Hyperuricemia and Kidney Disease May Be Predictors of Subsequent Flares in Patients With Gout

Researchers examined the changes in the presentation of incident gout in the last 20 years and determined risk for subsequent gout flares after an initial gout attack.

Hyperuricemia and renal dysfunction may be important risk factors for subsequent flares in patients with gout, according to study results published in The Journal of Rheumatology.

Gout is currently the most common form of inflammatory arthritis in the United States, with studies reporting an increased burden of comorbidities in patients with gout over the last 20 years.2 In this retrospective study, the researchers investigated whether there were changes in the presentation of incident gout over the last 20 years, determined the likelihood of subsequent flares after the first attack of gout, and investigated predictors of these subsequent flares.

Incident cases of gout were identified among individuals in the Olmsted County, Minnesota in 2 time intervals that were 20 years apart (January 1, 1989 to December 31, 1992, and January 1, 2009 to December 31, 2010). Patients with incident gout who met the 1977 American Rheumatism Association preliminary criteria or the New York or Rome criteria for gout were included in the study. Data from patients with incident gout (158 in the 1989-1992 cohort and 271 in the 2009-2010 cohort) were identified, and patients were followed up for a mean of 4.2 years. Most patients were male (73%), with mean age at gout onset of 59.7±17.3 years. Both cohorts were subsequently followed up for 5 years, until death, or migration out the county. Conditional frailty models and cumulative incidence and person-year (PY) methods were used to examine risk factors for subsequent gout flares, and compare flare rates, respectively.

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Study results revealed that body mass index, and comorbidities such as kidney disease, diabetes mellitus, hypertension, and hyperlipidemia increased significantly in the 2009-2010 cohort compared with the 1989-1992 cohort; however, classic podagra decreased significantly from 74% to 59% (P <.001). In the 5-year follow-up, despite the similar cumulative incidence of the first subsequent gout flare in both cohorts (P =.70), the incidence of all subsequent flares increased from 2.8 per 10 PY (95% CI, 2.4-3.3 per 10 PY) to 3.5 per 10 PY (95% CI, 3.2-3.9 per 10 PY), with a rate ratio of 1.24, (95% CI, 1.04-1.47) in patients with gout. Comorbidities including hyperuricemia (hazard ratio [HR], 1.59; 95% CI, 1.16-2.18) and kidney disease (HR, 1.34; 95% CI, 1.12-1.61) were identified as significant predictors for subsequent flares in patients with gout.

Study limitations included dependency on nonstandardized clinical documentation and systematic differences during the retrieval of clinical information between the 2 cohorts.

Researchers concluded, “[F]indings indicate that clinicians need to maintain a high level of suspicion for gout as a possible cause of joint pain and inflammation in atypical cases of inflammatory arthritis, and to guide the decision of whether a patient should be given uric acid-lowering therapy for flare prophylaxis.”


1. Elfishawi MM, Zleik N, Kvrgic Z, Michet CJ, Crowson CS Matteson EL, et al. Changes in the presentation of incident gout and the risk of subsequent flares: A population-based study over 20 years. J Rheumatol. 2020;47(4):613-618.

2. Elfishawi MM, Zleik N, Kvrgic Z, Michet CJ, Crowson CS, Matteson EL, et al. The rising incidence of gout and the increasing burden of comorbidities: a population-based study over 20 years. J Rheumatol. 2018;45:574-579.