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计算得出的胰岛素抵抗与高危结石患者结石形成的尿液代谢变化及更大的结石负荷相关。

Calculated insulin resistance correlates with stone-forming urinary metabolic changes and greater stone burden in high-risk stone patients.

作者信息

Tran Timothy Y, Flynn Mary, O'Bell John, Pareek Gyan

出版信息

Clin Nephrol. 2016 Jun;85(6):316-20. doi: 10.5414/CN108832.

DOI:10.5414/CN108832
PMID:27125629
Abstract

AIMS

Metabolic syndrome and diabetes are associated with nephrolithiasis. Proposed mechanisms of lithogenesis include insulin resistance causing low urine pH and hyperinsulinemia leading to hypercalciuria. Herein, we sought to determine whether insulin resistance was associated with differences in stone burden and lithogenic changes on 24-hour urine samples.

MATERIALS AND METHODS

All patients that underwent comprehensive metabolic workup including 24-hour urine samples and fasting insulin levels were included. Insulin resistance was defined as a homeostasis model assessment of insulin resistance value > 5 (HOMA-IR = (glucose×insulin)/405). Patients on active metabolic therapy were excluded or the 24-hour urine sample predating treatment was utilized for analysis. Stone burden was determined by totaling the maximal diameter of all stones noted on CT.

RESULTS

18 of 30 patients (60.0%) had HOMA-IR > 5. Among patients with calculated insulin resistance, stone burden was greater (17.6 mm vs. 6.3 mm, p = 0.002) and 24-hour urine samples revealed higher urine calcium (293 mg/d vs. 159 mg/d, p = 0.02) and lower urine pH and citrate (454 mg/d vs. 639 mg/d, p = 0.04 and 5.83 vs. 6.33, p = 0.04, respectively).

CONCLUSIONS

Previous studies have demonstrated a correlation between metabolic syndrome, diabetes, and nephrolithiasis. This report demonstrates a quantitative increase in stone burden among patients with calculated insulin resistance. The pathway for this greater stone burden may be related to the urinary metabolic changes noted among patients with insulin resistance. In the future, targeting reduction of fasting insulin levels may represent a key element of stone disease prevention.

摘要

目的

代谢综合征和糖尿病与肾结石有关。推测的结石形成机制包括胰岛素抵抗导致尿液pH值降低以及高胰岛素血症导致高钙尿症。在此,我们试图确定胰岛素抵抗是否与24小时尿液样本中结石负荷和致石性变化的差异有关。

材料与方法

纳入所有接受全面代谢检查的患者,包括24小时尿液样本和空腹胰岛素水平。胰岛素抵抗定义为稳态模型评估的胰岛素抵抗值>5(HOMA-IR =(血糖×胰岛素)/405)。正在接受积极代谢治疗的患者被排除,或使用治疗前的24小时尿液样本进行分析。结石负荷通过计算CT上所有结石的最大直径总和来确定。

结果

30例患者中有18例(60.0%)HOMA-IR>5。在计算出有胰岛素抵抗的患者中,结石负荷更大(17.6 mm对6.3 mm,p = 0.002),24小时尿液样本显示尿钙更高(293 mg/d对159 mg/d,p = 0.02),尿pH值和柠檬酸盐更低(分别为454 mg/d对639 mg/d,p = 0.04;5.83对6.33,p = 0.04)。

结论

先前的研究已证明代谢综合征、糖尿病与肾结石之间存在相关性。本报告显示,计算出有胰岛素抵抗的患者结石负荷有定量增加。这种更大结石负荷的途径可能与胰岛素抵抗患者中观察到的尿液代谢变化有关。未来,针对降低空腹胰岛素水平可能是预防结石疾病的关键因素。

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