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Abstract
Objective Protein-energy wasting is associated with chronic inflammation and advanced atherosclerosis in haemodialysis (HD) patients. We investigated association of geriatric nutritional risk index (GNRI), C reactive protein (CRP) with prediction of mortality after coronary revascularisation in chronic HD patients.
Methods We enrolled 721 HD patients electively undergoing coronary revascularisation. They were divided into tertiles according to preprocedural GNRI levels (tertile 1 (T1):<91.5, T2: 91.5–98.1 and T3:>98.1) and CRP levels (T1:≤1.4 mg/L, T2: 1.5–7.0 mg/L and T3:≥7.1 mg/L).
Results Kaplan-Meier 10 years survival rates were 32.3%, 44.8% and 72.5% in T1, T2 and T3 of GNRI and 60.9%, 49.2% and 23.5% in T1, T2 and T3 of CRP, respectively (p<0.0001 in both). Declined GNRI (HR 2.40, 95% CI 1.58 to 3.74, p<0.0001 for T1 vs T3) and elevated CRP (HR 2.31, 95% CI 1.58 to 3.43, p<0.0001 for T3 vs T1) were identified as independent predictors of mortality. In combined setting of both variables, risk of mortality was 5.55 times higher (95% CI 2.64 to 13.6, p<0.0001) in T1 of GNRI with T3 of CRP than in T3 of GNRI with T1 of CRP. Addition of GNRI and CRP in a model with established risk factors improved C-statistics (0.648 to 0.724, p<0.0001) greater than that of each alone.
Conclusion Preprocedural declined GNRI and elevated CRP were closely associated with mortality after coronary revascularisation in chronic HD patients. Furthermore, combination of both variables not only stratified risk of mortality but also improved the predictability.
- coronary artery disease
- risk factors
- risk stratification
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Footnotes
Presented at A part of this study was previously presented at European Society of Cardiology Congress 2017.
Contributorship Statement Conception and design of the study; YK, HI and HT. Generation, collection, assembly, analysis and/or interpretation of data; YK, SO, RI, NU and HT. Drafting and/or revision of the manuscript; YK, HI andHT. Approval of the final version of the manuscript; YK, HI, HT, SO, RI, NU and TM.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests HI received lecture fees from Astellas Pharma, Astrazeneca, Bayer Pharma, Bristol-Myers Squibb, Chugai Pharma, Daiichi Sankyo and Otsuka Pharma. TM received lecture fees from Bayer Pharmaceutical, Daiichi Sankyo, Dainippon Sumitomo Pharma, Kowa, MSD K.K., Mitsubishi Tanabe Pharma, Nippon Boehringer Ingelheim, Novartis Pharma K.K., Pfizer Japan, Sanofi-aventis K.K and Takeda Pharmaceutical. TM received unrestricted research grant for Department of Cardiology, Nagoya University Graduate School of Medicine from Astellas Pharma, Daiichi Sankyo, Dainippon Sumitomo Pharma, Kowa, MSD K.K., Mitsubishi Tanabe Pharma, Nippon Boehringer Ingelheim, Novartis Pharma K.K., Otsuka Pharma, Pfizer Japan, Sanofi-aventis K.K., Takeda Pharmaceutica, Teijin Pharma.
Patient consent for publication Not required.
Ethics approval The study protocol and chart reviews used were approved by the institutional ethics of both hospitals and conducted in accordance with the Declaration of Helsinki.
Provenance and peer review Not commissioned; externally peer reviewed.
Data availability statement Data are available on reasonable request.