慢性肾脏病5期患者25-羟维生素D3不足与缺乏

目的 评估慢性肾脏病(CKD)5期患者25-羟维生素D3[25 (OH) D3]不足与缺乏的患病率及其影响因素.方法 对本院96例CKD 5期患者的病史、实验室检查结果等进行回顾性分析.纳入研究的变量包括:血25 (OH) D3检测值,血白细胞(WBC)、血红蛋白(Hb)、血清尿素氮(BUN)、血清肌酐(Scr)、二氧化碳结合力(CO2CP)、血清白蛋白(Alb)、碱性磷酸酶(ALP)、总胆固醇(TCH)、高密度脂蛋白(HDL-C)、低密度脂蛋白(LDL-C)、甘油三脂(TG)、钙、磷、全段甲状旁腺激素(iPTH)等.分析25 (OH) D3水平与各项观察指标间的关系.结果 96例CKD 5期患者的25 (OH) D3平均水平为33.25(24.85～ 44.30) nmol/L,显著低于正常值(P＜0.01);非透析患者、维持性血液透析(以下简称血透)患者、维持性腹膜透析(以下简称腹透)患者25-羟维生素D3水平分别为32.70(25.30～43.70) nmol/L、37.00(29.20～ 48.65)nmoL/L和27.05(19.20 ～ 35.37) nmol/L.CKD5期患者的25 (OH) D3不足患病率为32.29％;在非透析、血透、腹透患者中分别为27.91％、45.45％和20％;CKD5期患者25 (OH) D3缺乏患病率为64.58％,在非透析、血透、腹透患者中分别为67.44％、51.52％和80％;25 (OH) D3缺乏及不足患病率为96.88％,非透析、血透、腹透患者中分别为95.35％、96.97％和100％,各患病率三组间差异无统计学意义.单因素相关分析结果显示,25 (OH) D3水平与Hb(r=0.222)、Alb(r=0.398)相关(P＜0.05).多元线性回归分析结果显示,Alb水平与25 (OH) D3水平呈正相关.结论 CKD5患者的维生素D缺乏和不足患病率高,普遍存在.Alb是CKD5期患者维生素D水平不足或缺乏的独立影响因素.     

肌注维生素D2治疗维持性血液透析患者25羟维生素D缺乏的临床观察

目的分析维持性血液透析患者的血清25-羟维生素D[25(OH)D]水平,探讨肌注维生素D2注射液治疗25羟维生素D缺乏的作用。 方法检测我院2020年12月至2021年2月170例维持性血液透析患者空腹血清25(OH)D水平,根据血清25(OH)D水平将患者分为严重缺乏组、缺乏组、不足组和正常组。分析血清25(OH)D水平与患者性别、年龄、透析龄、血红蛋白、白蛋白、血钙、血磷、全段甲状旁腺激素(iPTH)的相关性。其中86例维生素D缺乏或不足的血透患者,随机分为对照组(n＝43)和治疗组(n＝43),对照组给予常规治疗,治疗组在对照组基础上给予肌注维生素D2 (20万单位,1次/2周),连续3个月。比较患者治疗前后血清25(OH)D、血红蛋白、白蛋白、钙、磷、iPTH水平的变化,并观察不良反应情况。 结果170例患者中,维生素D严重缺乏组33例(19.4%),缺乏组33例(19.4%),不足组70例(41.2%),正常组34例(20%)。男性25(OH)D水平显著高于女性(P<0.05)。正常组与维生素D缺乏组和不足组在透析龄、血红蛋白、白蛋白差异方面均具有统计学意义(P<0.05)。血清25(OH)D与年龄、血钙、血磷、甲状旁腺激素无显著相关性(P>0.05)。多元线性逐步回归分析显示,血清25(OH)D与血红蛋白、白蛋白具有相关性(P<0.05)。肌注维生素D2 3月后可使血液透析患者的25(OH)D水平显著上升(P<0.05),同时血红蛋白、血清白蛋白、磷上升(P<0.05),对血钙、iPTH无显著影响(P>0.1)。 结论维持性血液透析患者维生素D缺乏发生率高,血清25(OH)D水平与性别、贫血、营养不良存在密切关系,肌注维生素D2可改善血透患者贫血、营养不良情况,但可能带来血磷升高。     

维持性腹膜透析患者发生不良心血管事件危险因素的分析

目的 探讨维持性腹膜透析患者发生不良心血管事件的危险因素.方法 选取维持性腹膜透析患者44例,透析时间≥3个月.根据不良心血管事件确认标准分为无心血管事件组24例,有心血管事件组20例.记录两组患者年龄、性别、原发病、透析龄;同时记录血生化指标:血尿酸、血色素、血浆白蛋白、总蛋白、胆固醇、甘油三酯、高密度脂蛋白、低密度脂蛋白、血钙、血磷、钙磷乘积、全段甲状旁腺素(iPTH)、25-(OH)D3、碱性磷酸酶、尿素氮、肌酐水平.结果 有心血管事件组血浆总蛋白、白蛋白、血肌酐、25-(OH)D3水平均低于无心血管事件组,而年龄、血胆固醇、尿酸水平则明显高于无心血管事件组(p＜0.05或p＜0.01);二分类Logistic回归分析显示血浆白蛋白、胆固醇、低密度脂蛋白、血尿酸、25-(OH)D3可能是腹膜透析患者发生不良心血管事件的危险因素.结论 心血管事件是腹膜透析患者常见的并发症之一,血脂异常、营养不良、高血尿酸、低血25-(OH)D3是腹膜透析患者发生不良心血管事件的重要危险因素.     

2型糖尿病患者血清25-经维生素D水平与骨密度的关系

目的 探讨2型糖尿病患者不同血清25-( OH) D水平与骨密度的关系。方法 选择住院的2型糖尿病患者288例,根据25-( OH) D水平对其进行分组：25-( OH) D>30ng/mL为维生素D充足组;20ng/mL <25-( OH ) D≤30 ng/mL为维生素D不足组;l0 ng/mL <25-( OH) D <20 ng/mL为维生素D缺乏组;25-( OH) D <10ng/mL为维生素D严重缺乏组。采用双能X线骨密度仪(DXA)测量受试者腰椎L1-4、股骨颈及全髓的骨密度。分析不同水平25-( OH ) D与骨密度的关系。结果 维生素D充足组、维生素D不足组、维生素D缺乏组、维生素D严重缺乏组的患者例数(所占比例)分别为10例(3. 5%) ,74例(25.7%) ,177例(61.5%) ,27例(9.3%)。不同性别组25-( OH ) D水平无明显差异,但是女性患者的腰椎L1-4、股骨颈、全髋的骨密度均较男性低。pearscm相关分析显示25-( OH) D水平与腰椎L1-4、股骨颈、全髓的骨密度均无相关性(分别为r=0.080 P=0.262;r=0. 139 P=0. 051;r=0.068 P=0. 342)。结论 2型糖尿病患者25-( OH) D水平与腰椎L1-4、股骨颈、全髓的骨密度均无明显相关性。     

2型糖尿病患者血清25-羟维生素D水平与骨密度的关系

目的探讨2型糖尿病患者不同血清25-(OH)D水平与骨密度的关系。方法选择住院的2型糖尿病患者288例,根据25-(OH)D水平对其进行分组:25-(OH)D30ng/mL为维生素D充足组;20ng/mL25-(OH)D≤30ng/mL为维生素D不足组;10ng/mL25-(OH)D≤20ng/mL为维生素D缺乏组;25-(OH)D≤10ng/mL为维生素D严重缺乏组。采用双能X线骨密度仪(DEXA)测量受试者腰椎L_(1-4)、股骨颈及全髋的骨密度。分析不同水平25-(OH)D与骨密度的关系。结果维生素D充足组、维生素D不足组、维生素D缺乏组、维生素D严重缺乏组的患者例数(所占比例)分别为10例(3.5%)、74例(25.7%)、177例(61.5%)、27例(9.3%)。不同性别组25-(OH)D水平无明显差异,但是女性患者的腰椎L_(1-4)、股骨颈、全髋的骨密度均较男性低。pearson相关分析显示25-(OH)D水平与腰椎L_(1-4)、股骨颈、全髋的骨密度均无相关性(分别为r=0.080 P=0.262;r=0.139 P=0.051;r=0.068 P=0.342)。结论 2型糖尿病患者25-(OH)D水平与腰椎L_(1-4)、股骨颈、全髋的骨密度均无明显相关性。     

慢性肾脏病患者维生素D缺乏与动脉僵硬度的相关性

目的 探讨慢性肾脏病患者维生素D缺乏与动脉僵硬度的相关性.方法 选取慢性肾脏病(CKD l～5期)患者300例,根据血25(OH)D3浓度分为维生素D缺乏组[25 (OH)D3＜20 μg/L]和维生素D非缺乏组[25(OH)D3≥20 μg/L].采集临床资料数据,测定动脉僵硬度指标肱踝脉搏波传导速度(baPWV).对血25(OH)D3水平与baPWV间的关系进行单因素相关分析及多元线性回归分析. 结果 维生素D缺乏组188例(62.7％),维生素D非缺乏组112例(37.3％).全部CKD患者25(OH)D3平均浓度为(17.62±8.54) μg/L,维生素D缺乏组和非缺乏组分别为(12.38±4.55) μg/L与(26.44±6.05) μg/L(P＜0.01).维生素D缺乏组baPWV值高于非缺乏组[(1 827.34±429.11) cm/s比(1 555.31±353.14) cm/s,P＜0.01].单因素相关分析显示全体CKD患者(r=-0.38,P＜0.01)以及CKD 2～5期患者[r=-0.30,P＜0.05;r=-0.26,P＜0.05;r=-0.46,P＜0.01;r=-0.57,P＜0.01]血25(OH)D3浓度与baPWV均呈负相关.多元线性回归分析显示血25 (OH)D3浓度下降与baPWV的增加独立相关(模型1:β=-0.18,P＜0.01;模型2:β=-0.17,P=0.01),回归模型1与模型2均可解释baPWV变化的50％.结论 CKD患者普遍存在维生素D缺乏,维生素D缺乏与动脉僵硬度增加相关.维生素D替代治疗可能影响CKD患者的心血管预后,但有待未来研究的进一步明确.     

育龄期女性终末期肾病血液透析患者性激素水平检测及其与血清25-羟维生素D关系的探讨

目的探讨育龄期女性终末期肾病血液透析患者性激素水平与血清25-羟维生素D[25(OH)D]的关系探讨。方法选取2016年5月至2019年11月西电集团医院收治的91例育龄期女性终末期肾病血液透析患者作为透析组,另选取87例同期体检健康的育龄期女性作为健康组,均行性激素[黄体生成素(luteinizing hormone, LH)、卵泡刺激素(follicle stimulating hormone, FSH)、催乳素(prolactin, PRL)、雌二醇(estradiol, E_2)、孕酮(progesterone, P)、睾酮(testosterone, T)]水平及血清25(OH)D水平检测。对比2组性激素各项指标及血清25(OH)D水平,并采用Pearson相关性分析法分析透析组LH、FSH、PRL、E_2、P、T与25(OH)D水平的关系。结果透析组血清LH、FSH、PRL水平均高于健康组,透析组E_2、P、T水平均低于健康组,差异均有统计学意义(P0.05);透析组血清25(OH)D水平明显低于健康组(P0.05),透析组维生素D缺乏或不足总占比为83.52%,明显高于健康组的12.64%(P0.05);透析组血清LH、FSH水平与25(OH)D水平呈显著负相关性(P0.05),血清E_2水平与25(OH)D水平呈显著正相关性(P0.05),而血清PRL、P、T水平与25(OH)D水平无明显相关性(P0.05)。结论育龄期终末期肾病血液透析女性患者存在性激素水平紊乱及维生素D缺乏或不足现象,且LH、FSH、E_2水平与血清25(OH)D水平具有一定相关性。     

慢性肾脏病患者25-羟维生素D3水平的改变及其影响因素分析

目的检测慢性肾脏病(chronickidneydisease,CKD)患者不同进展阶段25-羟维生素D3[25(OH)D3]的浓度,25(OH)D3水平与CKD发生、发展的关系,进一步探讨活性维生素D在CKD患者中的合理应用。方法收集2014年11月至2015年11月中国医科大学附属第一医院肾脏内科住院的非血液净化的CKD患者885例及急性肾损伤患者11例,分别测定25(OH)D3及血红蛋白(hemoglobin,Hb)、血肌酐(SCr)、尿素氮(BUN)、血清胱抑素C(Cystatin C,Cys-C)、血钙、血磷、血碳酸氢根(HCO)3)、血尿酸(uric acid,UA)、血总胆固醇(total cholesterol,TC)、三酰甘油(triglyceride,TG)、低密度脂蛋白胆固醇(low density lipoprotein cholesterol,LDL-C)、高密度脂蛋白胆固醇(high density lipoprotein cholesterol,HDL-C)、血白蛋白(albumin,Alb)、血清碱性磷酸酶(alkaline phosphates,ALP)、C反应蛋白(C-reactive protein,CRP)、糖化血红蛋白(-HbAlC)及采用化学发光法测量血清全段甲状旁腺素(immunoreactive parathyroid hormone,讧TH)。统计CKD不同阶段25(OH)D3不足及缺乏的发生率,分析不同维生素D水平分组下各项生化指标的变化趋势并进行相关性分析。结果①随肾脏病的进展,维生素D严重缺乏的发生率呈升高趋势。急性肾损伤患者25(OH)D3水平为(15.8±9.16)ng/ml,明显高于CKD各期(P0.05)。随25(OH)D3水平下降,患者的血压(收缩压、舒张压)水平升高,尿蛋白的程度加重,血白蛋白水平下降,钙磷代谢紊乱(血钙下降,血磷升高)及血脂代谢异常加重,不同维生素D水平分组间差异有统计学意义(P0.05),而年龄、左室射血分数、肾功能相关指标、骨代谢指标、血尿酸、血红蛋白、C反应蛋白则无统计学差异(P0.05);②25(OH)D3水平与尿蛋白程度相关,中度尿蛋白组和大量尿蛋白组25(OH)D3浓度均明显低于正常尿蛋白组和低尿蛋白组(P0.05);且随着蛋白尿病情加重,维生素D严重缺乏的发生率升高,在各尿蛋白组间差异有统计学意义(χ~2=251.75,P=0.000)。③25(OH)D3水平与血白蛋白、血钙、血红蛋白水平呈正相关;与收缩压、舒张压、尿蛋白定量、磷、血脂水平呈负相关。血白蛋白、收缩压、尿蛋白定量、血红蛋白是25(OH)D3水平的独立危险因素。结论我国东北地区CKD患者维生素D缺乏更加严重。25(OH)D3水平与CKD临床重要指标相关。血白蛋白、收缩压、24 h尿蛋白定量、血红蛋白是25(OH)D3水平的独立危险因素。     

糖尿病肾病患者维生素D水平与肾素、血管紧张素Ⅱ水平及蛋白尿的关系

目的:探讨糖尿病肾病患者血清25-羟维生素D与肾素、血管紧张素Ⅱ水平及蛋白尿的关系。方法:选取2019年1月—2019年10月在西安医学院附属医院肾内科住院的糖尿病肾病患者217例,测量其身高、体重,测定其空腹25-羟维生素D、肾素、血管紧张素Ⅱ水平,24 h尿白蛋白排泄率及糖脂代谢指标;根据患者检测结果分为,25-羟维生素D水平正常组(30μg/L)、25-羟维生素D水平不足组(20～30μg/L)和25-羟维生素D水平缺乏组(20μg/L),观察其与肾素、血管紧张素Ⅱ水平及尿白蛋白排泄率的关系。结果:维生素D缺乏组患者TC、TG、LDL-C水平与维生素D不足和正常组比较,差异有统计学意义(P0.05);维生素D缺乏组肾素、血管紧张素Ⅱ水平及尿白蛋白排泄率显著高于维生素D不足和正常组(P0.05);血清25-羟维生素D水平与肾素、血管紧张素Ⅱ水平及尿白蛋白排泄率呈负相关(r=-0.751、r=-0.769、r=-1.673,P0.05)。结论:维生素D缺乏和不足会影响到糖尿病肾病患者糖脂代谢;维生素D水平与患者肾素、血管紧张素Ⅱ水平、蛋白尿及血脂等危险因素有相关性。     

慢性肾脏病患者维生素D不足与缺乏

目的 了解慢性肾脏病(CKD)患者维生素D不足与缺乏的患病率,为合理的维生素D治疗提供依据。 方法 对358例住院CKD患者的临床资料进行回顾性分析。用酶标法测定血清25（OH）D3水平,并常规检测血红蛋白（Hb）、Scr、BUN、CO2CP、白蛋白(Alb)、血清钙、磷、全段甲状旁腺激素（iPTH）等。分析25（OH）D3水平与临床指标的关系。 结果 358例患者的25（OH）D3平均水平为（18.58±11.7） µg/L,显著低于正常值（P < 0.01）;CKD1~5期患者25（OH）D3水平分别为（25.84±9.71）、（20.76±6.99）、（20.40±17.02）、（19.49±11.29）和（14.16±7.98） µg/L。维生素D缺乏患病率为39.66%;在CKD1~5期中分别为5.00%、17.50%、37.21%、42.37%和57.14%,患病率随CKD分期逐级增加。维生素D不足患病率为44.97%,在CKD1~5期中分别为72.50%、47.50%、45.35%、33.90%和40.60%。维生素D缺乏及不足患病率为84.63%,在CKD1~5期中分别为77.50%、65.00%、82.56%、76.27%和97.74%,CKD各期间差异无统计学意义。单因素相关分析显示,25（OH）D3与Hb（r = 0.163）、Alb（r = 0.291）、Scr（r = -0.236）、eGFR（r = 0.156）和iPTH（r = -0.178）相关（P < 0.01）。多元线性回归分析显示,25（OH）D3与Alb呈正相关,而和iPTH、Scr呈负相关。CRP、钙磷乘积等与25（OH）D3无相关。按K/DOQI指南,根据25（OH）D3和iPTH水平,CKD3~5期患者符合维生素D治疗指征的比例分别为87.20%、83.05%和26.31%;而仅根据iPTH水平,符合治疗指征的比例仅为16.28%、35.59%和26.31%。 结论 CKD患者维生素D缺乏和不足患病率高。Alb、Scr和iPTH是CKD患者维生素D水平的重要影响因子。应在CKD人群中开展维生素D水平检测,并早期、合理治疗维生素D缺乏和不足。     

Relationship between serum 25-hydroxycholecalciferol deficiency and the risk of peritoneal dialysis associated peritonitis

Objective To investigate the relationship between serum 25-hydroxycholecalciferol[25(OH)D3] deficiency and the risk of peritoneal dialysis associated peritonitis. Methods Baseline clinical data (before the peritoneal dialysis catheter insertion) of peritoneal dialysis patients treated with CAPD in the First Affiliated Hospital of Guangxi Medical University from May 1, 2013 to February 1, 2016 were retrospective analyzed. All the patients were followed-up until July 31, 2016. According to the baseline serum 25(OH)D3 levels, patients were divided into deficiency group (25(OH)D3＜15 ng/ml) and non deficiency group (25(OH)D3 ≥15 ng/ml), the baseline clinical data of the two groups were also analyzed. Kaplan-Meier method was used to compare the time-to-peritonitis of two groups. Cox proportional hazard model was used to analyze the relationship between the 25(OH)D3 deficiency and the risk of peritonitis. ROC curve was used to analyze the predictive value of the baseline serum 25(OH)D3 for the risk of PDAP in peritoneal dialysis patients. Results Compared with the 25(OH)D3 non deficiency group, 25(OH)D3 deficiency group had a significant increase incidence of peritonitis, high diastolic blood pressure and mean arterial pressure, but serum albumin, total serum protein decreased significantly (P＜0.05). Kaplan-Meier survival analysis showed that, compared with 25(OH)D3 non deficiency group, the time-to-peritonitis episode of patients with 25(OH)D3 deficiency were shorter (P＜0.05). Cox proportional hazard model showed that after adjusting for age, sex, hemoglobin, serum albumin, C-reactive protein, total Kt/V, eGFR, diabetes or not, 25(OH)D3 deficiency is the independent risk factor of peritoneal dialysis associated peritonitis (HR 5.247, 95%CI 1.180-23.340, P＜0.05). ROC curve showed the area under the curve that baseline serum 25(OH)D3 deficiency predict the occurrence of PDAP was 0.714, and the best cut-off point of baseline serum 25(OH)D3 was 11.35 ng/ml (sensitivity 75%, specificity 63%). Conclusions Peritoneal dialysis associated peritonitis occurred earlier in peritoneal dialysis patients whose baseline serum 25(OH)D3 deficiency. Baseline serum 25(OH)D3 deficiency is the independent risk factor of peritoneal dialysis associated peritonitis, which may predict the incidence of peritoneal dialysis associated peritonitis.     

Opinion: Which of the K/DOQI Guidelines for Bone Disease in Dialysis Patients Should be Changed?

The K‐DOQI guidelines for bone metabolism in chronic kidney disease recommend measuring 25(OH) vitamin D levels and correcting deficiencies in stages 3 and 4 but not in ESRD. Most nephrologists are not concerned with 25(OH) vitamin D deficiency, despite evidence in hemodialysis patients that deficient vitamin D status [as measured by 25(OH) vitamin D levels] plays a role in bone disease. PD patients are often deficient in 25(OH) vitamin D in part because of peritoneal effluent losses, and correction may decrease muscle and bone complaints. Data from other populations are indicative of the importance of vitamin D in cancer surveillance and immune functioning. Randomized controlled trials of correction of 25(OH) vitamin D deficiency in both hemodialysis and peritoneal dialysis patients are urgently needed. vitamin D).     

Serum 25(OH)-vitamin D levels and bone metabolism in patients on maintenance hemodialysis

AIMS: An increasing amount of evidence suggests that 25-hydroxy vitamin D3 (25(OH)D3) may contribute to the bone health of patients with chronic kidney disease (CKD). The underlying vitamin D status of these patients, however, has often been neglected. In a cross-sectional study we assessed the association between vitamin D status and parathyroid function, bone turnover, bone mass and structure in patients on maintenance hemodialysis. METHODS: 69 patients on maintenance hemodialysis were assessed by bone densitometry (DEXA) and quantitative bone ultrasound (QUS). Serum 25-hydroxy vitamin D3 levels, serum markers of bone turnover and clinical data were tabulated. RESULTS: A high prevalence of potentially significant vitamin D3 deficiency was found in this patient group: 59% of the patients had a 25(OH)D3 level below 20 nmol/l. There was a significant negative correlation between serum 25(OH)D3 levels and serum intact parathyroid hormone (iPTH) (r = -0.231, p < 0.05), and this association remained significant after controlling for potential covariables. Furthermore, we show here that serum 25(OH)D3 concentration is positively correlated with bone mineral density (BMD) measured at the radius (r = 0.424, p < 0.01). Finally, we show for the first time that 25(OH)D3 levels are significantly and independently correlated with broadband ultrasound attenuation (beta = 0.262, p < 0.05) measured with calcaneal quantitative bone ultrasound (QUS) in patients with chronic renal failure. CONCLUSION: Vitamin D3 deficiency may contribute to the impaired bone health of patients on maintenance dialysis.     

Serum levels of 1,25-dihydroxyvitamin D, 24,25-dihydroxyvitamin D, and 25-hydroxyvitamin D in nondialyzed patients with chronic renal failure

BACKGROUND: In patients with chronic renal failure (CRF), abnormalities in vitamin D metabolism are known to be present, and several factors could contribute to the abnormalities. METHODS: We measured serum levels of three vitamin D metabolites, 1,25(OH)2D, 24, 25(OH)2D and 25(OH)D, and analyzed factors affecting their levels in 76 nondialyzed patients with CRF (serum creatinine> 1.6 and < 9.0 mg/dl), 37 of whom had diabetes mellitus (DM-CRF) and 39 of whom were nondiabetic (nonDM-CRF). RESULTS: Serum levels of 1,25(OH)2D were positively correlated with estimated creatinine clearance (CCr; r = 0.429; P < 0.0001), and levels of 24,25(OH)2D were weakly correlated with CCr (r = 0.252, P < 0.05); no correlation was noted for 25(OH)D. Serum levels of all three vitamin D metabolites were significantly and positively correlated with serum albumin. Although there were no significant differences in age, sex, estimated CCr, calcium and phosphate between DM-CRF and nonDM-CRF, all three vitamin D metabolites were significantly lower in DM-CRF than in nonDM-CRF. To analyze factors influencing vitamin D metabolite levels, we performed multiple regression analyses. Serum 25(OH)D levels were significantly and independently associated with serum albumin, presence of DM and serum phosphate (R2 = 0.599; P < 0.0001). 24,25(OH)2D levels were significantly and strongly associated with 25(OH)D (beta = 0.772; R2 = 0.446; P < 0.0001). Serum 1,25(OH)2D levels were significantly associated only with estimated CCr (R2 = 0. 409; P < 0.0001). CONCLUSIONS: These results suggest that hypoalbuminemia and the presence of DM independently affect serum 25(OH)D levels, probably via diabetic nephropathy and poor nutritional status associated with diabetes, and that 25(OH)D is actively catalyzed to 24,25(OH)2D in CRF, probably largely via extrarenal 24-hydroxylase. Serum levels of 1,25(OH)2D were significantly affected by the degree of renal failure. Thus, this study indicates that patients with CRF, particularly those with DM, should receive supplements containing the active form of vitamin D prior to dialysis.     

单次人体成分分析参数对住院尿毒症透析患者的预后价值

目的探讨生物电阻抗单次测定的营养及液体负荷指标对住院尿毒症患者预后的预测价值。 方法前瞻性连续纳入2014年1月至2016年12月在南京医科大学第一附属医院肾内科住院的成年维持性透析患者(包括血液透析、腹膜透析患者),患者入院后前3 d内均使用人体成分检测仪测定透析前人体成分。使用Kaplan-Meier法绘制生存曲线,使用Cox回归分析瘦体重指数(LTI)、脂肪组织指数(FTI)、细胞外液(ECW)与体细胞质量(BCM)比值(ECW/BCM)、过多水负荷(OH)与预后的关系,并进行多因素校正Cox回归分析。 结果(1)排除失访患者12例及随访期间行肾移植患者20例后共纳入819例患者,其中血液透析患者696例,腹膜透析患者123例。平均随访时间(28.1±9.7)月,172例(21%)患者随访期间死亡。(2)按照OH<-1L、-1～1 L及>1L将患者分为3组、按照OH/ECW比值将患者分为液体负荷过量(fluid overload)和液体平衡(fluid balance)两组、按照LTI、FTI、ECW/BCM的四分位数将患者各分为4组。生存分析发现不同OH组患者的死亡无显著差异(χ²＝ 2.4767,P＝0.2899),而不同体液状态的两组患者、不同LTI、FTI、ECW/BCM的4组患者的死亡有显著差异(体液状况2个组比较,χ²＝12.3874, P＝0.0004;LTI 4个组比较,χ²＝ 57.0897,P<0.0001;FTI 4个组比较,χ² ＝ 10.5650, P＝0.0143;ECW/BCM 4个组比较,χ²＝69.5081,P<0.0001)。其中,液体负荷组、LTI越低组,FTI越高组,ECW/BCM越高组,死亡风险趋向增高。多因素COX回归显示在校正透析龄、糖尿病、感染、舒张压、FTI、ECW/BCM后,高龄、高Charlson评分、低白蛋白、低LTI均是透析患者死亡的独立危险因素(HR_age＝1.03, P<0.001; HR_Charlson＝1.18, P＝0.003; HR_Alb＝0.94, P<0.001; HR_LTI＝0.84, P<0.001)。(3)按Alb和LTI的中位数将人群分为4组,发现预后按以下分组顺序依次变差：Alb>35.2、LTI>11.5组,Alb>35.2、LTI≤11.5组,Alb≤35.2、LTI>11.5组,Alb≤35.2、LTI≤11.5组。交互作用分析显示血Alb和LTI不存在交互作用。(4)亚组分析显示,血液透析亚组(n＝696)结果与总体类似,而腹膜透析亚组(n＝123)显示LTI、FTI与患者预后关系不明显。 结论低LTI、高FTI、高ECW/BCM、液体负荷过量与患者中期死亡显著相关,而单个点的OH与中期死亡无显著相关。即使在校正年龄、Charlson共病评分后,LTI仍独立于Alb与预后相关,且两者间无交互作用,提示LTI联合血清Alb可评价尿毒症患者的营养指标和判断预后。     

25‐OH‐Vitamin D Deficiency and Cellular Alloimmunity as Measured by Panel of Reactive T Cell Testing in Dialysis Patients

Primed antidonor alloreactive T cells are detrimental to transplant outcome, but factors that impact the strength of this immune response prior to transplantation are unknown. We tested peripheral blood mononuclear cells from dialysis patients, against panels of allogeneic, primary B‐cell lines in a newly standardized IFNγ ELISPOT panel of reactive T cell (PRT) assay. Results were correlated with known alloantibody‐sensitizing events and other clinical parameters. As 25‐OH‐vitamin D deficiency is associated with enhanced cellular immunity, is common in dialysis patients and is correctable, we assessed the relationship between serum 25‐OH‐vitamin D and the PRT. Using independent test and validation cohorts we found that low serum levels of 25‐OH‐vitamin D (<26 ng/mL) correlated with high‐PRT values (in the upper 50th percentile, OR 0.02, p = 0.01) independent of age, sex, race, previous transplant, transfusion, pregnancy, time on dialysis, panel of reactive antibody, iPTH, and treatment with 1,25‐OH‐vitamin D. The data provide a potential mechanism for the possible relationship between vitamin D deficiency and poor posttransplant outcome, and support studies to test the impact of 25‐OH‐vitamin D repletion on alloimmunity and allograft injury in kidney transplant candidates.     

Vitamin D deficiency, CD4+CD28null cells and accelerated atherosclerosis in chronic kidney disease

Aim: Cardiovascular disease (CVD) is the leading cause of death among chronic kidney disease (CKD) patients. The role of vitamin D remains controversial in this process. We evaluated the relationship between 25‐hydroxyvitamin D, abnormal T helper cells (CD4+CD28null cells), systemic inflammation and atherosclerosis in CKD patients. Methods: A total of 101 stage 4–5 non‐dialysis CKD patients and 40 healthy controls were studied. Common carotid artery intima media thickness (CCA‐IMT) was measured with an ultrasound system. 25(OH) vitamin D and highly sensitive C‐reactive protein (hsCRP) were measured in serum by enzyme linked immunosorbent assay. The frequency of circulating CD4+CD28null cells was evaluated by flowcytometry. Results: CKD subjects exhibited higher CCA‐IMT (0.71 ± 0.01 vs 0.56 ± 0.01 mm, P < 0.0001), hsCRP (90.7 ± 5.8 vs 50.1 ± 8.6 µg/mL, P < 0.0001), CD4+CD28null cell frequency (9.1 ± 0.9 vs 3.6 ± 0.5%, P < 0.0001) and lower 25(OH) vitamin D levels (17.9 ± 1.9 vs 26.9 ± 3.5 ng/mL, P < 0.0001). In CKD subjects, serum 25 (OH) vitamin D level showed a strong inverse correlation with CCA‐IMT (r = ?0.729, P < 0.0001) and correlated with CD4+CD28null cell frequency (r = ?0.249, P = 0.01) and hsCRP (r = ?0.2, P = 0.047). We also noted correlation of IMT with patient age (r = 0.291, P = 0.004) and CD4+CD28null cells (r = 0.34, P = 0.001). On multiple regression analysis, 25(OH) vitamin D level, diabetic status and CD4+CD28null cell frequency exhibited independent association with IMT in CKD subjects. Conclusions: Vitamin D deficiency, inflammatory activation and higher frequency of CD4+CD28null T lymphocyte population correlate with preclinical atherosclerotic changes in CKD population. These findings suggest possible linkage between vitamin D metabolism and T cell modulation – abnormalities that may contribute to development of atherosclerosis in CKD.     

Abnormalities of the PTH-vitamin D axis and bone turnover markers in children,adolescents and adults with cystic fibrosis: comparison with healthy controls

Abnormalities of calcium and vitamin D metabolism in cystic fibrosis (CF) are well documented. We tested the hypothesis that alterations in calcium metabolism are related to vitamin D deficiency, and that bone resorption is increased relative to accretion in patients with CF. Calcitropic hormones, electrolytes, osteocalcin (OC) and bone alkaline phosphatase (BAP), (markers of bone mineralisation), urinary deoxypyridinoline [total (t) Dpd, a marker of bone resorption] and lumbar spine bone mineral density (LS BMD), expressed as a z-score, were measured in 149 (81 M) CF and 141 (61 M) control children aged 5.3-10.99 years, adolescents aged 11-17.99 years and adults aged 18-55.9 years. Data were analysed by multiple regression to adjust for age. In patients, FEV(1)% predicted and CRP (as disease severity markers), genotype and pancreatic status (PS) were recorded. The distribution of PTH differed between groups ( P<0.0001), with CF levels both below and above the control range. 25OH vitamin D (25OHD) was not different in control and CF subjects ( P=0.06). Active hormonal vitamin D (1,25(OH)(2)D) was lower in the CF group ( P<0.0001), not explained by 25OHD or disease severity, as was serum magnesium ( P<0.0001). OC was decreased in CF adults ( P=0.004), and tDpd increased in CF adolescents ( P=0.003) and adults ( P=0.03). The ratio of OC to tDpd (a measure of bone coupling) was similar in CF and control children, but decreased in CF adolescents ( P=0.04) and adults ( P=0.02), suggesting decreased overall bone accrual in CF adolescents and uncoupling of bone balance in adults. 1,25(OH)2D was weakly correlated with OC in CF children ( r=0.43, P=0.01), and with tDpd in CF and control adolescents ( r=0.33, P=0.05 and r=0.36, P=0.02, respectively); thus there was limited evidence of association of calcitropic hormones, which had an abnormal pattern in all age groups, with bone turnover. There was no association between calcitropic hormones or bone turnover markers and LS BMD z-score. Despite vitamin D sufficiency, abnormalities of calcium metabolism and bone turnover markers were still apparent and bone accretion was decreased relative to resorption in the CF adolescent and adult groups. These changes were not fully explained by disease severity or genotype, but are consistent with reports of decreased BMD and unique bone histomorphometry in older subjects with CF.