2型糖尿病患者血清尿酸与原发性高血压、进行性蛋白尿和肾功能损害的关系

Aziz Kma
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摘要

2型糖尿病是一种代谢紊乱,有很多并发症。尿酸(UA)最近被发现是2型糖尿病发展的风险生物标志物。一些研究发现高尿酸血症与高血压(HTN)、肾脏并发症和心血管疾病有显著关联。然而,没有研究发现高尿酸血症与2型糖尿病患者的原发性高血压、肾病和糖尿病肾病(DKD)的发展有关。此外,过去没有研究发现血清尿酸对于糖尿病患者DKD/CKD发展具有敏感性和特异性的截断点,本研究实现了这一点。我们以横断面回顾性的方式收集了超过15年的10300例2型糖尿病患者的数据。17%为高尿酸血症,16%为DKD。血清UA与其他变量(血清肌酐、收缩压和舒张压、微量白蛋白和斑点尿蛋白)存在显著相关性。在HTN、肾病和DKD患者中UA水平升高(p<0.0001)。同样,高尿酸血症组血清肌酐、收缩压和舒张压、微量白蛋白尿和斑点尿蛋白均高于对照组(p<0.0001)。Pearson 's (χ²)和logistic回归显示高尿酸血症与HTN显著相关(比值比2.5;95% CI 1.8 ~ 23.4;p < 0.0001)。同样,高尿酸血症与肾病和DKD/CKD的发展显著相关;优势比2.1 (95% CI 1.46 ~ 2.8;p<0.0001)和27.3 (95% CI 14 ~ 53;分别为p < 0.0001)。此外,血清UA与血清肌酐的回归模型也相互显著相关,证明了我们的假设,即UA线性导致血肌酐升高,关系如下:血清肌酐=0.221 + [0.154 ×血清UA]。DKD和血清UA的ROC结果显示,AUC为0.98 (95% CI 0.961 ~ 0.986), UA水平为6.8时,DKD/CKD的敏感性为91%,特异性为79%,且与DKD/CKD显著相关(p<0.0001)。这是同类研究中首次证明UA与HTN、肾病和DKD有显著关联。是时候修改2型糖尿病患者的正常尿酸水平,并开始定期筛查高尿酸血症,以防止进一步的糖尿病并发症。
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Involvement of Serum Uric Acid in Essential Hypertension, Progressive Proteinuria and Impairment in Renal Function among Type-2 Diabetic Patients
Type-2 diabetes is a metabolic disorder with vast complications. Uric acid (UA) was recently discovered as a risk biomarker for the development of type-2 diabetes. Several studies have found a significant association of Hyperuricemia with Hypertension (HTN), renal complications and cardiovascular disease. However, no study has found an association of hyperuricemia with the development of essential hypertension, nephropathy and Diabetic Kidney Disease (DKD) among type-2 diabetics. Moreover, in the past no study has found cut off points for serum uric acids for the development of DKD/CKD among diabetics with sensitivity and specificity, which was achieved in the current study. We collected 10,300 type-2 diabetics data for more than 15 years in a cross sectional retrospective manner. 17% demonstrated hyperuricemia while 16% were found to be DKD. Significant correlations were found between serum UA and other variables (serum creatinine, systolic and diastolic BP, microalbumin and spot urine protein). Levels of UA were observed to be elevated among patients with HTN, nephropathy and DKD (p<0.0001). Similarly, serum creatinine, systolic and diastolic BP, microalbuminuria and spot urine protein were higher for the group with hyperuricemia (p<0.0001). Pearson’s (χ²) and logistic regression with odds ratio demonstrated that hyperuricemia was significantly associated with HTN (odds ratio 2.5; 95% CI 1.8 to 23.4; p<0.0001). Similarly, hyperuricemia was significantly associated with the development of nephropathy and DKD/CKD; odds ratio 2.1 (95% CI 1.46 to 2.8; p<0.0001) and 27.3 (95% CI 14 to 53; p<0.0001), respectively. Moreover, regression model between serum UA and serum creatinine was also significantly associated with each other and proves our hypothesis that UA linearly causes an increase in the blood creatinine with the following relationship : Serum creatinine=0.221 + [0.154 × serum UA]. ROC for DKD and serum UA demonstrated that with AUC of 0.98 (95% CI 0.961 to 0.986), UA level of 6.8 was 91% sensitive and 79% specific for the development and significant association with DKD/CKD (p<0.0001). This is the first study of its kind that has demonstrated significant associations of UA with HTN, nephropathy and DKD. It is the time to revise the normal levels of UA among type-2 diabetics and to initiate regular screening for hyperuricemia to prevent further diabetes complications.
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