We found a strong, incremental elevation in the prevalence of hyperuricemia and gout with increasing levels of BP, BMI, and total cholesterol, and with decreasing levels of estimated GFR and HDL cholesterol. Notably, regardless of survey period, individuals with uncontrolled BP and two additional CVD risk factors demonstrated a 4-fold or greater prevalence of hyperuricemia, and at least a 3-fold or greater prevalence of gout compared to normotensive individuals without these risk factors.
Our results are consistent with prior studies demonstrating an association between hyperuricemia or gout and the metabolic syndrome 
. However, metabolic syndrome, in its aggregate formulation, may not be the most suitable exposure for evaluating gout prevalence. Whereas many CVD risk factors are components of the metabolic syndrome and associate positively with hyperuricemia and gout, one component - serum glucose concentration - exhibits an inverse relationship at high concentrations 
. We observed this inverse association with greater levels of hemoglobin A1c. Furthermore, other CVD risk factors, such as reduced eGFR, are not among the characteristics comprising metabolic syndrome 
. As a result, our findings suggest that gout prevalence may be optimally characterized in relation to individual and additional CVD risk factors rather than as an aggregated syndrome. Moreover, these component factors are both intuitive and readily ascertained in the ambulatory care setting.
Hypertension is strongly associated with serum uric acid 
. In our analysis, the prevalence of hyperuricemia among individuals with uncontrolled BP, in the absence of other CVD risk factors, was ~10–15% compared to 7–8% in healthy individuals. Furthermore, in each survey period, we observed an incrementally greater prevalence of hyperuricemia with each successive stage of BP. The underlying mechanism is unknown. Some report that hyperuricemia is not an independent risk factor for hypertension 
, while other laboratory 
and epidemiologic studies suggest that uric acid plays a causal role in the development of hypertension 
. Furthermore, prospective studies describe hypertension as a risk factor for hyperuricemia 
and of gout 
. Regardless of mechanism, it is clear that hypertension and hyperuricemia are positively related, with about a quarter of all individuals with a blood pressure in the hypertensive range (i.e. uncontrolled blood pressure) also meeting criteria for hyperuricemia (Supplemental Table S1, Table S2, Table S3, Table S4
Hypertension is frequently present with other health conditions 
. CVD risk factors, including kidney disease, dyslipidemia, and obesity, along with hypertension, are among the most common reasons for ambulatory medical visits in the US 
. Our analyses indicate that each of these risk factors is individually and incrementally associated with a greater prevalence of hyperuricemia and gout ( and Table S1, Table S2, Table S3, Table S4
). Furthermore, the addition of two risk factors was sufficient for the prevalence of hyperuricemia and gout to be as high as 35% and 7% of the American population, respectively.
In 2008, hypertension was diagnosed in about 46,000 ambulatory visits in the US, making it the most commonly diagnosed condition 
. Based on our prevalence estimates, roughly 10,000 (15%) of these visits included individuals with hyperuricemia. Treating physicians are likely to initiate a thiazide agent as a first-line antihypertensive per the JNC VII guidelines 
. In fact, our analysis suggests that thiazide use has increased from 1.5% to 5.6% over the past 20 years. New thiazide use has been shown to increase serum urate levels by 0.55 mg/dL and increase the risk of gout by 44% 
. We recognize that widespread public health benefit can be achieved by small, marginal reductions in CVD risk factors 
. Conversely, population-based increases in serum uric acid, mediated by the use of thiazide and other diuretic agents, may have a detrimental effect on the burden of gout in the US population. Given the high prevalence of hyperuricemia among hypertensive individuals, particularly in those with additional CVD risk factors, it is important that primary care providers be aware of these associations, especially when evaluating a patient with concomitant joint pain and swelling. Furthermore, future BP management guidelines should consider screening for hyperuricemia and gout in candidates with a thiazide indication, as well as discuss alternative medications with fewer serum urate-related effects 
This study has a number of important limitations. Although NHANES is well-suited for describing the prevalence of hyperuricemia and gout in the US population, its cross-sectional design does not account for temporality, limiting causal inference. Furthermore, in this study, gout was ascertained via survey question rather than a clinical diagnosis, which precludes synovial fluid analysis for detection of confirmatory urate crystals 
. Although a crystal-proven diagnosis is the gold standard diagnostic approach in clinical practice, self-report is a reliable 
and practical tool in the context of epidemiologic research. Nevertheless, when in a sensitivity analysis, we restricted the outcome of self-reported, physician-diagnosed gout to those NHANES participants with hyperuricemia or receiving urate-lowering agents, the findings were unchanged.
The prevalence of hyperuricemia and gout is substantially and significantly greater among individuals with uncontrolled BP and additional CVD risk factors. When initiating medical therapy and in subsequent follow-up visits for hypertensive patients, particularly those harboring one or more additional CVD risk factors, health care providers should be vigilant for underlying hyperuricemia and risk of gout.