Journal
INTERNATIONAL JOURNAL OF EPIDEMIOLOGY
Volume 51, Issue 4, Pages 1317-1327Publisher
OXFORD UNIV PRESS
DOI: 10.1093/ije/dyac042
Keywords
RCC; diastolic blood pressure; systolic blood pressure; Mendelian randomization; kidney cancer
Categories
Funding
- Cancer Research UK [C18281/A29019, 14136, C8221/A29017]
- Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London
- NIHR Imperial Biomedical Research Centre
- Danish Cancer Society (Denmark)
- Ligue Contre le Cancer
- Institut Gustave Roussy
- Mutuelle Generale de l'Education Nationale
- Institut National de la Sante et de la Recherche Medicale (Inserm) (France)
- German Cancer Aid
- German Cancer Research Center (DKFZ)
- Federal Ministry of Education and Research (BMBF)
- Associazione Italiana per la Ricerca sul CancroAIRC-Italy
- National Research Council (Italy)
- Dutch Ministry of Public Health, Welfare and Sports (VWS), Netherlands Cancer Registry (NKR), LK Research Funds
- Dutch Prevention Funds
- Dutch ZON (Zorg Onderzoek Nederland)
- World Cancer Research Fund
- Health Research Fund (FIS)-Instituto de Salud Carlos III (ISCIII)
- Swedish Cancer Society
- Swedish Research Council
- County Councils of Skane
- Vasterbotten (Sweden)
- Medical Research Council [1000143, MR/M012190/1]
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Diastolic blood pressure (DBP) appears to play an important role in the etiology of renal cell carcinoma (RCC), while the association between systolic blood pressure (SBP) and RCC risk is less clear and seems to be dependent on DBP.
Background The relation between blood pressure and kidney cancer risk is well established but complex and different study designs have reported discrepant findings on the relative importance of diastolic blood pressure (DBP) and systolic blood pressure (SBP). In this study, we sought to describe the temporal relation between diastolic and SBP with renal cell carcinoma (RCC) risk in detail. Methods Our study involved two prospective cohorts: the European Prospective Investigation into Cancer and Nutrition study and UK Biobank, including >700 000 participants and 1692 incident RCC cases. Risk analyses were conducted using flexible parametric survival models for DBP and SBP both separately as well as with mutuality adjustment and then adjustment for extended risk factors. We also carried out univariable and multivariable Mendelian randomization (MR) analyses (DBP: n(instruments) = 251, SBP: n(instruments) = 213) to complement the analyses of measured DBP and SBP. Results In the univariable analysis, we observed clear positive associations with RCC risk for both diastolic and SBP when measured >= 5 years before diagnosis and suggestive evidence for a stronger risk association in the year leading up to diagnosis. In mutually adjusted analysis, the long-term risk association of DBP remained, with a hazard ratio (HR) per standard deviation increment 10 years before diagnosis (HR10y) of 1.20 (95% CI: 1.10-1.30), whereas the association of SBP was attenuated (HR10y: 1.00, 95% CI: 0.91-1.10). In the complementary multivariable MR analysis, we observed an odds ratio for a 1-SD increment (ORsd) of 1.34 (95% CI: 1.08-1.67) for genetically predicted DBP and 0.70 (95% CI: 0.56-0.88) for genetically predicted SBP. Conclusion The results of this observational and MR study are consistent with an important role of DBP in RCC aetiology. The relation between SBP and RCC risk was less clear but does not appear to be independent of DBP.
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