目的　研究肾组织钠 /二羧基转运蛋白 1(hNaDC1)表达变化与肾结石发病的的关系。方法　 85例肾结石患者分为、尿枸橼酸正常结石组和低枸橼酸尿结石组。并设 5 0例对照为非结石患者。采用RT PCR及Northern印迹法检测其中部分肾结石患者肾组织的hNaDC1mRNA水平 ;免疫组化检测hNaDC1蛋白表达的变化 ;常规生化方法测定血、尿枸橼酸、草酸等生化指标。结果　低枸橼酸尿结石组结石复发率 (36 .1% ) ,显著高于尿枸橼酸正常结石组 (16 .3% ,P <0 .0 1)。hNaDC1mRNA在正常肾组织中有表达 ,分布于近端肾小管刷状缘 ;低枸橼酸尿结石患者hNaDC1mRNA/18sRNA比值 (0 .6 5± 0 .2 1)显著高于对照组 (0 .36± 0 .11,P <0 .0 1) ;而尿枸橼酸正常结石患者 (0 .4±0 .13)与对照组比较差异无显著意义 (P >0 .0 5 ) ;低枸橼酸尿结石组hNaDC1蛋白表达也显著高于对照组及尿枸橼酸正常结石组 (P <0 .0 1) ,而后两组间差异无显著意义 (P >0 .0 5 )。低枸橼酸尿结石组尿pH值、尿钠水平显著低于尿枸橼酸正常结石组和对照组 ;尿钙、尿草酸水平均显著高于对照组 ,与尿枸橼酸正常结石组无显著差异。结论　肾组织hNaDC1表达上调可能是低枸橼酸尿的重要原因 ,与肾结石的形成和复发存在某种内在联系 Objective To investigate the relationship between the expression of sodium / dicotransporter 1 (hNaDC1) and the pathogenesis of kidney stones in renal tissues. Methods Eighty-five patients with nephrolithiasis were divided into two groups: normal urine citrate group and low citrate urine stone group. And set 50 cases of non-control patients with stones. RT-PCR and Northern blotting were used to detect hNaDC1mRNA in renal tissues of patients with renal calculi. The expression of hNaDC1 protein was detected by immunohistochemistry. Biochemical indexes such as blood, urine citrate and oxalic acid were determined by routine biochemical methods. Results The recurrence rate of stones in low citrate urolith (36.1%) was significantly higher than that in urinary citrate normal stone (16.3%, P <0.01). The expression of hNaDC1mRNA in normal renal tissue was distributed in the brush border of proximal tubule. The hNaDC1mRNA / 18sRNA ratio (0.65 ± 0.21) in patients with low citrate urolithiasis was significantly higher than that in control group (0.36 ± 0.11, P <0.01). There was no significant difference between the normal urinary citrate patients (0.4 ± 0.13) and the control group (P> 0.05) The expression of hNaDC1 protein in aciduria group was also significantly higher than that in control group and normal urine citrate group (P <0.01), but there was no significant difference between the two groups (P> 0.05). Urinary calcium and urinary oxalate levels were significantly lower in the patients with low citrate urolithiasis than those in the normal urines with citric acid and controls Significant differences. Conclusion The upregulation of hNaDC1 in renal tissue may be an important reason for low citrate aciduria, and there is some intrinsic connection with the formation and recurrence of kidney stones