作者
Anne‐Laure Faucon,Oriane Lambert,Ziad A. Massy,Tilman B. Drüeke,Christian Combe,Denis Fouque,Luc Frimat,Christian Jacquelinet,Maurice Laville,Sophie Liabeuf,Roberto Pecoits–Filho,Marie Hauguel-Moreau,Mansencal Nicolas,Natália Alencar de Pinho,Bénédicte Stengel,Raymond Azar,Xavier Belenfant,Dominique Besnier,Jean Philippe Bourdenx,Stéphane Burtey,Dominique Chauveau,Charles Chazot,Gabriel Choukroun,Christian Combe,Michel Delahousse,Benjamin Deroure,Marie Essig,François Glowacki,Thierry Hannedouche,Maxime Hoffmann,M Hourmant,Mohamed Jamali,Laurent Juillard,Nassim Kamar,Adrien Keller,Alexandre Klein,F Kuentz,Adeline Lacraz,G Lambrey,Isabelle Landru,Philippe Lang,G. Lebrun,Thierry Lobbedez,Éric Magnant,Sébastien Mailliez,N. Maisonneuve,Séverine Martin,Bruno Moulin,Christian Noël,Viktor Panescu,Hacène Sekhri,Mustafa Smati,Angelo Testa,Éric Thervet,Pablo Ureña-Torres,Carlos Vela,Philippe Zaoui
摘要
Rationale & Objective Sex differences in cardiovascular disease (CVD) are well-established, but whether chronic kidney disease (CKD) modifies these risk differences, and whether they differ between atheromatous (ACVD) and non-atheromatous (N-ACVD) CVD is unknown. Assessing this interaction was the principal goal of this study. Study Design Prospective cohort study. Setting & Participants Adults enrolled in the CKD-Renal Epidemiology and Information Network (CKD-REIN) cohort from from 2013 to 2020, a nationally representative sample of 40 nephrology clinics in France. Exposure Sex. Outcomes Fatal and non-fatal composite ACVD events (ischaemic coronary, cerebral, and peripheral artery disease) and composite N-ACVD events (heart failure, haemorrhagic stroke, and arrhythmias). Analytical Approach Multivariable cause-specific Cox proportional hazards models. Results 1,044 women and 1,976 men with moderate to severe CKD (median age, 67 vs. 69; mean estimated glomerular filtration rate [eGFR], 32±12 vs. 33±12 mL/min/1.73m2) were studied. Over a median follow-up of 5.0 (interquartile range, 4.8;5.2) years, the ACVD rate (per 100 patient-years) was significantly lower in women than men: 2.1 (95% confidence interval: 1.6-2.5) vs 3.6 (3.2-4.0) (P<0.01), while the N-ACVD rate was not: 5.7 (5.0-6.5) vs 6.4 (5.8-7.0) (P=0.55). N-ACVD had a steeper relationship with eGFR than did ACVD. There was an interaction (P<0.01) between sex and baseline eGFR and the ACVD hazard: the adjusted hazard ratio for women compared to men was 0.42 (0.25;0.71) at 45 mL/min/1.73m2 and gradually attenuated at lower levels of eGFR, reaching 1.00 (0.62;1.63) at 16 mL/min/1.73m2. In contrast, the N-ACVD hazard did not differ between the sexes across the eGFR range studied. Limitations Cardiovascular biomarkers and sex hormones were not assessed. Conclusion This study shows how the lower risk of ACVD among women compared to men attenuates fully with kidney disease progression. The equal risk of N-ACVD between sexes across CKD stages and its steeper association with eGFR suggest an important contribution of CKD to the development of this CVD type.