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·1.73m2)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·1.73m2, 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 non-dialysis-dependent CKD patients, the ability to promote renal excretion of phosphorus reached the maximum.
[1]Streja E, Lau WL, Goldstein L,et al.Hyperphosphatemia is a combined function of high serum PTH and high dietary protein intake in dialysis patients. Kidney Int Suppl(2011).2013 Dec; 3(5):462-468.
[2]国家肾脏疾病临床医学研究中心.中国慢性肾脏病矿物质和骨异常诊治指南概要[J].肾脏病与透析肾移植杂志, 2019, 28(1):27-57
[3]Evenepoel P, Bover J, Urena Torres P.Parathyroid hormone metabolism and signaling in health and chronic kidney disease[J].Kidney Int, 2016, 90(6):1184-1190
[4]张昆, 路燕燕, 刘熹, 余晨.血磷正常的慢性肾脏病患者矿物质骨代谢异常的相关性因素分析[J].世界临床医学, 2018, 12(1):1-3
[5]Craver L，Marco MP，Martinez I, et al.Mineral metabolism parameters throughout chronic kidney disease stages 1-5-achivevement of KDOQI target ranges[J].Nephrol Dial Transplant, 2007, 22(4):1171-1176
[6]Vassalotti JA, Uribarri J, Chen SC, et al.Trends in mineral metabolism:Kidney Early Evaluation Program(KEEP) and the National Health and Nutrition Examination Survey (NHANES)1999-2004[J].Am J Kidney Dis, 2008, 51(4 Suppl 2):S56-58
[7]Fukagawa M, Yokoyama K, Koiwa F, et al.Clinical practice guideline for the management of chronic kidney disease-mineral and bone disorder[J].Ther Apher Dial, 2013, 17(3):247-288
[8]Fukagawa M, Kazama J, Shigematsu T.Skeletal resistance to PTH as a basic abnormality underlying uremic bone diseases[J].American Journal of Kidney Diseases, 2001, 38(4):S152-S155
[9]高志红.钙、磷、镁的代谢[J].中国医刊, 2002, 37(11):6-7
