Impact of Cardio-Renal-Metabolic Comorbidities on Cardiovascular Outcomes and Mortality in Type 2 Diabetes Mellitus.


Journal

American journal of nephrology
ISSN: 1421-9670
Titre abrégé: Am J Nephrol
Pays: Switzerland
ID NLM: 8109361

Informations de publication

Date de publication:
2020
Historique:
received: 25 09 2019
accepted: 03 11 2019
pubmed: 10 12 2019
medline: 9 2 2021
entrez: 9 12 2019
Statut: ppublish

Résumé

We evaluated the incremental contribution of chronic kidney disease (CKD) to the risk of major adverse cardiovascular (CV) events (MACE), heart failure (HF), and all-cause mortality (ACM) in type 2 diabetes mellitus (T2DM) patients and its importance relative to the presence of other cardio-renal-metabolic (CaReMe) comorbidities. Patients (≥40 years) were identified at the time of T2DM diagnosis from US (Humedica/Optum) and UK (Clinical Practice Research Datalink) databases. Patients were monitored post-diagnosis for modified MACE (myocardial infarction, stroke, ACM), HF, and ACM. Adjusted hazard ratios were obtained using Cox proportional-hazards regression to evaluate the relative risk of modified MACE, HF, and ACM due to CKD. Patients were stratified by the presence or absence of atherosclerotic CV disease (ASCVD) and age. Between 2011 and 2015, of 227,224 patients identified with incident T2DM, 40,063 (17.64%) had CKD. Regardless of prior ASCVD, CKD was associated with higher risk of modified MACE, HF, and ACM; this excess hazard was more pronounced in older patients with prior ASCVD. In time-to-event analyses in the overall cohort, patients with T2DM + CKD or T2DM + CKD + hypertension + hyperlipidemia had increased risks for modified MACE, HF, and ACM versus patients with T2DM and no CaReMe comorbidities. Patients with CKD had higher risks for and shorter times to modified MACE, HF, and ACM than those without CKD. In T2DM patients, CKD presence was associated with higher risk of modified MACE, HF, and ACM. This may have risk-stratification implications for T2DM patients based on background CKD and highlights the potential importance of novel renoprotective strategies.

Sections du résumé

BACKGROUND
We evaluated the incremental contribution of chronic kidney disease (CKD) to the risk of major adverse cardiovascular (CV) events (MACE), heart failure (HF), and all-cause mortality (ACM) in type 2 diabetes mellitus (T2DM) patients and its importance relative to the presence of other cardio-renal-metabolic (CaReMe) comorbidities.
METHODS
Patients (≥40 years) were identified at the time of T2DM diagnosis from US (Humedica/Optum) and UK (Clinical Practice Research Datalink) databases. Patients were monitored post-diagnosis for modified MACE (myocardial infarction, stroke, ACM), HF, and ACM. Adjusted hazard ratios were obtained using Cox proportional-hazards regression to evaluate the relative risk of modified MACE, HF, and ACM due to CKD. Patients were stratified by the presence or absence of atherosclerotic CV disease (ASCVD) and age.
RESULTS
Between 2011 and 2015, of 227,224 patients identified with incident T2DM, 40,063 (17.64%) had CKD. Regardless of prior ASCVD, CKD was associated with higher risk of modified MACE, HF, and ACM; this excess hazard was more pronounced in older patients with prior ASCVD. In time-to-event analyses in the overall cohort, patients with T2DM + CKD or T2DM + CKD + hypertension + hyperlipidemia had increased risks for modified MACE, HF, and ACM versus patients with T2DM and no CaReMe comorbidities. Patients with CKD had higher risks for and shorter times to modified MACE, HF, and ACM than those without CKD.
CONCLUSION
In T2DM patients, CKD presence was associated with higher risk of modified MACE, HF, and ACM. This may have risk-stratification implications for T2DM patients based on background CKD and highlights the potential importance of novel renoprotective strategies.

Identifiants

pubmed: 31812955
pii: 000504558
doi: 10.1159/000504558
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

74-82

Informations de copyright

© 2019 S. Karger AG, Basel.

Auteurs

David Z I Cherney (DZI)

Division of Nephrology, University Health Network and Department of Medicine, University of Toronto, Toronto, Ontario, Canada, david.cherney@uhn.ca.

Enrico Repetto (E)

Cardiovascular, Renal and Metabolism, Global Medical Affairs, AstraZeneca, Gaithersburg, Maryland, USA.

David C Wheeler (DC)

Department of Renal Medicine, University College London, London, United Kingdom.
The George Institute for Global Health and University of New South Wales, Sydney, New South Wales, Australia.

Suzanne V Arnold (SV)

Saint Luke's Mid America Heart Institute and University of Missouri-Kansas City, Kansas City, Missouri, USA.

Sharon MacLachlan (S)

Department of Real World Evidence, Evidera, London, United Kingdom.

Philip R Hunt (PR)

Cardiovascular, Renal and Metabolism, Global Medical Affairs, AstraZeneca, Gaithersburg, Maryland, USA.

Hungta Chen (H)

Cardiovascular, Renal and Metabolism, Global Medical Affairs, AstraZeneca, Gaithersburg, Maryland, USA.

Jiten Vora (J)

Department of Diabetes and Endocrinology, University of Liverpool, Liverpool, United Kingdom.

Mikhail Kosiborod (M)

Saint Luke's Mid America Heart Institute and University of Missouri-Kansas City, Kansas City, Missouri, USA.
The George Institute for Global Health and University of New South Wales, Sydney, New South Wales, Australia.

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