草酸盐肾病引起的急性肾损伤（acute kidney injury，AKI）是临床上AKI长期容易被忽视的原因之一。该文报道经肾活检确诊的继发性草酸盐肾病并发急性肾损伤2例，经积极治疗后患者肾功能恢复。该文复习了草酸盐肾病相关文献，以期提高临床医师对草酸盐肾病的认识。

目的:分析无锡地区2 529例泌尿系结石标本的结石成分，为泌尿系结石的临床预防和治疗提供参考。方法:回顾性分析2009年3月至2021年10月在江苏无锡地区收集的2 529例泌尿系结石标本，采用红外光谱分析法分析结石成分，并结合患者的临床资料进行分析。结果:共检测出19种结石成分，其中单一成分结石9种，共990例；混合成分结石10种，共1 539例。单一成分结石以草酸钙为主，共840例；混合成分结石以草酸钙＋碳酸磷灰石为主，共1 335例。草酸钙类和尿酸类结石中男性患者的发生率高于女性患者；而在感染性结石中，女性患者的发生率高于男性患者(均 P<0.05)。36～60年龄段的结石发病人数最多。在各个年龄段中，发生率最高的结石成分为草酸钙类。尿酸类结石在61～86年龄段的发病率较其他年龄段高，差异均有统计学意义(均 P<0.05)。在各个不同部位，发生率最高的结石成分为草酸钙类。尿酸类结石在膀胱中的发生率明显高于其他部位，差异均有统计学意义(均 P<0.05)。在各个不同年龄段中，上尿路结石的发生率明显高于下尿路结石。膀胱结石在61～86年龄段的发生率最高，与其他年龄段比较，差异均有统计学意义(均 P<0.05)。 结论:无锡地区泌尿系结石成分主要以草酸钙类结石为主，草酸钙类结石在不同性别、年龄和部位分布存在差异，对于泌尿系结石的临床预防和治疗有重要的参考价值。

Oxalate is an organic dicarboxylic acid that is a common component of plant foods.The kidneys are essential organs for oxalate excretion,but excessive oxalates may induce kidney stones.Jupiter micro-tubule associated homolog 2(JPT2)is a critical molecule in Ca2+mobilization,and its intrinsic mecha-nism in oxalate exposure and kidney stones remains unclear.This study aimed to reveal the mechanism of JPT2 in oxalate exposure and kidney stones.Genetic approaches were used to control JPT2 expression in cells and mice,and theJPT2 mechanism of action was analyzed using transcriptomics and untargeted metabolomics.The results showed that oxalate exposure triggered the upregulation of JPT2,which is involved in nicotinic acid adenine dinucleotide phosphate(NAADP)-mediated Ca2+mobilization.Tran-scriptomic analysis revealed that cell adhesion and macrophage inflammatory polarization were inhibited by JPT2 knockdown,and these were dominated by phosphatidylinositol 3-kinase(PI3K)/AKT signaling,respectively.Untargeted metabolomics indicated that JPT2 knockdown inhibited the produc-tion of succinic acid semialdehyde(SSA)in macrophages.Furthermore,JPT2 deficiency in mice inhibited kidney stones mineralization.In conclusion,this study demonstrates that oxalate exposure facilitates kidney stones by promoting crystal-cell adhesion,and modulating macrophage metabolism and in-flammatory polarization via JPT2/PI3K/AKT signaling.