1 Department of Endocrinology, Prince Charles Hospital, Cwm Taf University Health Board, Merthyr Tydfil, UK.
2 Department of Endocrinology, University Hospital of Wales, Cardiff and Vale University Health Board, Cardiff, UK.
Ann Clin Biochem. 2019 Jan;56(1):155-162. doi: 10.1177/0004563218797979. Epub 2018 Sep 11.
Microalbuminuria represents vascular and endothelial dysfunction. Thyroid hormones can influence urine albumin excretion as it exerts crucial effects on the kidney and on the vascular system. This study explores the relationship between serum thyrotropin and urine albumin excretion in euthyroid patients with diabetes.
A total of 433 patients with type 1 or 2 diabetes were included in this retrospective cross-sectional study. Data included anthropometric measurements and biochemical parameters from diabetes clinic. Males with urine albumin creatinine ratio >2.5 and female's >3.5 mg/mmoL were considered to have microalbuminuria.
34.9% of the patients had microalbuminuria. Prevalence of microalbuminuria increased according to TSH quartiles (26.9, 34.6, 38.5 and 44.9%, P for trend = 0.02). In a fully adjusted logistic regression model, higher TSH concentrations were associated with high prevalence of microalbuminuria (adjusted odds ratio 2.06 [95% CI: 1.14-3.72]; P = 0.02), while comparing the highest with the lowest quartile of TSH. Multiple linear regression analysis showed an independent association between serum TSH and urine albumin creatinine ratio (β = 0.007, t = 2.03 and P = 0.04). The risk of having microalbuminuria was higher with rise in TSH concentration in patients with younger age (<65 years), raised body mass index (≥25 kg/m), hypertension, type 2 diabetes and hyperlipidaemia and age was the most important determinant ( P for interaction = 0.02).
Serum TSH even in the euthyroid range was positively associated with microalbuminuria in euthyroid patients with diabetes independent of traditional risk factors. This relationship was strongest in patients with components of the metabolic syndrome.
微量白蛋白尿代表血管和内皮功能障碍。甲状腺激素可影响尿白蛋白排泄,因为它对肾脏和血管系统有重要影响。本研究探讨了甲状腺刺激素与甲状腺功能正常的糖尿病患者尿白蛋白排泄之间的关系。
这项回顾性横断面研究纳入了 433 名 1 型或 2 型糖尿病患者。数据包括糖尿病诊所的人体测量和生化参数。男性尿白蛋白肌酐比值>2.5mg/mmol,女性>3.5mg/mmol 被认为有微量白蛋白尿。
34.9%的患者有微量白蛋白尿。根据 TSH 四分位值,微量白蛋白尿的患病率增加(26.9%、34.6%、38.5%和 44.9%,趋势 P=0.02)。在完全调整的逻辑回归模型中,较高的 TSH 浓度与较高的微量白蛋白尿患病率相关(调整后的比值比 2.06[95%可信区间:1.14-3.72];P=0.02),而比较 TSH 的最高四分位值与最低四分位值。多元线性回归分析显示,血清 TSH 与尿白蛋白肌酐比值之间存在独立关联(β=0.007,t=2.03,P=0.04)。在年龄<65 岁、体重指数(BMI)升高(≥25kg/m)、高血压、2 型糖尿病和血脂异常的患者中,随着 TSH 浓度的升高,发生微量白蛋白尿的风险更高,年龄是最重要的决定因素(交互作用 P=0.02)。
即使在甲状腺功能正常范围内,血清 TSH 与甲状腺功能正常的糖尿病患者的微量白蛋白尿呈正相关,独立于传统危险因素。这种关系在代谢综合征的患者中最强。