Kong Xianglei, Ma Xiaojing, Zhang Chengyin, Su Hong, Xu Dongmei
Department of Nephrology, Qianfoshan Hospital, Shandong University, No. 16766, Jingshi Road, Jinan, 250014, People's Republic of China.
Department of Health Examination Center, Qianfoshan Hospital, Shandong University, No. 16766, Jingshi Road, Jinan, 250014, People's Republic of China.
Int Urol Nephrol. 2017 Apr;49(4):661-667. doi: 10.1007/s11255-016-1452-3. Epub 2016 Nov 7.
Patients either with hyperhomocysteinemia or chronic kidney disease (CKD) have an increased risk of cardiovascular disease. Little is known regarding whether hyperhomocysteinemia can increase the risk of CKD in a Chinese middle-aged and elderly population. To help clarify this we conducted a prospective cohort study to measure the association of hyperhomocysteinemia with CKD.
A total of 5917 adults aged 56.4 ± 9.6 years without CKD at baseline were enrolled. The highest homocysteine quartile (≥15 μmol/L) was defined as hyperhomocysteinemia. CKD was defined as decreased estimated glomerular filtration rate (eGFR < 60 mL/min/1.73 m) or presence of proteinuria (urine protein ≥ 1+) assessed using a repeated dipstick method.
During 3 years of follow-up, 143 (2.4%) patients developed CKD, 85 (1.4%) patients with proteinuria and 59 (1.0%) patients with decreased eGFR. After adjusted for potential confounders, both homocysteine (per 1 μmol/L increase) and hyperhomocysteinemia were independently associated with increased risk of decreased eGFR [with a fully adjusted OR of 1.07 (95% CI 1.04-1.10) and 3.05 (95% CI 1.71-5.46)] and CKD [with a fully adjusted OR of 1.04 (95% CI 1.02-1.07) and 1.62 (95% CI 1.11-2.35)], respectively. By contrast, neither homocysteine (per 1 μmol/L increase) nor hyperhomocysteinemia were associated with proteinuria in the multivariable logistic regression analysis.
The study revealed that hyperhomocysteinemia increases the risk of decreased eGFR. This suggests that homocysteine could be considered as a useful molecular markers for delaying the development of CKD.
高同型半胱氨酸血症患者或慢性肾脏病（CKD）患者发生心血管疾病的风险增加。关于在中国中老年人群中，高同型半胱氨酸血症是否会增加CKD风险，目前知之甚少。为了阐明这一点，我们进行了一项前瞻性队列研究，以测量高同型半胱氨酸血症与CKD之间的关联。
共纳入5917名年龄在56.4±9.6岁、基线时无CKD的成年人。同型半胱氨酸最高四分位数（≥15μmol/L）定义为高同型半胱氨酸血症。CKD定义为使用重复试纸法评估的估计肾小球滤过率降低（eGFR<60mL/min/1.73m²）或存在蛋白尿（尿蛋白≥1+）。
在3年的随访期间，143名（2.4%）患者发生了CKD，85名（1.4%）患者出现蛋白尿，59名（1.0%）患者eGFR降低。在调整潜在混杂因素后，同型半胱氨酸（每增加1μmol/L）和高同型半胱氨酸血症均分别与eGFR降低风险增加独立相关[完全调整后的OR分别为1.07（95%CI 1.04-1.10）和3.05（95%CI 1.71-5.46）]以及CKD风险增加独立相关[完全调整后的OR分别为1.04（95%CI 1.02-1.07）和1.62（95%CI 1.11-2.35）]。相比之下，在多变量逻辑回归分析中，同型半胱氨酸（每增加1μmol/L）和高同型半胱氨酸血症均与蛋白尿无关。
该研究表明，高同型半胱氨酸血症会增加eGFR降低的风险。这表明同型半胱氨酸可被视为延缓CKD进展的有用分子标志物。
