Abstract
Background: Elevated uric acid (UA) is a recognized risk factor for chronic kidney disease (CKD). This study aimed to investigate whether this association exists in dyslipidemic patients receiving multifactorial treatment.
Methods: An observational study conducted in Greece including 1,269 dyslipidemic individuals followed-up in a lipid clinic for ≥3 years. Estimated glomerular filtration rate (eGFR) was calculated by CKD-EPI equation and CKD was defined as ≤60 mL/min/1.73 m2. The correlation was assessed between UA levels and the CKD risk after adjusting for potential confounding factors, after defining the following UA quartiles: Q1: < 4, Q2: 4–5, Q3: 5–6, and Q4: > 6 mg/dL.
Results: After excluding patients with baseline eGFR <60 mL/min/1.73 m2, gout and those taking UA-lowering drugs, 1,095 individuals were eligible; of those, 91% and 69% were treated with statins and anti-hypertensive drugs, respectively. During their follow-up (6 years; IQR = 4–10), 11.9% of the subjects developed CKD, whereas the median annual eGFR decline was 0.69 mL/min/1.73 m2 (IQR = 0.45–2.33). Multivariate analysis showed that baseline UA levels (HR = 1.26; 95% CI = 1.09–1.45, p = .001), female gender (HR = 1.74; 95% CI = 1.14–2.65, p = .01), age (HR = 1.10; 95% CI = 1.07–1.12, p < .001), diabetes (HR = 1.67; 95% CI = 1.05–2.65, p = .03), cardiovascular disease (HR = 1.62; 95% CI = 1.02–2.58, p = .04), decreased baseline renal function (eGFR <90 mL/min/1.73 m2) (HR = 2.38; 95% CI = 1.14–4.81, p = .02), and low-density lipoprotein cholesterol reduction (HR = 0.995; 95% CI = 0.991–0.998, p = .01) were associated with incident CKD. Additionally, patients with UA ≥6 mg/dL exhibited a higher risk of incident CKD compared with those in the lowest UA quartile (HR = 2.01; 95% CI = 1.11–3.65, p = .02).
Conclusion: Higher UA levels are correlated with a higher risk of incident CKD in dyslipidemic individuals taking multifactorial treatment.
Transparency
Declaration of funding
There was no support/funding for the present study.
Declaration of financial/other relationships
The authors have received no payment in preparation of this manuscript and declare conflicts of interest outside the submitted work. FB reports personal fees from Amgen, Boehringer Ingelheim, and Sanofi. EL reports personal fees from AstraZeneca, Amgen, MSD, and Sanofi, Dr. R. Kalaitzidis reports personal fees from Sanofi. GL reports personal fees from Angelini, Bayer, Menarini, and Sanofi. ME reports personal fees from Astra Zeneca, grants and personal fees from MSD, personal fees from Pfizer, personal fees and non-financial support from Abbott, personal fees and non-financial support from Sanofi, non-financial support from Boehringer Ingelheim, personal fees and non-financial support from Eli Lilly, non-financial support and other from GSL, outside the submitted work. CMRO peer reviewers on this manuscript have no relevant financial or other relationships to disclose.