Abstract
Hyperuricemia accompanies many pathologies that contribute to overall death rate. The population-based multifaceted study of older adults in Poland made it possible to assess the effect of serum uric acid (SUA) on overall mortality. The PolSenior study performed between 2007–2011 included 3926 participants aged 65 years or above (mean age 79 ± 9 years) not treated with xanthin oxidase inhibitors (XOI) who were stratified by sex and SUA concentration into six subgroups increasing by 1 mg/dL. In 2019, survival data were retrieved from the population register. The crude risk of death was significantly higher in men and women with SUA ≥ 7 mg/dL. After adjustment to statistically significant factors, SUA remained a risk factor of death in men with SUA ≥ 8 mg/dL only, potentially due to the limited number of women with high SUA levels. Furthermore, age, heart failure, diabetes, and activities of daily living ≤ 4 pts were identified as factors increasing mortality risk regardless of sex. The risk of death increased also with smoking, past stroke, COPD/asthma, and hs-CRP > 3 mg/dL for men; and eGFR < 45 mL/min/1.73 m2, mini nutritional assessment ≤ 7 pts, and loop diuretics use for women. Mild hyperuricemia is a significant health status marker and an independent risk factor for overall mortality in older Caucasians not receiving XOI. Increased mortality is mostly limited to subjects with SUA levels ≥ 8 mg/dL.
Highlights
Uric acid (UA) has been a subject of medical interest for many years
Results similar to Japanese and Taiwanese data were obtained by the authors of a study examining the effect of serum uric acid (SUA) on mortality in the Irish adult population (>18 years old) [43]
Increased mortality rate in the group with the lowest SUA levels was explained by the highest incidence of malnutrition (11.4% and 21.1% in men and women, respectively) and a high incidence of dependency in activities of daily living, resulting in low ADL scores among these patients
Summary
Uric acid (UA) has been a subject of medical interest for many years. The prevalence of hyperuricemia ranges between 5–16% in the general populations of Western Europe, reaching 85% of the Marshall Islands population [1,2]. Hyperuricemia is caused by an increased production and/or a reduced elimination of UA Both these processes can be altered by the lifestyle (eating habits, alcohol intake, physical activity), comorbidities (obesity, metabolic syndrome, chronic kidney disease, myelo- and lymphoproliferative diseases) and medications (diuretics, aspirin, urate-lowering therapy (ULT), oncological treatment) [14]. SUA concentration is determined by the expression of genes encoding UA transporters in the kidneys and intestine [15]. Variations of these genes in the form of risk alleles favor a higher rate of hyperuricemia and occur more frequently in Chinese, Japanese, Africans in Southwest USA, and Mexicans compared to Europeans [16]
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