Background: Renal cell carcinoma and hypertension (a well-established renal cancer risk factor) are both more frequent among blacks than whites in the United States. The association between hypertension and renal cell carcinoma has not been examined in black Americans. We investigated the hypertension–renal cancer association by race, and we assessed the role of hypertension in the racial disparity of renal cancer incidence.
Methods: Participants were enrolled in a population-based case-control study in Detroit and Chicago during 2002–2007 (number of cases: 843 whites, 358 blacks; number of controls: 707 whites, 519 blacks). Participants reported their history of hypertension and antihypertensive drug use. We used unconditional logistic regression to calculate odds ratios (ORs) and 95% confidence intervals (CIs), adjusted for demographic characteristics, smoking, body mass index, and family history of cancer.
Results: Hypertension doubled renal cancer risk (OR = 2.0 [CI = 1.7–2.5]) overall. For whites, the OR was 1.9 (CI = 1.5–2.4), whereas for blacks it was 2.8 (2.1–3.8) (P for interaction = 0.11). ORs increased with time after hypertension diagnosis (P for trend <0.001), reaching 4.1 (CI = 2.3–7.4) for blacks and 2.6 (CI = 1.7–4.1) for whites after 25 years. ORs for poorly controlled hypertension were 4.5 (CI = 2.3–8.8) for blacks and 2.1 (CI = 1.2–3.8) for whites. If these estimates correctly represent causal effects and if, hypothetically, hypertension could be prevented entirely among persons aged 50–79 years, the black/white disparity in renal cancer could be reversed among women and reduced by two-thirds among men.
Conclusions: Hypertension is a risk factor for renal cancer among both blacks and whites, and might explain a substantial portion of the racial disparity in renal cancer incidence. Preventing and controlling hypertension might reduce renal cancer incidence, adding to the known benefits of blood pressure control for heart disease and stroke reduction, particularly among blacks.
From the aDivision of Cancer Epidemiology and Genetics, Department of Health and Human Services, National Cancer Institute, National Institutes of Health, Bethesda, MD; bKarmanos Cancer Institute and Department of Family Medicine & Public Health Sciences, Wayne State University, Detroit, MI; cDepartment of Epidemiology and Biostatistics, School of Public Health, University of Illinois at Chicago, Chicago, IL; and dWestat, Inc., Rockville, MD.
Submitted 22 November 2010; accepted 30 June 2011; posted 31 August 2011.
Supported by the Intramural Research Program of the National Institutes of Health and the National Cancer Institute with contracts N02-CP-10128 (Westat, Inc.), N02-CP-11004 (Wayne State University), and N02-CP-11161 (University of Illinois at Chicago).
The authors reported no financial interests related to this research.
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Correspondence: Joanne S. Colt, National Cancer Institute, Occupational and Environmental Epidemiology Branch, 6120 Executive Boulevard, Room 8002, Bethesda, MD 20892-7240. E-mail: firstname.lastname@example.org.