Background: This thesis is a composition of three studies that explore the role of statins in kidney cancer. Furthermore, I evaluate the potential for different interpretations from the same data depending on the method of classifying medication use. Methods: The first study was a population-based case-control study evaluating the association of statin use with risk of incident kidney cancer. The second study was a systematic review and meta-analysis reviewing the current evidence relating statins with kidney cancer survival outcomes. The final study was a population-based cohort study evaluating the association of statin use with survival. In the observational studies, I used fractional polynomials for the primary analysis to allow for a non-linear relationship between cumulative exposure and the risk of the outcome. I also compared risk estimates obtained by different methods of classifying medication exposure. Results: The population-based case-control study included 10,377 incident cases of kidney cancer and 35,939 matched controls. Increasing cumulative use of statins was not associated with kidney cancer risk. I identified 12 studies for inclusion in the systematic review and meta-analysis and found that statin use was significantly associated with markedly improved cancer-specific and overall survival. However, none of these studies evaluated cumulative use. In the population-based cohort study of 9124 patients with incident kidney cancer, increasing cumulative use of statins was associated with minimal improvement in cancer-specific and overall survival. The association of statin use with kidney cancer risk or survival varied depending on the method of classifying exposure. Conclusions: This thesis does not support the use of statins for the prevention or adjunctive treatment in kidney cancer. Furthermore, risk estimates in pharmacoepidemiology may be sensitive to the method of classifying exposure.
carcinoma, renal cell, drug utilization, HMG-CoA reductase inhibitor, humans, pharmacoepidemiology
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