慢性肾脏病患者维生素D3水平变化及其相关因素分析

目的:分析慢性肾脏病(CKD)患者活性维生素D3水平变化及其相关因素。方法:检测2013年4月~2014年6月本院新诊断的143例非透析CKD患者及19例同期健康体检者维生素D3水平,分析其与肾功能、成纤维细胞生长因子23(血FGF-23)、血钙、血磷、甲状旁腺素(PTH)等指标的关系。结果:CKD1~5期患者维生素D3水平分别为(22.03±4.39)ng/ml、(20.29±4.66)ng/ml、(16.88±3.00)ng/ml、(13.71±2.99)ng/ml、(9.76±2.97)ng/ml,与对照组(25.68±4.08)ng/ml相比,各组间维生素D3水平逐渐下降(P<0.05)。维生素D3水平与血肌酐(r=-0.676)、尿素氮(r=-0.554)、血磷(r=-0.248)、钙磷乘积(r=-0.178)、PTH(r=-0.636)、FGF-23(r=-0.690)呈负相关(P<0.05),与血钙(r=0.157)、白蛋白(r=0.164)、肾小球滤过率e GFR(r=0.759)呈正相关(P<0.05),多元逐步回归分析显示维生素D3与e GFR呈正相关,与PTH呈负相关。回归方程为Y=13.196+0.092X1-0.016X2(Y为维生素D3,X1为e GFR,X2为PTH,13.196为常数)。结论:随着CKD的进展,患者活性维生素D3缺乏日益严重,且与钙磷代谢紊乱、继发性甲旁亢及FGF-23升高相关。     

成纤维细胞生长因子-23与慢性肾病患者钙磷代谢的相关性研究

目的：检测CKD3～5期患者血中成纤维细胞生长因子23（FGF-23）水平,探讨FGF-23与钙磷代谢的关系。方法：采用酶联免疫分析法（ELISA）对108例CKD3～5慢性肾脏疾病患者及20例健康志愿者进行血清全段FGF-23测定,同时测定血清25（OH）D3、iPTH、血清肌酐（Scr）、血钙（Ca2＋）、磷（P3-）、碱性磷酸酶（ALP）、血红蛋白（Hb）、白蛋白（Alb）、C反应蛋白等指标。观察各期患者以上指标的变化,及其与FGF-23的关系。结果：（1）CKD各组患者血清FGF-23水平均显著高于对照组。CKD各期FGF-23水平逐步升高,组间差异有统计学意义。（2）Pearson相关分析结果显示：非透析组血清FGF-23水平与肌酐清除率、血红蛋白、校正血钙、血磷存在显著负相关关系（P〈0.01）;与钙磷乘积、全段甲状旁腺激素（P〈0.01）和白蛋白（P〈0.05）存在直线正相关关系。透析组血清FGF-23水平与全段甲状旁腺激素及C-反应蛋白（P〈0.01）存在正相关关系。（3）非透析组多元回归结果显示：血磷、iPTH、肌酐清除率是血清FGF-23水平的独立相关因素,其回归方程为：Y（FGF-23）=1.700＋0.106（P）＋0.048（LogPTH）-0.003（Ccr）。透析组PTH、CRP是影响FGF-23的主要变量。结论：CKD患者血FGF-23明显升高,血磷和甲状旁腺激素可能是CKD患者血FGF-23水平的调节因子。     

慢性肾脏疾病3～5期矿物质异常的横断面研究

目的了解湖北地区慢性肾脏疾病（chronic kidney diseases,CKD）3～5期患者矿物质代谢异常的现状及影响因素,为非透析CKD3～5期矿物质及骨代谢紊乱的患者提供诊治依据。方法将湖北省中医院肾内科门诊及住院的123例CKD3～5期患者分为3组（根据肾小球滤过率分组：CKD3组、CKD4组、CKD5组）,比较CKD患者的血钙、血磷、钙磷乘积、碱性磷酸酶（alka—linephos phatase,ALP）、全段甲状旁腺素（immunoreactive parathyroid hormone,iPTH）水平,并评估继发性甲状旁腺功能亢进的发病率及其相关影响因素。结果患者血钙、血磷、钙磷乘积、ALP及iPTH水平在CKD3～5期之间比较均有统计学差异（P〈0．01,P〈0．001）。随着CKD病程的进展,血钙逐渐下降,血清磷、钙磷乘积及iPTH水平逐渐上升。根据统计结果,CKD5期血钙水平较CKD3、4期明显下降（P〈0．05,P〈O．001）,CKD5期患者的钙磷乘积、ALP水平比CKD3、4期明显升高（P〈0．01,P〈O．001）,CKD3期患者血清磷、钙磷乘积及iPTH水平与CKD4期相比有显著统计学差异（P〈0．05,P〈O．001）,而CKD3期和CKD4期患者的血钙、ALP水平无显著差异（P〉0．05）。以iPTH为因变量,性别、年龄、病程、血钙、血磷、钙磷乘积、ALP和肾小球滤过率（glomerularfiltrationrate,GFR）为自变量线性相关分析,结果提示iPTH水平与血钙、GFR成负相关（P〈0．001）、与血磷、ALP成正相关（P〈0．01）,与钙磷乘积无相关性,再次基础上做多元相关回归分析,结果显示相关回归系数R：0．51,血钙、ALP、GFR是iPTH升高的独立相关因素（P〈0．01和P〈O．001）。结论CKD患者的钙磷代谢紊乱在疾病的早期即存在,且随疾病的进展而不断加重。继发性甲状旁腺功能亢进的发病与CKD进程、血钙及ALP有密切关系。     

糖尿病肾病患者血清BMP2、BMP7水平与钙磷代谢的关系

目的探讨糖尿病肾病患者血清骨形态蛋白-2(BMP2)、骨形态蛋白-7(BMP7)水平与钙磷代谢的关系。方法选取2016年11月至2018年11月西电集团医院收治的126例糖尿病肾病患者作为研究组,采用系统性回顾性分析法分析研究组临床资料,根据不同分期阶段慢性肾脏病(CKD)将患者分为5组,分别为CKD 1组22例、CKD 2组21例、CKD 3组27例、CKD 4组31例、CKD 5组25例,另选取36例同期于西电集团医院门诊体检的健康人群作为对照组,测定患者血清BMP2、BMP7、血磷、血钙、肌酐(Scr)、甲状旁腺激素(iPTH),分析血清BMP2、BMP7与钙磷代谢的关系。结果①对照组与CKD 1~2期在血磷、血钙、Scr、iPTH、BMP2、BMP7水平之间差异无明显统计学意义(P>0.05);与对照组比较,CKD 4期以后血钙及血清BMP7水平明显降低(P<0.05);CKD 3期以后血清Scr、iPTH、BMP2水平明显开始升高、血清BMP7水平明显开始降低(P<0.05);CKD 4期以后血磷、Scr、iPTH、BMP2水平明显升高,血钙、BMP7水平明显降低;CKD 5期的变化情况同CKD 4期;②经Pearson积差相关分析,血清BMP2与血磷、Scr及iPTH呈正相关,与血钙呈负相关(P<0.05);BMP7与血钙呈正相关,与血磷、Scr及iPTH呈负相关(P<0.05);③经多因素多元逐步回归分析,血磷、血钙、Scr及iPTH均为影响糖尿病肾病患者血清BMP2、BMP7水平的相关因素(P<0.05)。结论CKD 3期以后血清BMP2开始升高、BMP7开始降低,且血清BMP2与血钙呈明显负相关,BMP7与血磷、Scr及iPTH呈明显负相关;钙磷代谢情况可能是糖尿病肾病患者血清BMP2升高、BMP7降低的重要相关因素。     

腹膜透析患者成纤维细胞生长因子23与骨代谢的关系

目的 探讨腹膜透析患者成纤维细胞生长因子23（FGF-23）与钙磷代谢及骨密度的关系。 方法 研究对象为中南大学湘雅医院持续性不卧床腹膜透析（CAPD）患者59例,按照世界卫生组织骨密度评分标准将CAPD患者分为骨质正常、骨质降低、骨质疏松3组,另设健康对照组30例。酶联免疫吸附法检测FGF-23、1,25（OH）2VitD3;免疫化学发光法检测甲状旁腺激素（PTH）;自动生化分析仪测量血钙（Ca）、磷（P）;双能X射线吸收仪测量骨密度（BMD）。 结果 CAPD患者股骨颈部位的骨质疏松率为23.7%,腰椎部位的骨质疏松率为35.6%。3组间FGF-23水平差异无统计学意义,但CAPD组FGF-23水平显著高于健康对照组（P ＜ 0.01）。Pearson相关分析显示log[FGF-23]与血磷呈正相关（r = 0.604,P ＜ 0.01）;与肾小球滤过率（GFR）、1,25（OH）2VitD3呈负相关（r = -0.651,P ＜ 0.01;r = -0.401,P ＜ 0.05）;与 PTH、Ca、T值、透析龄无相关。 结论 CAPD患者血FGF-23显著增高,血磷、肾功能状态、1,25（OH）2VitD3均可调节血FGF-23水平,但FGF-23与骨密度降低无直接关系。     

慢性肾脏病患者血管钙化与成纤维细胞生长因子23-Klotho轴的关系

目的 阐明成纤维细胞生长因子FGF23-Klotho轴与慢性肾脏病(chronic kidneydisease,CKD)患者血管钙化之间的关系,以及CKD患者成纤维细胞生长因子-23 (FGF-23)、Klotho的检测及差异.方法 应用酶联免疫分析(ELISA)法检测65例CKD 3～5期未透析患者与15名健康对照组全段FGF-23、Klotho和1,25二羟基维生素D3[1,25(OH)2-VitD3]的水平,同时测定血清肌酐(creatinine,CREA)、钙(calcium,Ca)、磷(phosphate,P)、碱性磷酸酶(alkaline phosphatese,ALP)、尿酸(uric acid,UA)、全段甲状旁腺激素(parathyroid hormone,iPTH)等指标,分析FGF-23与各指标的关系.结果 CKD患者血清FGF-23水平随肾功能下降而逐渐升高,CKD各期与对照组相比、各期组间相比差异存在统计学意义(P＜0.05).Klotho与FGF-23存在显著正相关,1,25(OH)2-VitD3随肾功能损害的程度加重而下降.相关分析结果显示:CKD 3～5期患者血清FGF-23与血清Klotho、CREA、P、Ca×P、iPrH存在显著正相关(r分别为0.338、0.542、0.402、0.423、0.342,均P＜0.01),与eGFR存在显著负相关(r为-0.627,P＜0.01).多元回归分析显示:CREA、eGFR、P、Ca×P、iPTH、Klotho是血清FGF-23水平的独立影响因素.Ca、CREA、iPTH、Klotho、1,25(OH)2-VitD3、eGFR等指标无明显差异(P＞0.05).无血管钙化组和血管钙化组比较,患者的FGF-23、年龄、Ca×P、P、ALP水平有显著性差异(P＜0.05).血管钙化的危险因素采用多因素Logistic回归分析:年龄、P可能是发生血管钙化的主要危险因素(r值分别为-1.446、-1.454,P值分别为0.011、0.029).结论 CKD 3～5期患者血清FGF-23显著升高,CREA、eGFR、P、Ca×P、iPTH、Klotho可能是血清FGF-23水平的影响因素.年龄、P可能为血管钙化的危险因素.     

益肾汤经结肠透析对慢性肾脏病颈动脉钙化患者血镁及炎症因子的影响

目的:研究益肾汤经结肠透析对慢性肾脏病(CKD)颈动脉钙化患者血镁及炎症因子的影响。方法:收集我院门诊及住院的CKD3-4期患者,随机分为对照组、结肠透析组、益肾汤经结肠透析组。对照组予以常规内科治疗,结肠透析组在对照组基础上行结肠透析,益肾汤经结肠透析组在结肠透析组基础上用益肾汤灌肠。收集患者一般资料、治疗后生化指标,比较各组患者Scr、BUN、血尿酸、Hb、血镁、i PTH、血钙、血磷、ALB、血脂检测、NF-κB及TNF-α等指标的变化。结果:(1)经过4周后的治疗观察,结果发现益肾汤经结肠透析组与对照组比较,Scr、BUN、血磷、血镁、血尿酸、NF-κB及TNF-α明显改善,P<0.05;结肠透析组与对照组比较,Scr、BUN、血磷、血镁、血尿酸、NF-κB及TNF-α明显改善,P<0.05。(2)血清镁浓度与颈动脉钙化呈负相关(r=-0.65,P<0.01);与i PTH呈负相关(r=-0.29,P<0.05);与血磷浓度呈负相关(r=-0.264,P<0.05);与血钙浓度无相关性(r=0.174,P>0.05)。结论:血管钙化是CKD患者常见并发症,血清镁浓度与颈动脉钙化、i PTH、血磷有一定的相关性。益肾汤经结肠透析可能通过调节血镁及炎症因子表达,从而缓解CKD患者颈动脉钙化,其具体机制有待于进一步研究。     

慢性肾脏病钙、磷及甲状旁腺激素水平变化的对比分析

目的 观察各期慢性肾脏病(CKD)患者的钙、磷及甲状旁腺激素(PTH)水平并分析其临床特征,为早期防治提供依据.方法 选择2006年1月至2010年12月在新疆自治区人民医院肾病科住院的CKD患者294例,检测血清磷(P)、钙(Ca)、肌酐(Cr)、血清白蛋白(ALB)、CaP及血清甲状旁腺激素(PTH)的浓度.并进行回顾性分析.结果 CKD1 ～2期患者血清钙、磷与对照组比较无显著性差异.CKD2期患者血清肌酐与对照组比较有显著性差异(P＜0.05).CKD3～5期患者血清钙浓度低于对照组(P＜0.05),与CKD1 ～2期比较有差异,CKD5期患者血清钙浓度明显低于CKD3 ～4期有显著性差异.CKD3 ～5期患者血磷高于对照组及CKD1 ～2期,有显著性差异(P＜0.01),血磷增高明显与血钙和PTH有显著性差异(P＜0.05).CKD2 ～5期患者血肌酐高于对照组及CKD1期患者有显著性差异(P＜0.01),与各组间比较亦无明显差异.结论 对于CKD3期患者我们应该积极给予降低血磷的综合治疗,以防治继发性甲状旁腺功能亢进发生.     

FGF23在慢性肾脏病中的改变及意义的研究进展

成纤维细胞生长因子23(FGF-23)是一个新近发现的钙磷代谢的调节因子,可通过与肾小管细胞膜受体Klotho等分子结合,增加尿磷排泄.在慢性肾脏病(CKD)患者,血清FGF23水平升高先于血磷的升高.临床研究表明,血清FGF-23升高是心肌肥厚和血管内皮损伤的独立危险因素,也是CKD患者肾功能进行性恶化的重要预测因子;在维持性血液透析患者,血清FGF-23升高者透析一年后的死亡率明显上升.针对FGF-23的干预治疗可能是延缓CKD进展的重要措施.     

骨化三醇治疗对血液透析患者矿物质、骨代谢紊乱及FGF23的影响

目的:评价骨化三醇不同给药方案对血液透析患者矿物质及骨代谢紊乱(CKD-MBD)及FGF23的影响。方法:选取血甲状旁腺素(PTH)水平在300~621 pg/ml(正常的4~9倍)之间的血液透析患者,随机分成骨化三醇常规治疗组(常规组,22例)和间歇给药组(间歇组,26例),疗程16周,检测治疗前后血清FGF-23水平、钙磷代谢等指标变化。结果:(1)两组患者治疗终点与治疗前比较,血PTH均明显下降、血维生素D及FGF23均明显升高(P0.05)。间歇组在治疗终点,血钙明显升高、碱性磷酸酶明显下降(P0.05),而持续组,治疗前后血钙、碱性磷酸酶无明显变化。(2)在不同治疗时间点,持续组PTH明显下降(P0.05);间歇组PTH、碱性磷酸酶明显下降,血钙明显升高(P0.05)。治疗第4周、第8周,间歇组PTH下降较持续组明显(P0.05)。(3)治疗期间,持续组有6例患者血磷升高,间歇组无血磷升高患者。治疗期间无高钙血症发生。结论:骨化三醇不同给药方案能不同程度下降患者血PTH、升高FGF23,间歇组较持续组明显;间歇给药组血钙明显升高、碱性磷酸酶明显下降。两组治疗方案均能改善继发性甲状旁腺功能亢进,间歇给药组降PTH效果更佳。骨化三醇治疗轻中度继发性甲状旁腺功能亢进安全有效。     

Postprandial mineral metabolism and secondary hyperparathyroidism in early CKD

Normophosphatemia and normocalcemia are maintained in chronic kidney disease (CKD) by increased levels of fibroblast growth factor-23 (FGF-23) and parathyroid hormone (PTH), but the stimuli for secretion of these hormones in early CKD are incompletely understood. Most human physiologic studies have focused on random or fasting measurements of phosphorus, calcium, FGF-23, and PTH, but in this study, the hypothesis was that measurements in the postprandial state may reveal intermittent stimuli that lead to increased FGF-23 and PTH levels. The 4-h postprandial response in 13 patients with CKD and fasting normophosphatemia and normocalcemia (mean GFR 41 +/- 8 ml/min per m(2)) was compared with 21 healthy volunteers. Compared with healthy subjects, fasting patients with CKD had significantly higher levels of FGF-23 and fractional excretion of phosphorus; lower fractional excretion of calcium; and no difference in serum calcium, phosphorus, and PTH levels. After standardized meals, urinary phosphorus excretion in both groups increased despite unchanged serum phosphorus and FGF-23 levels. Postprandial urinary calcium excretion also increased in both groups, and this was accompanied by significantly reduced serum calcium and increased PTH levels in patients with CKD only; therefore, FGF-23 does not seem to be an acute postprandial regulator of phosphaturia in CKD or in health, but inappropriate postprandial calciuria with episodic, relative hypocalcemia may represent a previously unreported mechanism of secondary hyperparathyroidism in CKD.     

成纤维细胞生长因子23在血液透析患者磷和维生素D代谢中的作用

目的 探讨成纤维细胞生长因子23（FGF-23）在维持性血液透析（MHD）患者磷和维生素D代谢中的作用及相关调控机制。 方法 采用酶联免疫分析法（ELISA）对59例MHD患者（血透组）及20例健康志愿者（对照组）进行血清全段FGF-23测定，同时应用放免法测定血清1，25-二羟维生素D（1,25(OH)2VitD）水平。血透组患者测定血清白蛋白（Alb）、血红蛋白（Hb）、血肌酐（Scr）、尿素氮（BUN）、钙（Ca）、磷（P）及全段甲状旁腺激素（iPTH）等指标。 结果 血透组血清FGF-23水平明显高于对照组[（215.23±123.55）比（28.72±11.49） ng/L，P < 0.01]，而血清1,25(OH)2VitD水平明显低于对照组[（13.25±8.73）比（42.24±12.45） μg/L，P < 0.01]。Pearson相关分析显示，血透组血清FGF-23水平与血清P、Scr、Ca、iPTH及透析疗程时间呈正相关（P < 0.05）；与血清1,25(OH)2VitD水平和年龄呈负相关（P < 0.05）；而与性别、血压、血清Alb、Hb、BUN等指标无相关。多元回归分析显示，血清P、Ca、Scr、iPTH和1,25(OH)2VitD是影响血清FGF-23的主要变量，5者组成的模型解释了总变异的约62%（R2=0.623，P < 0.01）。 结论 MHD患者血清全段FGF-23水平明显增高，而1,25(OH)2VitD水平明显降低。FGF-23的调控是由复杂的多种因素共同作用的结果，血清P、Ca、Scr、iPTH和1,25(OH)2VitD是影响血清FGF-23水平的主要调控因子。     

Fibroblast growth factor 23 is elevated before parathyroid hormone and phosphate in chronic kidney disease

Fibroblast growth factor 23 (FGF23) regulates phosphorus metabolism and is a strong predictor of mortality in dialysis patients. FGF23 is thought to be an early biomarker of disordered phosphorus metabolism in the initial stages of chronic kidney disease (CKD). We measured FGF23 in baseline samples from 3879 patients in the Chronic Renal Insufficiency Cohort study, which is a diverse cohort of patients with CKD stage 2-4. Mean serum phosphate and median parathyroid hormone (PTH) levels were in the normal range, but median FGF23 was markedly greater than in healthy populations, and increased significantly with decreasing estimated glomerular filtration rate (eGFR). High levels of FGF23, defined as being above 100 RU/ml, were more common than secondary hyperparathyroidism and hyperphosphatemia in all strata of eGFR. The threshold of eGFR at which the slope of FGF23 increased was significantly higher than the corresponding threshold for PTH based on non-overlapping 95% confidence intervals. Thus, increased FGF23 is a common manifestation of CKD that develops earlier than increased phosphate or PTH. Hence, FGF23 measurements may be a sensitive early biomarker of disordered phosphorus metabolism in patients with CKD and normal serum phosphate levels.     

Fibroblast growth factor-23 mitigates hyperphosphatemia but accentuates calcitriol deficiency in chronic kidney disease

Hyperphosphatemia, calcitriol deficiency, and secondary hyperparathyroidism (SHPT) are common complications of chronic kidney disease (CKD). Fibroblast growth factor-23 (FGF-23) is a novel phosphaturic hormone that also inhibits renal 1alpha-hydroxylase activity and thus may be involved in the pathogenesis of SHPT. Several hypotheses were tested: that FGF-23 increases as renal function declines; is linearly associated with serum phosphate levels; is associated with increased phosphaturia independent of parathyroid hormone (PTH); and is associated with decreased calcitriol levels independent of renal function, hyperphosphatemia, and vitamin D stores. FGF-23, PTH, 25(OH)D3, calcitriol, calcium, phosphate, and urinary fractional excretion of phosphate (Fe(PO4)) were measured in 80 CKD patients. Multiple linear regression was used to test the hypotheses. FGF-23 and PTH were inversely associated with estimated GFR (eGFR), whereas calcitriol levels were linearly associated with eGFR. Hyperphosphatemia and hypocalcemia were present in only 12 and 6% of patients, respectively, all of whose eGFR was <30. Increased Fe(PO4) was associated with decreased eGFR, and both increased FGF-23 and PTH were independently associated with increased Fe(PO4). Increased FGF-23 and decreased 25(OH)D3 were independent predictors of decreased calcitriol, but the effects on calcitriol levels of renal function itself and hyperphosphatemia were completely extinguished by adjusting for FGF-23. It is concluded that FGF-23 levels increase early in CKD before the development of serum mineral abnormalities and are independently associated with serum phosphate, Fe(PO4), and calcitriol deficiency. Increased FGF-23 may contribute to maintaining normal serum phosphate levels in the face of advancing CKD but may worsen calcitriol deficiency and thus may be a central factor in the early pathogenesis of SHPT.     

Circulating concentration of FGF-23 increases as renal function declines in patients with chronic kidney disease, but does not change in response to variation in phosphate intake in healthy volunteers

BACKGROUND: Hyperphosphatemia is a risk factor for the development of several different complications of chronic kidney disease (CKD), including secondary hyperparathyroidism and cardiovascular complications, due to the formation of calcium-phosphate deposits. Fibroblast growth factor-23 (FGF-23) is a recently discovered protein that is mutated in autosomal-dominant hypophosphatemic rickets, an inherited phosphate wasting disorder, and it may represent a novel hormonal regulator of phosphate homeostasis. We therefore hypothesized that FGF-23 levels may be altered in hyperphosphatemia associated with renal failure and that its concentration changes in response to different levels of phosphate intake. METHODS: Using a two-site enzyme-linked immunosorbent assay (ELISA) detecting the C-terminal portion of FGF-23, serum concentration was measured in 20 patients with different stages of renal failure (creatinine range 155 to 724 micromol/L), in 33 patients with end-stage renal disease (ESRD) on dialysis treatment, and in 30 patients with functioning renal grafts. Furthermore, six healthy males were given oral phosphate binders in combination with low dietary phosphate intake for 2 days followed by 3 days of repletion with inorganic phosphate. FGF-23 levels were determined at multiple time points. RESULTS: FGF-23 serum levels were significantly elevated in CKD with a strong correlation between serum creatinine and FGF-23 concentration. Independent correlations were also seen between FGF-23 and phosphate, calcium, parathyroid hormone (PTH), and 1,25(OH)2D3. No changes in serum FGF-23 levels were observed in volunteers following ingestion of oral phosphate binders/low dietary phosphate intake, which led to a decline in phosphate excretion or during the subsequent repletion with inorganic phosphate through oral phosphate and a normal diet. CONCLUSION: Circulating FGF-23 was significantly elevated in patients with CKD and its concentration correlated with renal creatinine clearance. In healthy volunteers, FGF-23 levels did not change after phosphate deprivation or phosphate loading.     

The impact of diabetes mellitus on vitamin D metabolism in predialysis patients

Although diabetes mellitus (DM) disturbs bone metabolism, little is known concerning its effects on laboratory abnormalities in chronic kidney disease-mineral and bone disorders (CKD-MBD). We extracted data for 602 patients from the Osaka Vitamin D Study in patients with CKD (OVIDS-CKD), an observational study enrolling predialysis outpatients. No enrolled patients received vitamin D, bisphosphonate, estrogen or raloxifene. We measured 1– 84 PTH, 25-hydroxyvitamin D (25D), calcitriol, fibroblast growth factor-23 (FGF-23), calcium (Ca), and phosphate (P). Since there were 112 DM patients (group D), we extracted 112 age-, sex-, and eGFR-matched non-DM counterparts (group N). We compared biochemical markers between groups, and then performed multiple regression analyses for all 602 subjects to confirm the results obtained. Group D had significantly higher corrected Ca and P than group N throughout all stages of CKD. In group D, 25D decreased as renal function declined, while in group N it remained constant (interaction P < 0.05). Despite higher P and poorer vitamin D status in DM, there were no differences in 1– 84 PTH level between group D and group N stratified by stage of CKD, resulting in significantly lower calcitriol levels in group D in late CKD. Multiple regression analyses revealed that DM was significantly associated with low vitamin D status even with adjustment for urinary protein, and that this poorer vitamin D status in DM was responsible for lower calcitriol level associated with DM. Despite higher P, lower FGF-23 in early CKD (stages 1 + 2) and comparable level of FGF-23 in late stages of CKD (stages 3, 4, and 5) were observed in group D. We interpreted these results to indicate that inappropriate production of FGF-23 in DM might explain higher serum phosphate in DM. Multiple regression analysis with adjustment for covariates confirmed an independent relationship between DM and low FGF-23, implying the existence of dysfunction or decreased density of osteocytes in DM. Given the origin of these phosphaturic hormones, DM may thus have markedly deleterious effects on parathyroid and bone. Poorer vitamin D status and higher CaP product might be partly responsible for functional and structural changes of vasculature, respectively, in DM.