This article aims to summarize the recent epidemiological studies that have been conducted on the potential effects of urate (uric acid) on diseases, specifically focusing on studies that used a Mendelian randomization approach. As is generally the case with cardiometabolic diseases, urate epidemiology has resorted to Mendelian randomization to disentangle causal relationships. The Mendelian randomization approach utilizes genetic variants as an instrumental variable to address whether a given biomarker has a causal effect on the disease, or whether it is simply a non-causal marker (perhaps a consequence of the disease); thus, this approach allows addressing causality in the presence of potential confounding factors. Most Mendelian randomization studies on urate have suggested modest or negligible degrees of causal effect of urate on many diseases and that reverse causality may explain the associations of urate with cardiometabolic biomarkers, such as adiposity, which are repeatedly observed in conventional epidemiology. Conflicting results have been reported partly due to the use of different sets of genetic variants, which emphasizes the importance of physiological and epidemiological characterizations of individual genetic variants and codified proteins. With improved sets of genetic variants and methods to infer causal effects in the presence of invalid genetic variants (for example, those with pleiotropy), further Mendelian randomization analyses may uncover subtle causal effects of urate on cardiovascular and kidney outcomes.