Background Obesity and hypertension have been implicated asrisk factors for the development of renal-cell cancer.
Methods We examined the health records of 363,992 Swedish menwho underwent at least one physical examination from 1971 to1992 and were followed until death or the end of 1995. Men withcancer (renal-cell cancer in 759 and renal-pelvis cancer in136) were identified by cross-linkage of data with the nationwideSwedish Cancer Registry. Poisson regression analysis was usedto estimate relative risks, with adjustments for age, smokingstatus, body-mass index, and diastolic blood pressure.
Results As compared with men in the lowest three eighths ofthe cohort for body-mass index, men in the middle three eighthshad a 30 to 60 percent greater risk of renal-cell cancer, andmen in the highest two eighths had nearly double the risk (Pfor trend, <0.001). There was also a direct association betweenhigher blood pressures and a higher risk of renal-cell cancer(P for trend, <0.001 for diastolic pressure; P for trend,0.007 for systolic pressure). After the first five years offollow-up had been excluded to reduce possible effects of preclinicaldisease, the risk of renal-cell cancer was still consistentlyhigher in men with a higher body-mass index or higher bloodpressure. At the sixth-year follow-up, the risk rose furtherwith increasing blood pressures and decreased with decreasingblood pressures, after adjustment for base-line measurements.Men who were current or former smokers had a greater risk ofboth renal-cell cancer and renal-pelvis cancer than men whowere not smokers. There was no relation between body-mass indexor blood pressure and the risk of renal-pelvis cancer.
Conclusions Higher body-mass index and elevated blood pressureindependently increase the long-term risk of renal-cell cancerin men. A reduction in blood pressure lowers the risk.
Kidney cancers account for 2 to 3 percent of new cases of cancerin the United States. In more than 80 percent of these cases,the cancer arises from the renal parenchyma and consists ofadenocarcinoma (renal-cell carcinoma); most renal-pelvis cancersare transitional-cell carcinomas. In the United States, renal-cellcarcinoma is among the most rapidly increasing of all typesof tumors in incidence, particularly among black persons, whereasthe rates of renal-pelvis cancer have declined during the pasttwo decades.1
Obesity increases the risk of renal-cell cancer, although thisassociation has not been consistently observed in men.2,3 Hypertensionis also a risk factor, but quantitative data according to levelsof blood pressure are limited.4 A small case–control studybased on medical records found that the risk of renal-cell cancerwas higher with higher blood pressures within 5 to 10 yearsbefore a diagnosis of renal-cell cancer.5 Cohort studies withmeasurements of blood pressure have not distinguished amongdifferent types of renal cancer, although a dose–responserelation was reported in two studies.6,7 In general, renal-pelviscarcinoma has not been linked to obesity or hypertension, althoughan association with hypertension has been suggested.8 Cigarettesmoking increases the risk of both types of kidney cancer, andthe increase is greater for renal-pelvis cancer than for renal-cellcancer.9,10
To clarify these associations, we conducted a study of newlydiagnosed kidney cancer during a follow-up period of as longas 25 years in a large cohort of men in whom measurements ofheight, weight, and blood pressure were obtained at an initialexamination. In a subgroup of the men, who underwent multipleexaminations, we also evaluated the effect of changes in body-massindex and blood pressure on the risk of kidney cancer.
Methods
The Study Cohort
In 1968, Bygghälsan, the Swedish Foundation for OccupationalSafety and Health of the Construction Industry, was establishedto coordinate all activities concerning occupational safetyand health among construction workers,11,12 including the provisionof preventive medical care to all workers in this industry nationwide.Workers were invited to undergo health examinations at intervalsof two to five years. Data from the health examinations, whichincluded measurements of height, weight, and blood pressure,were registered in a central data base beginning in 1971.
Between January 1971 and December 1992, information from 389,135workers was registered in the data base, after the exclusionof information on 605 workers whose national registration numbers(unique numbers assigned to each Swedish resident) had beenentered incorrectly. We then excluded the 19,418 workers whowere women, because they constituted only 5 percent of the cohortand because only 5 of them were found to have kidney cancer,and the 5725 men (1.5 percent) who emigrated before the first(base-line) examination or for whom we did not have completedata on weight, height, or blood pressure. Of the 363,992 menincluded in the study, 234,297 (64 percent) had, in additionto the base-line examination, one or more follow-up visits.
Follow-Up
The men who were given a diagnosis of kidney cancer were identifiedwith the use of information from the population-based SwedishCancer Registry, according to the men's national registrationnumbers. This cancer registry was established in 1958 and hasbeen found to be more than 98 percent complete in its documentationof cases.13 In addition, dates of death or emigration duringthe follow-up period were obtained by cross-linkage with thenationwide Mortality Registry and Migration Register. The menwere followed from the date of entry into the cohort (definedas the date of the initial examination) until the date of adiagnosis of kidney cancer, emigration, or death or the endof the observation period (December 31, 1995), whichever camefirst.
Statistical Analysis
Kidney cancers were classified as renal-cell cancer (codes 180.0and 180.9 of the International Classification of Diseases, 7thRevision [ICD-7]) or renal-pelvis or ureteral cancer (ICD-7codes 180.1 and 181.1).14 The relative risks of cancer (with95 percent confidence intervals) were estimated with Poissonregression analysis, with adjustments for age (as a continuousvariable), smoking status (nonsmoker, former smoker, or currentsmoker at base line), body-mass index (the weight in kilogramsdivided by the square of the height in meters), and diastolicblood pressure. Body-mass index and blood pressure, as continuousvariables, were used for adjustment and for the testing of lineartrends. To calculate estimates of risk, body-mass index wasdivided into eight categories (from 20.75 to 27.76), with anapproximately equal number of men in each category, and bloodpressure was divided into increments of 10 mm Hg (diastolicpressure from <70 to 110 mm Hg and systolic pressure from<120 to 160 mm Hg). Effect modification was assessed by examinationof the risk of cancer associated with body-mass index or bloodpressure within each level of a second variable, such as age.The significance of interactions between body-mass index andblood pressure was evaluated by adding an interaction term tothe model.
The main analysis was based on data from the base-line examinationfor the entire cohort. To provide more stable information forbody-mass index and blood pressure, separate analyses were conductedwith the average values from the base-line examination and thefirst follow-up examination within three years after the base-lineexamination; in these analyses, person-years were consideredto have begun accumulating after the first follow-up visit.The effects of changes over time in body-mass index and diastolicblood pressure were also evaluated with respect to the differencesin these values between the base-line examination and the examinationconducted during approximately the sixth year of follow-up.
Results
The workers entered the cohort at an average age of 44.2 years.They were followed for an average of 16 years, for a cumulativetotal of 5,783,888 person-years of follow-up. At the time ofentry, 52 percent of them smoked cigarettes or had smoked inthe past (Table 1). They had a mean (±SD) body-mass indexof 24.5±3.1, a mean diastolic blood pressure of 84±13 mm Hg, and a mean systolic blood pressure of 140±18mm Hg. The mean body-mass index varied little according to age,whereas the mean blood pressure was higher in older men thanin younger men.
Table 1. Characteristics of the 363,992 Men in the Cohort.
During follow-up, renal-cell cancer was diagnosed in 759 menand renal-pelvis cancer in 136 men. Men who were current orformer cigarette smokers at base line had a significantly higherrisk of renal-cell cancer and an even higher risk of renal-pelviscancer than men who had never smoked (relative risk of renal-cellcancer, 1.3 [95 percent confidence interval, 1.0 to 1.6] forformer smokers and 1.6 [95 percent confidence interval, 1.3to 1.9] for current smokers; relative risk of renal-pelvis cancer,1.6 [95 percent confidence interval, 0.9 to 3.1] for formersmokers and 3.5 [95 percent confidence interval, 2.1 to 5.8]for current smokers) (Table 2). Furthermore, the risk of renal-cellcancer was significantly higher among men with a higher body-massindex than among those who were leaner (P for trend, <0.001);the risk was nearly doubled for men in the highest eighth ofthe cohort for body-mass index (relative risk as compared withthe leanest subgroup, 1.9; 95 percent confidence interval, 1.3to 2.7) (Table 2). Height was not consistently related to therisk of either type of cancer (data not shown).
Table 2. Relative Risk of Renal-Cell Cancer and Renal-Pelvis Cancer among Men in the Cohort, According to Smoking Status, Body-Mass Index, and Blood Pressure.
Blood pressure was positively related to the risk of renal-cellcancer; the dose–response relation was clearer for diastolicpressure (P for trend, <0.001) than for systolic pressure(P for trend, 0.007). The risk of renal-cell cancer in men witha diastolic pressure of 90 mm Hg or more was more than doublethe risk in men with a diastolic pressure below 70 mm Hg. Therisk of this type of cancer was 60 to 70 percent higher in menwith a systolic pressure of 150 mm Hg or more than in thosewith a systolic pressure below 120 mm Hg. The risks associatedwith body-mass index and blood pressure were independent ofeach other. In contrast, the risk of renal-pelvis cancer wasnot related to body-mass index or blood pressure, either interms of the relative risks or in terms of a dose–responserelation (Table 2).
The risk of renal-cell cancer in relation to body-mass indexand blood pressure varied according to age at the time of entryinto the cohort; men who were initially less than 50 years oldhad the highest risks (Table 3). For men who entered the cohortat an age of 60 years or older, the excess risk, if present,was small. Those with a high body-mass index had a significantlyhigher risk throughout the follow-up period, even more than15 years after the base-line examination. The association betweenthe risk of renal-cell cancer and diastolic blood pressure,however, was strongest during the first five years of follow-up.Smoking status also appeared to modify the association betweenthis risk and body-mass index, with the highest increases inrisk found among nonsmokers. In addition, the association betweenthe risk of renal-cell cancer and body-mass index and the associationbetween this risk and blood pressure were similar for men recruitedfrom 1971 through 1979 and those recruited from 1980 through1992 (data not shown).
Table 3. Relative Risk of Renal-Cell Cancer among Men in the Cohort, According to Body-Mass Index and Diastolic Blood Pressure, with Stratification According to Selected Characteristics.
We also examined the combined effect of body-mass index andblood pressure on the risk of renal-cell cancer after excludingthe men in whom cancer was diagnosed during the first five yearsof follow-up and after excluding all the person-years the cohortaccumulated during that period (to reduce the possible effectof increases in blood pressure due to preclinical cancer) (Table 4).The risk of renal-cell cancer rose consistently with increasingbody-mass index at each level of diastolic blood pressure analyzed.Conversely, it tended to rise, though not consistently, withincreasing diastolic pressure at each level of body-mass indexanalyzed.
Table 4. Combined Effect of Diastolic Blood Pressure and Body-Mass Index on the Relative Risk of Renal-Cell Cancer.
To increase the stability of the base-line measurements of bloodpressure, we averaged the results of the first two examinationsfor men who had a second examination within three years afterthe initial examination. Among these men, the risk of renal-cellcarcinoma increased steadily with higher average diastolic orsystolic blood pressure and was generally higher than the riskfor the entire cohort, calculated with data from only the initialexamination (data not shown).
We also examined the effects of changes in body-mass index ordiastolic blood pressure (actual changes and percent changes)between the base-line examination and the sixth-year follow-upvisit (Table 5). The risk of renal-cell cancer was more thandoubled in men whose diastolic pressure rose by more than 14mm Hg (relative risk, 2.3; 95 percent confidence interval, 1.4to 3.7) or by more than 19 percent (relative risk, 2.2; 95 percentconfidence interval, 1.3 to 3.7) as compared with men who hadlittle change in diastolic blood pressure. In contrast, a decreasein diastolic blood pressure during this period reduced the riskby 40 percent in those whose diastolic pressure decreased bymore than 14 mm Hg (relative risk, 0.6; 95 percent confidenceinterval, 0.3 to 1.3) and in those whose diastolic pressuredecreased by more than 9 percent (relative risk, 0.6; 95 percentconfidence interval, 0.3 to 0.9). This pattern persisted overeach 5-year period of follow-up after the sixth-year examination(0 to 5, 6 to 10, and >10 years after this examination) (datanot shown). The risk of renal-cell cancer in relation to changesin body-mass index between the time of the base-line examinationand the sixth-year visit was not statistically significant.The risk in men with the largest increases in body-mass indexwas 1.6 to 2.0 times the risk in men who had little change inbody-mass index. The risks related to changes in body-mass indexor blood pressure were independent of those associated withthe degree of obesity or hypertension at base line.
Table 5. Relative Risk of Renal-Cell Cancer among Men in the Cohort According to Changes in Diastolic Blood Pressure and Body-Mass Index.
Discussion
In this study of Swedish men, we found independent dose–responserelations between body-mass index and the risk of renal-cellcancer and between diastolic and systolic blood pressure andthe risk of renal-cell cancer, with a greater risk observedin men with an even slightly higher body-mass index or bloodpressure than in their counterparts with lower values. Changesin blood pressure over time influenced this risk independentlyof the effect of hypertension at base line, suggesting thata reduction in blood pressure may help to prevent renal-cellcancer. The specificity of the association between high bloodpressure and high body-mass index and the risk of renal-cellcancer, as opposed to renal-pelvis cancer, in this relativelyhomogeneous population, as well as the persistent increasesin this risk during more than 15 years of follow-up, arguesagainst the presence of any confounding factor or other potentialsource of bias as an explanation for our findings. Furthermore,our study confirmed the results of previous studies10 that indicatedthat cigarette smoking increases the risk of both types of renalcancer.
Previous studies of the relation between renal-cell cancer andblood pressure were based on relatively small numbers of subjects.5,6,7In our study, the number of men with renal-cell cancer was sufficientto show a clear dose–response relation over a wide rangeof blood-pressure levels. Even slightly higher blood pressuresconferred some excess risk, whereas increases in blood pressureover time further raised the risk independently of the presenceof hypertension at base line. Of special interest was the decreasein risk associated with a reduction in blood pressure over time,although further studies will be needed to confirm this finding.
Whereas the excess risk of renal-cell cancer associated withobesity was consistent throughout the follow-up period, therisk related to hypertension was highest during the first fiveyears of follow-up. Renal tumors in their early stages, beforediagnosis, may cause increases in blood pressure15 and thuscontribute to the apparent risk associated with hypertensionduring the initial years of follow-up. However, even after weexcluded the men in whom cancer was diagnosed and the person-yearsaccumulated by the cohort during the first five years of follow-up,the risk of renal-cell cancer still was significantly higherat higher blood pressures, suggesting that the association isnot an artifact of routine health examinations.
Epidemiologic studies have not been able to distinguish theeffects of hypertension from those of diuretics or other antihypertensivedrugs on the risk of renal-cell cancer.4,5 We did not collectdata on the use of antihypertensive drugs; however, severalof our findings — the monotonic, dose–response relationassociated with increments in blood pressure, the excess riskseen with only slightly elevated blood pressures (which maynot prompt treatment), and the reduced risk associated withdecreased blood pressure at subsequent visits — implicatehypertension as a risk factor for renal-cell carcinoma. Indeed,our data indicate that effective control of hypertension maylower the risk of renal-cell cancer.
Several other potential limitations of our study should be considered.Only a subgroup of the men in the cohort had a follow-up visitafter the initial, base-line examination. However, the men whohad more than one examination were more likely to be activeand healthy than those who did not have a follow-up examination.It therefore seems unlikely that increases in the risk of renal-cellcancer associated with worsening hypertension over time weredue to selection bias in this subgroup. In addition, althoughour results provide strong evidence of a dose–responserelation with body-mass index and blood pressure in men, theymay not apply to the same extent in women.
Our finding that obesity and hypertension independently increasethe risk of renal-cell cancer suggests that these factors actto increase this risk through different mechanisms. Obese personshave high serum concentrations of free insulin-like growth factorI,16 an important mitogen that affects the cell cycle.17 Highserum insulin-like growth factor I concentrations have beenlinked to an increased risk of several cancers, including cancersof the breast, prostate, lung, and colorectum,17 but the levelof this growth factor has not been reported to be related tothe risk of renal-cell cancer. Obesity may also increase therisk by increasing the serum concentrations of free estrogens,18,19which have been linked to the risk of renal-cell cancer in studiesin animals,20 but epidemiologic studies of renal-cell canceramong women have found no clear association between the riskof this cancer and the use of exogenous estrogens.21,22
As for hypertension, a variety of angiogenic and other growthfactors, the levels of which are increased in persons with hypertensivedisease, may be involved in renal carcinogenesis.23,24 Subtlechanges in renal function that precede the development of overthypertension25,26 may render the kidney susceptible to carcinogensand tumor growth. A long-term cohort study of men who underwenthealth examinations at the time they entered college27 revealeda tripling of the risk of kidney cancer among those who hadproteinuria.
Our findings underscore the importance of even small excessesin body-mass index and blood pressure in the development ofrenal-cell cancer and suggest that effective control of weightand hypertension may be useful in the prevention of this increasinglycommon type of cancer.
Supported in part by a contract (NO2-CP-71100) with the NationalCancer Institute.
We are indebted to Dr. Anders Englund, medical director of Bygghälsan,for designing the health-surveillance program and record-keepingsystem used in this cohort study; to Ulrik Wallström, chairmanof the steering committee of the health-surveillance registryof Swedish construction workers; and to Winnie Ricker of InformationManagement Services for computing support.
Source Information
From the Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Md. (W.-H.C., G.G., J.F.F.); and the Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden (B.J.).
Address reprint requests to Dr. Chow at the National Cancer Institute, 6120 Executive Blvd., EPS 8100, Bethesda, MD 20892-7240, or at choww{at}mail.nih.gov.
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20.75 to 
27.76), with an approximately equal number of men in each category, and blood pressure was divided into increments of 10 mm Hg (diastolic pressure from <70 to 
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