Rave Klaus, Nosek Leszek, Posner John, Heise Tim, Roggen Kerstin, van Hoogdalem Ewoud-Jan
Profil Institut für Stoffwechselforschung GmbH, Neuss, Germany.
Nephrol Dial Transplant. 2006 Aug;21(8):2166-71. doi: 10.1093/ndt/gfl175. Epub 2006 Apr 20.
The purpose of this study was to investigate renal glucose excretion as a function of blood glucose concentration and to evaluate the within-subject variability and between-subject variability in subjects with type 2 diabetes.
Twenty-two subjects with type 2 diabetes [age 58 (12) years, diabetes duration 7 (6) years, endogenous creatinine clearance 117 (38) ml min(-1) 1.73 m(-2); median (inter-quartile range, IQR)] underwent two five-period hyperglycaemic glucose clamp experiments at intervals of 7-21 days. Starting from an initial blood glucose level of 12.2 mmol l(-1), subsequent glucose clamp levels were chosen using an algorithm based on urinary glucose concentrations measured at the end of the preceding glucose clamp period. That is, blood glucose was either stepwise decreased or increased depending on whether urinary glucose concentration was above or below 11.1 mmol l(-1), respectively.
As expected, increasing the blood glucose from 7.8 to 13.3 mmol l(-1) during the glucose clamps resulted in a steep increase of urinary glucose excretion from 0.06 to 0.77 mmol min(-1). With decreasing blood glucose, a measurable glucosuria persisted up to a blood glucose level of 7.8 mmol l(-1). When defining the (pseudo)threshold for renal glucose excretion (PRT(G)) as the highest blood glucose level during glucose clamps associated with a concomitant glucose concentration in urine of <2.8 mmol l(-1), median (IQR) PRT(G) was 11.0 (1.1) mmol l(-1). The within-subject variability of PRT(G), i.e. the difference between two assessments, was low, 0.1 (0.0) mmol l(-1) while the between-subject variability of PRT(G) was high, ranging from 7.7 to 12.2 mmol l(-1).
Renal glucose excretion increases in a proportional manner with increasing blood glucose. When decreasing blood glucose to euglycaemic blood glucose levels, glucosuria persists so that the classical concept of a renal threshold for glucose excretion cannot be upheld in subjects with type 2 diabetes.
本研究旨在探讨肾葡萄糖排泄与血糖浓度的关系，并评估2型糖尿病患者的个体内变异性和个体间变异性。
22例2型糖尿病患者[年龄58（12）岁，糖尿病病程7（6）年，内生肌酐清除率117（38）ml·min⁻¹·1.73 m⁻²；中位数（四分位间距，IQR）]在7 - 21天的间隔内进行了两次为期五个阶段的高血糖葡萄糖钳夹实验。从初始血糖水平12.2 mmol·l⁻¹开始，后续葡萄糖钳夹水平根据前一葡萄糖钳夹期结束时测得的尿葡萄糖浓度，使用一种算法来选择。也就是说，根据尿葡萄糖浓度分别高于或低于11.1 mmol·l⁻¹，血糖要么逐步降低要么逐步升高。
正如预期的那样，在葡萄糖钳夹期间将血糖从7.8 mmol·l⁻¹提高到13.3 mmol·l⁻¹导致尿葡萄糖排泄从0.06 mmol·min⁻¹急剧增加到0.77 mmol·min⁻¹。随着血糖降低，可测量的糖尿一直持续到血糖水平7.8 mmol·l⁻¹。当将肾葡萄糖排泄（PRT(G)）的（伪）阈值定义为葡萄糖钳夹期间与尿中葡萄糖浓度<2.8 mmol·l⁻¹同时出现的最高血糖水平时，PRT(G)的中位数（IQR）为11.0（1.1）mmol·l⁻¹。PRT(G)的个体内变异性，即两次评估之间的差异较低，为0.1（0.0）mmol·l⁻¹，而PRT(G)的个体间变异性较高，范围为7.7至12.2 mmol·l⁻¹。
肾葡萄糖排泄随血糖升高成比例增加。当血糖降至正常血糖水平时，糖尿仍然存在，因此在2型糖尿病患者中不能维持经典的肾葡萄糖排泄阈值概念。
