −2.76 (−2.82 to −2.71), with a Δslope of −1.09 (−1.16 to −1.02) for HF; −1.09 (−1.20 to −0.98) vs. −1.87 (−1.92 to −1.81), with a Δslope of −0.78 (−0.85 to −0.70) for CHD; and −1.00 (−1.37 to −0.63) vs. −0.99 (−1.19 to −0.78), with a Δslope of 0.02 (−0.24 to 0.27) for stroke. The accelerated declines in eGFR after HF and CHD were consistent across the spectrum of eGFR, although pre-event eGFR slopes were steeper in lower eGFR (e.g. pre-event eGFR slope for HF −0.64 (−0.76 to −0.53) for eGFR ≥60 mL/min/1.73 m2, −1.43 (−1.57 to −1.30) for eGFR 30–59 mL/min/1.73 m2, and −2.42 (−2.71 to −2.12) for eGFR <30 mL/min/1.73 m2). Conclusions: Incident hospitalization with cardiac diseases (i.e. HF and CHD) was significantly associated with a subsequent acceleration of eGFR decline.
AB - Aims: The cardiorenal syndrome refers to a bidirectional relationship between the kidney and the heart. However, epidemiological evidence of cardiovascular disease (CVD) as a risk factor for chronic kidney disease (CKD) progression is actually scarce. Methods and results: We examined the slopes of estimated glomerular filtration rate (eGFR) decline in the 2 years before vs. after an incident hospitalization with heart failure (HF) (n = 20 420), coronary heart disease (CHD) (n = 18 152), or stroke (n = 1808) using data from a complete laboratory data collection in Stockholm, Sweden between 2006 and 2011. eGFR slopes were estimated using mixed-effect models with unstructured residual correlation. Overall, incident hospitalization with HF and CHD, but not stroke, was significantly associated with a subsequent accelerated decline in eGFR, with a faster eGFR decline and greater slope change after HF than CHD. The pre-event vs. post-event eGFR slopes (mL/min/1.73 m2 per year) were −1.67 (−1.77 to −1.57) vs. −2.76 (−2.82 to −2.71), with a Δslope of −1.09 (−1.16 to −1.02) for HF; −1.09 (−1.20 to −0.98) vs. −1.87 (−1.92 to −1.81), with a Δslope of −0.78 (−0.85 to −0.70) for CHD; and −1.00 (−1.37 to −0.63) vs. −0.99 (−1.19 to −0.78), with a Δslope of 0.02 (−0.24 to 0.27) for stroke. The accelerated declines in eGFR after HF and CHD were consistent across the spectrum of eGFR, although pre-event eGFR slopes were steeper in lower eGFR (e.g. pre-event eGFR slope for HF −0.64 (−0.76 to −0.53) for eGFR ≥60 mL/min/1.73 m2, −1.43 (−1.57 to −1.30) for eGFR 30–59 mL/min/1.73 m2, and −2.42 (−2.71 to −2.12) for eGFR <30 mL/min/1.73 m2). Conclusions: Incident hospitalization with cardiac diseases (i.e. HF and CHD) was significantly associated with a subsequent acceleration of eGFR decline.
KW - Cardiorenal syndrome
KW - Cardiovascular disease
KW - Chronic kidney disease
KW - Coronary heart disease
KW - Heart failure
KW - Stroke
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U2 - 10.1002/ejhf.1968
DO - 10.1002/ejhf.1968
M3 - Article
C2 - 32683762
AN - SCOPUS:85089595089
SN - 1388-9842
VL - 22
SP - 1790
EP - 1799
JO - European Journal of Heart Failure
JF - European Journal of Heart Failure
IS - 10
ER -