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.     

慢性肾脏病患者成纤维细胞生长因子23与肾功能及钙磷代谢的关系

目的 探讨慢性肾脏病（CKD）患者随着肾功能的变化,其成纤维细胞生长因子23（FGF23）与钙磷代谢的关系。 方法 研究对象为2008年8月至2009年4月在上海交通大学附属第一人民医院肾内科住院的初诊CKD患者72例,按照肾小球滤过率（GFR）水平分为5组,另设健康对照组20例。抽取受试者静脉血并分离血清,以酶联免疫法检测FGF23、25（OH）VitD3、1,25（OH）2VitD3;全自动生化分析仪测量钙（Ca）、磷（P）、血肌酐（Scr）、尿素氮（BUN）、白蛋白（Alb）水平;免疫放射法测定全段甲状旁腺激素（iPTH）。 结果 CKD患者血清FGF23水平随GFR降低逐渐升高,在CKD4期和5期时,血FGF23、P、iPTH上升明显,1,25（OH）2VitD3显著下降,与CKD1期差异有统计学意义（均P < 0.05）。CKD2~3期与CKD1期的FGF23、P、Ca、iPTH、活性维生素D水平差异均无统计学意义。血Ca、25（OH）VitD3随着肾功能下降有降低趋势,但各期间差异均无统计学意义。Pearson相关分析显示,CKD1~5期logFGF23与P、logiPTH呈正相关（r = 0.653,P < 0.01;r = 0.800,P < 0.01）,与GFR、1,25（OH）2VitD3呈负相关（r = -0.753,P < 0.01;r = -0.265,P < 0.05),与Ca、25（OH）VitD3无相关。CKD1~3期logFGF23与logiPTH呈正相关(r = 0.374,P < 0.05),而与Ca、P、25（OH）VitD3、1,25（OH）2VitD3、GFR均无相关。CKD4~5期log FGF23与P、logiPTH呈正相关（r = 0.381,P < 0.05;r = 0.515,P < 0.01）,与GFR呈负相关（r = -0.654,P < 0.01）,与Ca、25（OH）VitD3、1,25（OH）2VitD3无相关。 结论 随着肾功能减退,血清FGF23、P、iPTH水平逐渐升高,活性维生素D水平逐渐下降,尤以CKD4~5期明显。在肾脏病早期阶段（CKD1~3期）血iPTH水平与FGF23有关。当GFR<30 ml/min时,肾功能状态、血磷、血iPTH均可影响血FGF23水平。     

慢性肾脏病3～4期患者骨矿物质代谢紊乱的调查

目的 调查慢性肾脏病（chronickidney disease,CKD）3 ～4期患者慢性肾脏病矿物质及骨代谢紊乱（chronic kidney disease-mineral and bone disorder,CKD-MBD）的状况和检测有关骨代谢的指标.方法 检测111例CKD3～4期患者的血钙、血磷、血清全段甲状旁腺素（intact parathyroid hormone,iPTH）,并随机对其中20例患者行25羟维生素D[25（OH）D]及骨性碱性磷酸酶（bone-alkaline phosphare,b-ALP）的检测.结果 CKD3 ～4期患者矫正钙分别为（2.25 ±0.12 mmol/L）和（2.20±0.14 mmol/L）,血磷分别为（1.20 ±0.23 mmol/L）和（1.36 ±0.28 mmol/L）,iPTH分别为（73.18±51.77pg/mL）和（118.95±64.97pg/mL）,低钙血症的发生率分别为2.22％和6.06％,高磷血症的发生率分别为0％和7.58％,SHPT的发生率分别为37.78％和48.48％.CKD4期患者与CKD3期的患者相比,血钙显著性下降（P＜0.05）,iPTH水平显著升高（P＜0.05）,iPTH水平与血磷（r=0.103,P＞0.05）成正相关,与GFR（r=-0.422,P＜0.01）、血钙（r=-0.268,P＜0.01）成负相关.多元逐步回归分析显示,血钙、血磷、GFR是iPTH的独立影响因素（复相关系数R=0.482,p＜0.05）.CKD3～4期患者b-ALP（74.476±56.056ng/mL）,显著高于健康人（24.141±14.741ng/mL）（P＜0.01）,而25（OH）D（173.763±52.375ng/mL）显著低于健康人（306.995±93.085ng/mL）（P＜0.05）.结论 CKD早期患者存在CKD-MBD及骨代谢异常,且随着疾病的进展而愈加明显,应重视并早期干预,从而改善预后.     

558例非透析慢性肾脏病患者骨代谢指标的分析

目的 调查我院非透析慢性肾脏病患者骨代谢指标,为早期监测慢性肾脏病的矿物质及骨代谢异常提供依据。方法 回顾性分析我科住院的非透析慢性肾脏病患者558例,检测血甲状旁腺素(iPTH) , β-胶原特殊序列测定(β-CTX )、骨钙素、25-羟基维生素D3[25(OH)D3]、钙、磷、碱性磷酸酶(AKP)、肌酐、白蛋白、血糖等指标,留取晨尿进行尿常规及24 h尿蛋白定量检查,并分析相关影响因素。结果558例CKD患者平均年龄(70.6±15. 6 )岁,其中男性51.1%,女性48.9%,骨代谢指标男女性别间差异无统计学意义(P > 0. 05)。iPTH , β-CTX、骨钙素、血磷在CKD1-3期患者间差异无统计学意义,但与CKD4、5期患者差异有统计学意义(P<0.001);AKP在CKD5期明显升高。25(OH)D3在CKD1-5期患者中差异无统计学意义,各期CKD患者均存在25(OH)D3的不足及缺乏,其患病率分别为24.7% ,70.1%。单因素相关分析显示,MDRD-eGFR与iPTH ( r=–0. 457 ) , β-CTX (r=–0. 501)、骨钙素(r=–0. 485 )、血磷(r=–0. 501) ,AKP( r=–0. 187 )、年龄(r=–0. 140 )水平相关,均P<0.01;与血钙(r =– 0. 084 )水平相关,P < 0. 05。结论 非透析CKD患者各骨代谢指标在CKD早期无明显差异,但随着肾功能的减退进行性升高,且其之间存在正相关关系。CKD患者普遍存在25(OH)D3的缺乏且在CKD早期即有。     

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.     

不同阶段慢性肾脏病患者的25（OH）D3水平及相关性分析

目的为了解本地区不同阶段慢性肾脏病（chronic kidney disease,CKD）患者血清中25（OH）D3的水平,并探讨其水平与其他检测指标的关系。方法选择2013年1月至3月在我院肾病科住院的CKD非透析患者119例及同时期在我院体检的健康对照者30名（健康对照组）,采用酶联免疫法检测所有入选者25（0H）D3的水平,比较2组间25（0H）D3含量的差异,并分析其与体内其他生化指标的相关性。结果与健康对照组相比,CKD3～5期患者血清25（0H）D3含量均显著降低（PG0．05）,CKD患者血清25（OH）D3缺乏率达37．8％,不足率高达60．5％;CKD3～5期患者的血清甲状旁腺激素（PTH）、血肌酐（SCr）水平均显著升高（PG0．05）,CKD5期患者的血磷水平显著升高（P〈0．05）;25（OH）I）3与SCr、PTH、年龄、血糖（GLU）呈负相关（r=-0．480、-0．217、-0．604、-0．183,均PG0．05）;25（0H）D3与估算肾小球滤过率（eGFR）、血红蛋白（Hb）、血白蛋白（Alb）、性别、原发病种类呈正相关（r=0．569、0．512、0．359、0．200、0．300,均PG0．05）。结论本地区CKD3～5期患者的25（0H）D3水平明显下降,且CKD患者的25（OH）D3水平与SCr、eGFR、Alb、Hb、PTH等均存在一定的相关性。     

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。     

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。     

山西地区2012年至2013年我院就诊人群血清维生素D水平状况调查

目的 探讨目前山西地区不同季节人群的维生素D状况。方法 通过对2012 年6 月至2013年7月山西医科大学第二医院就诊的1313例患者血清25 羟维生素D [ 25（OH）D] 和甲状旁腺激素（PTH）水平,应用电化学发光免疫法测定血清25-羟维生素D[25（OH）D]、甲状旁腺激素（PTH）,按不同季节、性别进行分析。结果 ①所有检测人员的血清25(OH)D平均水平: 男性（11.38±6.29）ng/mL,女性（9.04±5.71）ng/mL。按照IOF维生素D水平判定标准:严重缺乏者占62.2%;维生素D缺乏者占28.46%;维生素D不足者占6.1%;维生素D充足者占3.25%。②血清25(OH)D水平与季节有显著相关性（r=0.228,P<0.05）;③血清25(OH)D与PTH 呈负相关（r=-0.272,P<0.05）。结论 受各种因素影响,目前山西地区成年人群中存在严重的维生素D不足和缺乏状况,应受到广泛的关注并改善现状,降低维生素D相关疾病的发病率。     

Relationship between serum 25-hydroxyvitamin D3 and heart valvular calcification in chronic kidney disease patients stage 3-5

Objective To detect the prevalence of heart valvular calcification (VC) and its related risk factors, and to investigate correlation between serum 25-hydroxyvitamin D3[25(OH)D3] and VC in chronic kidney disease (CKD) stage 3-5 patients. Methods A total of 294 CKD patients stage 3-5 were admitted in The Second Affiliated Hospital of Anhui Medical University. Their clinical and laboratory data were collected, patients were classified into two groups according echocardiography: patients with VC were defined as VC group while others were defined as non-VC group. The differences of 25(OH)D3 level and other data in two group were assessed, and related risk factors of VC were analyzed. Results Among 294 CKD patients, 82 were with VC (27.9%) while 212 were without VC (72.1%); serum 25(OH)D3 level was significantly higher in VC group than in non-VC group [(11.9±9.3) μg/L vs (9.6±7.2) μg/L, P＜0.05]. Age, cystatin C, hypersensitive C-reactive protein, pulmonary artery pressure, proportion of secondary hyperparathyroidism, incidence of abdominal aortic calcification and taking active vitamin D proportion were higher in VC group than in non-VC group (P＜0.05). Two classification logistic regression analyses showed that advanced age, high intact parathyroid hormone (iPTH) and 25(OH)D3, pulmonary arterial hypertension were risk factors for VC in CKD stage 3-5 patients. Conclusions The prevalence of VC is high in CKD stage 3-5 patients. Advanced age, bone metabolic disorder and pulmonary arterial hypertension are associated with VC.     

Effect of ergocalciferol supplementation on serum parathyroid hormone and serum 25-hydroxyvitamin D in chronic kidney disease

AIM: To assess the impact of the administration of ergocalciferol on serum parathyroid hormone levels at different stages of chronic kidney disease (CKD). METHODS: A continuous series of 85 patients with stages 3-5 CKD but excluding patients on dialysis referred to the Kaiser Kidney Program were followed. Baseline serum intact parathyroid hormone (iPTH) and serum 25(OH)D levels were measured. All patients were administered ergocalciferol in doses ranging from 800 iu/day to 100,000 iu/week. We obtained serum levels of iPTH and 25(OH)D for a post-treatment endpoint after a median treatment period of 90 days. RESULTS: Pre- and post-treatment serum iPTH levels displayed a mean difference of 2.8 pmol/L (95% CI 1.3-4.4, P < 0.001). Patients with stage 4 CKD had a mean difference of 3.6 pmol/L (95% CI 1.7-5.5, P < 0.001) between pre- and post-iPTH levels. Serum iPTH levels decreased among CKD stages 3 and 5, but were not statistically significant. All CKD groups analysed in the present study had significant increases in serum 25(OH)D levels. None of the study population required cessation of vitamin D therapy and no adverse outcomes were reported. CONCLUSION: Ergocalciferol supplementation appears a safe and effective treatment for CKD populations which may raise levels of serum 25(OH)D levels and decrease iPTH levels.     

Vitamin D bioavailability and catabolism in pediatric chronic kidney disease

Background

Vitamin D-binding protein (DBP) and catabolism have not been examined in the clinical setting of childhood chronic kidney disease (CKD).

Methods

The concentrations of serum vitamin D {25-hydroxyvitamin D [25(OH)D], 1,25-dihydroxyvitamin D [1,25(OH)₂D], 24,25-dihydroxyvitamin D [24,25(OH)₂D]}, DBP, intact parathyroid hormone (iPTH), and fibroblast growth factor-23 (FGF23) were measured in 148 participants with CKD stages 2–5D secondary to congenital anomalies of the kidney/urinary tract (CAKUT), glomerulonephritis (GN), or focal segmental glomerulosclerosis (FSGS). Free and bioavailable 25(OH)D concentrations were calculated using total 25(OH)D, albumin, and DBP concentrations.

Results

The concentrations of all vitamin D metabolites were lower with more advanced CKD (p?<?0.001) and glomerular diagnoses (p?≤?0.002). Among non-dialysis participants, DBP was lower in FSGS versus other diagnoses (FSGS–dialysis interaction p?=?0.02). Winter season, older age, FSGS and GN, and higher FGF23 concentrations were independently associated with lower concentrations of free and bioavailable 25(OH)D. Black race was associated with lower total 25(OH)D and DBP, but not free or bioavailable 25(OH)D. 24,25(OH)₂D was the vitamin D metabolite most strongly associated with iPTH. Lower 25(OH)D and higher iPTH concentrations, black race, and greater CKD severity were independently associated with lower levels of 24,25(OH)₂D, while higher FGF23 concentrations and GN were associated with higher levels of 24,25(OH)₂D.

Conclusions

Children with CKD exhibit altered catabolism and concentrations of DBP and free and bioavailable 25(OH)D, and there is an important impact of their underlying disease.     

The impact of over-the-counter vitamin D supplements on vitamin D and parathyroid hormone levels in chronic kidney disease

BACKGROUND: In addition to the known disturbances in mineral metabolism and vitamin D activation, the majority of patients with chronic kidney disease (CKD) do not have sufficient vitamin D stores. The impact of supplementation with low-dose, nonactive forms of vitamin D (calciferol) on parathyroid hormone (PTH) levels in this population is unknown, however. METHODS: A cross-sectional evaluation of vitamin D levels, intact parathyroid hormone (iPTH) and other laboratory results in 108 stage 3 and stage 4 CKD patients according to their intake of over-the-counter vitamin D. RESULTS: 37 patients took 400 IU of vitamin D daily with supplemental calcium and 71 did not. Compared to subjects who did not take it, patients who were on the supplement had higher 25(OH)D (31 +/- 15 vs. 17 +/- 9) ng/ml, higher 1,25(OH)D (21 +/- 12 vs. 16 +/- 9) pg/ml, lower iPTH (75 +/- 48 vs. 144 +/- 100) pg/ml and were more likely to meet K-DOQI PTH guidelines. However, these subjects were more likely to have oversuppressed iPTH values. The groups did not differ with regard to demographics, glomerular filtration rate and calcium and phosphorus levels. CONCLUSIONS: Vitamin D supplements may be a valuable tool in the prevention and treatment of hyperparathyroidism in patients with stages 3 and 4 CKD. CKD patients who have oversuppressed PTH need to be asked about their vitamin supplement intake.     

慢性肾脏病患者骨代谢与尿蛋白量的关系

目的 研究慢性肾脏病（CKD）患者骨代谢状况与尿蛋白量的关系。 方法 随机挑选2008年1月至2009年5月在本院肾活检证实为原发性肾小球疾病的CKD患者71例为对象。按尿蛋白量分为3组：A组25例,尿蛋白量<1.0 g/24 h;B组16例,尿蛋白量 （1.0~<3.5） g/24 h;C组30例,尿蛋白量≥3.5 g/24 h。健康体检者58例为健康对照组。常规测定血清白蛋白、24 h尿蛋白量及血清钙、磷、PTH、25羟基维生素D3[25-(OH)D3]、骨钙素（BGP）、I型胶原吡啶交联C终端肽（CTx）及尿钙/肌酐（UCa/Cr）等骨代谢指标。双能X线骨密度仪检测患者骨密度（BMD）。对各因素间进行Pearson相关分析。 结果 与健康对照组比较,A、B、C组CKD患者血钙分别为（2.23±0.08）、（2.13±0.09）、（2.04±0.06）比 （2.37±0.12） mmol/L;血25-（OH）D3分别为（50.19±6.58）、（47.78±6.69）、（42.42±10.85）比（56.34±8.34） nmol/L（均P < 0.05）;而UCa/Cr显著升高,分别为0.25±0.11、0.34±0.13、0.41±0.05比0.14±0.06（均P < 0.05）。B、C组血BGP分别为（18.69±7.35）、（16.13±5.76） μg/L,显著低于健康对照组的（22.88±6.21） μg/L;血CTx分别为（413.59±114.93）、（516.21±314.25） ng/L,显著高于健康对照组的（304.53±234.15） ng/L（均P < 0.05）。A、B两组BMD与健康对照组差异无统计学意义;C组BMD显著低于健康对照组[（1.028±0.090）比（1.090±0.062） g/cm2,P < 0.05]。Pearson相关分析显示,24 h尿蛋白量与血钙、血 25-(OH)D3呈负相关,与UCa/Cr 呈正相关;UCa/Cr与血CTx 呈正相关,与血BGP呈负相关;25-(OH)D3与BGP呈正相关,与CTx呈负相关。 结论 原发性肾小球疾病CKD患者的骨代谢异常主要表现为骨形成降低,骨吸收增加,其变化与蛋白尿程度相关,而大量尿蛋白患者骨代谢显著异常。     

Vitamin D status in children with chronic kidney disease

Background

The role of vitamin D status in patients with renal insufficiency and its relation to dietary intake and parathyroid hormone (PTH) secretion is of utmost interest given the morbidity and mortality associated with the disordered mineral metabolism seen in chronic kidney disease (CKD).

Methods

We conducted a cross-sectional study of 100 pediatric patients with a diagnosis of CKD stage 1–5 at Children's Hospital Boston, measuring blood levels of 25-hydroxyvitamin D [25(OH)D], 1,25-dihydroxyvitamin D [1,25(OH)₂D], and parathyroid hormone and obtaining data on nutrient intake and other variables related to vitamin D status.

Results

Subjects ranged in age from 6 months to 18?years, and 60 were male, 40 female. Of the 100 patients, 16 % were deficient in 25(OH)D (≤20?ng/mL) and another 24 % were insufficient (≤30?ng/mL), with 40 % in the suboptimal range. Serum 25(OH)D and dietary vitamin D intake were not correlated.

Conclusions

We found a high prevalence of hyperparathyroidism in early-stage CKD and a significant relationship between 25(OH)D and PTH regardless of calcitriol level. Our study results support the suggestion that optimization of vitamin D levels may provide additional benefit in preventing or improving hyperparathyroidism in patients with early CKD and likely remains important as an adjunctive therapy in children with advanced CKD.