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作 者:杜晨露 王清华[3] 朱慧敏[4] 焦夏 梁琦晨 左力[1] DU Chen-lu;WANG Qing-hua;ZHU Hui-min;JIAO Xia;LIANG Qi-Chen;ZUO Li(Department of Nephrology,Peking University People’s Hospital,Beijing 100044,China;Department of Nephrology,Yuncheng Tongde Hospital,Shanxi 044000,China;Department of Nephrology,Shanxi Provincial People’s Hospital,Shanxi 030000,China;Department of Nephrology,Tianjin Fifth People's Hospital,Tianjin 300450,China)
机构地区:[1]北京大学人民医院肾内科,北京100044 [2]山西运城同德医院肾内科,山西044000 [3]山西省人民医院肾内科,山西030000 [4]天津市第五中心医院肾内科,天津300450
出 处:《中国血液净化》2023年第8期599-602,共4页Chinese Journal of Blood Purification
摘 要:目的对非透析依赖的慢性肾脏病(chronic kidney disease,CKD)患者的全段甲状旁腺激素(intact parathyroid hormone,iPTH)控制目标进行探讨。方法收集2016年3月一2022年10月在北京大学人民医院肾内科就诊的未行肾脏替代治疗的具有完整血尿生化结果的CKD患者,探讨估算的肾小球滤过率(estimated glomerular filtration rate,eGFR)、iPTH与尿磷排泄分数(fraction excretion of phosphate,FEP)之间的关系;利用R语言中的segmented函数绘制iPTH-FEP拟合曲线,查找FEP不再随着iPTH增加而增加的截断点。结果共纳入125例研究对象,当eGFR小于60 ml/(min·1.73m^(2))时,随着肾功能的下降,iPTH、FEP水平逐渐升高;当iPTH超过114.74 pg/ml后,FEP不再增加。结论当非透析依赖的CKD患者的iPTH升高到超过114.74 pg/ml时,其促进肾脏排泄磷的能力达到极限。Objective To investigate the control target of intact parathyroid hormone(iPTH)level in patients with non-dialysis-dependent chronic kidney disease(CKD).Methods The CKD patients with complete blood and urine biochemical results,not received renal replacement therapy and treated in the Outpatient/Inpatient Sections,Department of Nephrology,Peking University People's Hospital from March 2016 to October 2022 were recruited.The relationship between estimated glomerular filtration rate(eGFR),iPTH and fraction excretion of phosphate(FEP)in these patients were investigated.By using the segment function in R language,the iPTH-FEP fitting curve is depicted to find out the truncate point that FEP increases no longer with the increase of iPTH.Results A total of 125 subjects were enrolled in this study.When eGFR was<60 ml/min·1.73m^(2),iPTH and FEP levels gradually increased with the decline of renal function.When iPTH>114.74pg/ml,FEP no longer increased.Conclusion When iPTH increased to more than 114.74pg/ml in nondialysis-dependent CKD patients,the ability to promote renal excretion of phosphorus reached the maximum.
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