Abstract
BackgroundSerum uric acid (SUA) is associated with the development of diabetic kidney disease (DKD). Thyroid hormones can regulate metabolism and insulin resistance. The relationship between SUA and thyroid function in patients with DKD is still uncertain. In current study, we aimed to investigate the association between thyroid stimulating hormone (TSH) and SUA in type 2 diabetic patients with early-stage DKD.MethodsTwo hundred fifty-four type 2 diabetic patients with early-stage DKD were enrolled in current study and were further classified as high SUA group (SUA level > 420 μmol/L in males or > 360 μmol/L in females, n = 101) and normal SUA group (SUA level ≤ 420 μmol/L in males or ≤ 360 μmol/L in females, n = 153). Eighty-five control subjects were recruited as control group. The clinical characteristics were obtained via face-to-face surveys and medical records.ResultsCompared with normal SUA group and control group, high SUA group exhibited the increased SUA level, and the decreased TSH level (P < 0.017 for all), and no significant difference was detected in SUA and TSH between normal SUA group and control group. TSH was negatively associated with SUA (r = − 0.35, P < 0.001) in type 2 diabetic participants with early-stage DKD. Furthermore, the decreased TSH level was independently correlated with higher SUA level (β = − 25.69, P < 0.001), and retained a significant association with hyperuricemia (odds ratio = 1.73, P = 0.002) after adjusting for confounding factors in type 2 diabetic patients with early-stage DKD.ConclusionsTSH is negatively correlated with SUA, and decreased TSH is an independent risk factor for hyperuricemia in type 2 diabetic patients with early-stage DKD. These results indicate that thyroid hormones, TSH in particular, might participate in regulating uric acid metabolism in patients with early-stage DKD.
Highlights
Serum uric acid (SUA) is associated with the development of diabetic kidney disease (DKD)
A significant trend was observed for body mass index (BMI), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), TG, fasting blood glucose (FBG), Glycated hemoglobin (HbA1c), fasting insulin (FINS), homeostasis model assessment of insulin resistance (HOMA-IR), CR, estimated glomerular filtration rate (eGFR), urinary albumin-to-creatinine ratio (UACR), Free thyroxine (FT4), thyroid stimulating hormone (TSH) and SUA in three groups (P < 0.01 for all)
The levels of BMI, TG, FBG and HOMA-IR were significantly elevated in normal SUA group than those in control group (P < 0.017 for all), and no significant difference was detected in CR, eGFR and FT4 between normal SUA group and control group (P > 0.017 for all)
Summary
Serum uric acid (SUA) is associated with the development of diabetic kidney disease (DKD). We aimed to investigate the association between thyroid stimulating hormone (TSH) and SUA in type 2 diabetic patients with early-stage DKD. Diabetic kidney disease (DKD), one of the major microvascular complications of diabetes, is the main cause of end-stage renal disease and is associated with high morbidity and mortality. The increased serum uric acid (SUA) has been reported to be correlated with the progression of insulin resistance [2], metabolic (2021) 21:1 syndrome [3], and T2DM [4]. SUA has been documented to cause the development of microvascular diseases and thereby renal injury in DKD by several reported effects, including inducing the endothelial dysfunction [5], causing the inflammatory cascades [6], activating the profibrotic cytokine [7], and increasing the activity of the renin-angiotensin aldosterone system [6]. The elevated SUA has been regarded as one of the major predictors of DKD [9]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
