Risk of renal-cell cancer in relation to use of diuretics, other anti-hypertensive medications and hypertension was assessed in a multi-center, population-based, case-control study conducted in Australia, Denmark, Germany, Sweden and the United States, using a shared protocol and questionnaire. A total of 1,732 histologically confirmed cases and 2,309 controls, frequency-matched to cases by age and sex, were interviewed. The association between renal-cell cancer and the drugs was estimated by relative risks (RRs) and 95% confidence intervals (CIs). Risks were increased among users of diuretics and other anti-hypertensive medications. After adjustment for hypertension, risk for diuretics was reduced to unity, except among long-term (15+ years) users. Risk for use of non-diuretic anti-hypertensive drugs remained significantly elevated and increased further with duration of use. Overall risk was not enhanced when both classes of medications were used. Excess risk was not restricted to any specific type of diuretic or anti-hypertensive drug and no trend was observed with estimated lifetime consumption of any particular type of product. The RR for hypertension after adjustment for diuretics and other anti-hypertensive medications was 1.4 (95% CI = 1.2-1.7), although among non-users of any anti-hypertensive medications, there was little excess risk associated with a history of hypertension. Exclusion of drug use that first occurred within 5 years of cancer diagnosis or interview did not alter the associations. Our findings suggest small effects on renal-cell cancer risk associated with hypertension and use of diuretics and other anti-hypertensive medications. However, because of potential misclassifications of these highly correlated variables, it is difficult to distinguish the effect of treatment from its indication, hypertension.

The strength of the association between regular analgesic intake (RAI) and end-stage renal failure (EF) has been insufficiently established until now. A case-control study was conducted to estimate the relative risks (RR) of EF after RAI (defined as consumption of 15 or more analgesic doses per month for a continuous period of at least 1 year) for cumulative drug intake, single-ingredient analgesics, combinations, and specific compounds. The case group included all patients with EF undergoing renal replacement therapy in the area of West Berlin (1984–1986, n = 921). Control subjects, matched to cases by sex, age, and nationality, were selected from a group of patients in outpatient clinics. Matching was possible for 517 cases. The RR of EF after RAI of any analgesic was 2.44 (95% confidence interval: 1.77–3.39) and after RAI of combination drugs 2.65 (95% confidence interval 1.91–3.67). No significant increase was found, however, after RAI of single-ingredient analgesics. The RR after RAI of combination drugs and for the most preferred analgesic ingredients (phenacetin, paracetamol, acetylsalicylic acid, phenazones, caffeine) increased with dose. Furthermore, a dose-time-related RR after RAI of the longest used preparation was found. Thus, the results clearly show an increased RR of EF after RAI related to both dose and exposure time of mixed analgesic compounds, but not for the use of only single-ingredient analgesics.

PTX3 levels are markedly elevated in HD patients. The increase in PTX3 production in whole blood after HD indicates that the HD procedure itself contributes to elevated PTX3 levels in HD patients. The association between PTX3 and cardiovascular morbidity suggests a possible connection of PTX3 with atherosclerosis and cardiovascular disease in HD patients.

Although numerous studies have identified obesity or high relative weight as a risk factor for renal-cell cancer in women, the degree to which this effect is present in men remains unclear. A multicenter population-based case-control study concerning incident cases of histologically verified renal-cell cancer (n = 1,732) and age-and sex-matched controls (n = 2,309) was conducted in Australia, Denmark, Germany (2 centers), Sweden and the United States. Relative weight was estimated by the body mass index, and the association between this factor and other factors, such as height, physical activity and use of amphetamines, was measured by the relative risk estimated in logistic regression models. Body mass index was found to be a risk factor among women and, to a lesser extent, among men. A 3-fold increased risk (RR = 3.6, 95% CI = 2.3-5.7) was observed for women with a relative weight in the top 5% compared with those in the lowest quartile. Rate of weight change (estimated as weight change per annum in kilograms) appeared to be an independent risk factor among women but not among men. Physical activity and height were unrelated to risk of renal-cell cancer regardless of level of BMI, while use of amphetamines was associated with an increased risk among men, although no dose or duration effect was seen. Our findings verify the link between high relative weight and risk of renal-cell cancer, particularly among women. The mechanism that underlies this association is, however, still unclear, although the rate of weight change may play a role.(3 I995 Wiley-Liss. Inc.

On the 30th anniversary of the U.S. Surgeon General's report Smoking and Health, we present updated results from one of the original cohort studies that comprised the groundbreaking document. A 26-year follow-up of 248,046 U.S. veterans evaluating the risks of cigarette smoking revealed strong dose-response effects between smoking and total cancer and a large number of cancer sites. Over 50% of cancer deaths among current smokers and 23% of cancer deaths among former smokers were attributable to cigarette smoking. These findings further demonstrate the large and unique role cigarette smoking plays in cancer etiology and the importance of smoking cessation to reduce this enormous public health burden.

Habitual risks from smoking and intake of laxatives significantly contribute to the development of UC, especially of the renal pelvis and ureter cancer. Intake of at least 1 kg of analgesic substances (anilides, pyrazolones) as calculated from this study base is associated with increased but not significant risks for RPC. These data underline that restrictive and educational measurements focusing on common habits would have a strong impact on preventing UC in Germany.

A number of medical conditions have been linked with renal-cell cancer, although the evidence is not consistent in every case. In a large international case-control study of renalcell cancer, we examined, among other hypotheses, associations with a personal history of certain medical conditions and a family history of cancer of the kidney or thyroid. Relative risks (RR), adjusted for the effects of age, gender, body-mass index, tobacco smoking and study centre, were significantly increased by a history of kidney stones or thyroid or kidney disease. The RR were not altered by additional adjustment for hypertension, or when diagnoses were restricted to those made at least 5 or 10 years before 1987 (the usual "cut-off'' date). The link with kidney injury is particularly likely to be affected by recall bias. Increased RR of borderline significance were found for kidney infection (RR, 1. A number of medical conditions have been linked in analytical epidemiological studies with renal-cell cancer (RCC), although the evidence is not consistent in every case. Statistically significant associations have been reported for kidney stones (McLaughlin et al., 1984;Maclure and Willett, 1990;Talamini et al., 1990), kidney infection (McLaughlin et al., 1984), kidney cysts (McLaughlin et al., 1984), urinary-tract infection in women (Kreiger et al., 1993), urological disease (McCredie et al., 1988, hypertension (Raynor et al., 1981;McLaughlin et al., 1984McLaughlin et al., , 1992Fraser et al., 1990;Maclure and Willett, 1990), stroke (McLaughlin et al., 1984) and myocardial infarction (Wynder et al., 1974). Nonsignificant links have been reported with diabetes (McLaughlin et al., 1984(McLaughlin et al., , 1992Asal et al., 1988;Kreiger et al., 1993;Adami et al., 1993), also possible associations with thyroid disease (Rosenberg et al., 1990) and thyroid cancer (Tucker et al., 1985).Case reports have identified additional, less common conditions which appear to carry an increased risk of RCC. These include autosomal dominant inherited disease such as von Hippel-Lindau syndrome (Hudson and Wilson, 1979;Lynch and Walzak, 1980) and polycystic kidney disease (Bernstein et al., 1987), end-stage renal failure requiring dialysis (Port et al., 1989), where the risk appears to be associated with acquired cystic disease Matson and Cohen, 1990), and a family history of kidney cancer (Franksson et al., 1972;Cohen et al., 1979).A large international case-control study of RCC was carried out to examine, among other hypotheses, the associations with a personal history of certain medical conditions and a family history of cancer of the kidney or thyroid. SUBJECTS AND METHODSA complete description of the population-based ascertainment of cases and controls has been presented elsewhere (McLaughlin et at., 199%). Briefly, cases with a histologically verified diagnosis of RCC during the period 1989-1991 were identified through population-based registries in 4 study areas (Sydney, Denmark, Uppsala and Minnesota), while cases in Berlin and Heidelberg were ...

There has been concern about the role of analgesics in the development of renal-cell cancer, although a few studies have reported moderately elevated risks with regular or long-term use. In a large international case-control study of renal-cell cancer we examined, among other hypotheses, the effect of phenacetin-containing and of other types of analgesics: paracetamol (acetaminophen), salicylates (mainly aspirin) and pyrazolones (e.g., antipyrine or phenazone). Relative risks, adjusted for the effects of age, sex, body-mass index, tobacco smoking and study centre, were not significantly increased with intake of phenacetin, either when lifetime consumption was categorized at the level of > or = 0.1 kg or when subjects were subdivided further by amount. Nor were paracetamol, salicylates or pyrazolones linked with renal-cell cancer. No consistently increasing risks with consumption level was found. The lack of association was not altered by restricting analgesic use to that which occurred 5 or 10 years before the defined "cut-off" date or when analysis was restricted to exclusive users of a particular type of analgesic. Neither was the risk influenced by the rate of consumption or whether the consumption had occurred at a young age. Our study provides clear evidence that aspirin is unrelated to renal-cell cancer risk, and our findings do not support the hypothesis that analgesics containing phenacetin or paracetamol increase the risk, although the number of "regular" users and the amount of these types of analgesic consumed were too small to confidently rule out a minor carcinogenic effect of phenacetin and paracetamol.