中华肾脏病杂志
中華腎髒病雜誌
중화신장병잡지
2014年
12期
891-896
,共6页
许贺文%傅淑霞%张丽萍%靳敬伟
許賀文%傅淑霞%張麗萍%靳敬偉
허하문%부숙하%장려평%근경위
肾小球肾炎%糖皮质激素类%骨化二醇%糖调节受损
腎小毬腎炎%糖皮質激素類%骨化二醇%糖調節受損
신소구신염%당피질격소류%골화이순%당조절수손
Glomerulonephritis%Glucocorticoids%Calcifediol%Impaired glucose regulation
目的：探讨肾小球疾病患者血清25(OH)D水平及其对糖皮质激素治疗致糖代谢异常的影响。方法临床及肾活检确诊，首次应用泼尼松治疗的肾小球疾病患者61例，激素治疗前均做OGTT试验[糖耐量正常（NGR组，43例），糖代谢受损（IGR组，18例）]，ELISA法测血清25(OH)D浓度，化学发光法测血清胰岛素浓度，同期健康体检者16人为对照组。激素治疗后随访6周，各组资料进行统计学分析。结果（1）激素治疗前血清25(OH)D水平对照组[（64.09±13.53）nmol/L]高于NGR组[（50.81±12.44）nmol/L]，NGR组高于IGR组[（42.71±8.09） nmol/L ，均P＜0.05]。患者血清25(OH)D不足和缺乏分别为18例（29.5%）和39例（63.9%）。肾炎患者25(OH)D水平高于肾病患者[（56.94±10.41） nmol/L比（45.88±11.55） nmol/L ，P＜0.05]。（2）激素治疗6周时基线IGR组患者类固醇糖尿病（SDM）发生率显著高于NGR组（61.11%比20.93%，P＜0.05）。25(OH)D基线水平NGR组[（55.68±13.09） nmol/L]、IGR组[（48.97±9.91） nmol/L]均显著高于SDM组[（40.91±7.82）nmol/L，均P＜0.05]。（3）血清25(OH)D水平与Alb、校正血钙浓度呈正相关（r=0.455、0.317，均P＜0.05），与BMI、TC、餐后2 h血糖及尿蛋白排泄量呈负相关（r=-0.302、-0.27、-0.361、-0.339，均P＜0.05）。（4）Logistic回归示：基线血清25(OH)D＜50 nmol/L、HbA1c＞5.6%发生SDM的风险分别为＞50 nmol/L、＜5.6%者的5.6、5.2倍；年龄每增加10岁，胰岛素抵抗指数每增加1，发生SDM的风险分别增加2.4、2.8倍。结论绝大多数肾小球疾病患者血清25(OH)D不足或缺乏；低血清25(OH)D水平是糖皮质激素致类固醇糖尿病发生的主要危险因素之一。
目的：探討腎小毬疾病患者血清25(OH)D水平及其對糖皮質激素治療緻糖代謝異常的影響。方法臨床及腎活檢確診，首次應用潑尼鬆治療的腎小毬疾病患者61例，激素治療前均做OGTT試驗[糖耐量正常（NGR組，43例），糖代謝受損（IGR組，18例）]，ELISA法測血清25(OH)D濃度，化學髮光法測血清胰島素濃度，同期健康體檢者16人為對照組。激素治療後隨訪6週，各組資料進行統計學分析。結果（1）激素治療前血清25(OH)D水平對照組[（64.09±13.53）nmol/L]高于NGR組[（50.81±12.44）nmol/L]，NGR組高于IGR組[（42.71±8.09） nmol/L ，均P＜0.05]。患者血清25(OH)D不足和缺乏分彆為18例（29.5%）和39例（63.9%）。腎炎患者25(OH)D水平高于腎病患者[（56.94±10.41） nmol/L比（45.88±11.55） nmol/L ，P＜0.05]。（2）激素治療6週時基線IGR組患者類固醇糖尿病（SDM）髮生率顯著高于NGR組（61.11%比20.93%，P＜0.05）。25(OH)D基線水平NGR組[（55.68±13.09） nmol/L]、IGR組[（48.97±9.91） nmol/L]均顯著高于SDM組[（40.91±7.82）nmol/L，均P＜0.05]。（3）血清25(OH)D水平與Alb、校正血鈣濃度呈正相關（r=0.455、0.317，均P＜0.05），與BMI、TC、餐後2 h血糖及尿蛋白排洩量呈負相關（r=-0.302、-0.27、-0.361、-0.339，均P＜0.05）。（4）Logistic迴歸示：基線血清25(OH)D＜50 nmol/L、HbA1c＞5.6%髮生SDM的風險分彆為＞50 nmol/L、＜5.6%者的5.6、5.2倍；年齡每增加10歲，胰島素牴抗指數每增加1，髮生SDM的風險分彆增加2.4、2.8倍。結論絕大多數腎小毬疾病患者血清25(OH)D不足或缺乏；低血清25(OH)D水平是糖皮質激素緻類固醇糖尿病髮生的主要危險因素之一。
목적：탐토신소구질병환자혈청25(OH)D수평급기대당피질격소치료치당대사이상적영향。방법림상급신활검학진，수차응용발니송치료적신소구질병환자61례，격소치료전균주OGTT시험[당내량정상（NGR조，43례），당대사수손（IGR조，18례）]，ELISA법측혈청25(OH)D농도，화학발광법측혈청이도소농도，동기건강체검자16인위대조조。격소치료후수방6주，각조자료진행통계학분석。결과（1）격소치료전혈청25(OH)D수평대조조[（64.09±13.53）nmol/L]고우NGR조[（50.81±12.44）nmol/L]，NGR조고우IGR조[（42.71±8.09） nmol/L ，균P＜0.05]。환자혈청25(OH)D불족화결핍분별위18례（29.5%）화39례（63.9%）。신염환자25(OH)D수평고우신병환자[（56.94±10.41） nmol/L비（45.88±11.55） nmol/L ，P＜0.05]。（2）격소치료6주시기선IGR조환자류고순당뇨병（SDM）발생솔현저고우NGR조（61.11%비20.93%，P＜0.05）。25(OH)D기선수평NGR조[（55.68±13.09） nmol/L]、IGR조[（48.97±9.91） nmol/L]균현저고우SDM조[（40.91±7.82）nmol/L，균P＜0.05]。（3）혈청25(OH)D수평여Alb、교정혈개농도정정상관（r=0.455、0.317，균P＜0.05），여BMI、TC、찬후2 h혈당급뇨단백배설량정부상관（r=-0.302、-0.27、-0.361、-0.339，균P＜0.05）。（4）Logistic회귀시：기선혈청25(OH)D＜50 nmol/L、HbA1c＞5.6%발생SDM적풍험분별위＞50 nmol/L、＜5.6%자적5.6、5.2배；년령매증가10세，이도소저항지수매증가1，발생SDM적풍험분별증가2.4、2.8배。결론절대다수신소구질병환자혈청25(OH)D불족혹결핍；저혈청25(OH)D수평시당피질격소치류고순당뇨병발생적주요위험인소지일。
Objective To explore the levels of serum 25(OH)D in glomerular disease patients and investigate its influence on the impaired glucose metabolism after treated with glucocorticoid. Methods A total of 61 patients with glomerular disease confirmed by clinical diagnosis and renal biopsy were included in the case group before receiving steroid therapy. 16 cases were selected as control at the same period. Before and six weeks after the treatment of glucocorticoid, all subjects took oral glucose tolerance test (OGT). According to the results of OGT, patients were divided into normal glucose regulation (NGR) group, impaired glucose regulation (IGR) group and steroid diabetes mellitus (SDM) group. Serum 25(OH)D levels were detected with enzyme?linked immunosorbent assay (ELISA), and other clinical data including albumin(Alb), Scr and urine protein were collected. Results (1) Before treated with glucocorticoid, the serum 25(OH)D levels in the control group [(64.09±13.53) nmol/L]were significantly higher than that in NGR group [(50.81 ± 12.44) nmol/L], while the latter was significantly higher than that in IGR group [(42.71 ± 8.09) nmol/L, all P<0.05]. In the glomerular disease patients, 18 cases (29.51%) were 25(OH)D insufficiency and 39 cases(63.93%) were 25(OH)D deficiency. 25(OH)D levels in patients with nephritis were significantly higher than in patients with nephroitic syndrome[(56.94 ± 10.41) nmol/L vs (45.88 ± 11.55) nmol/L, P<0.05]. (2)6 weeks after the treatment, incidence of steroid diabetes in IGR group was significantly higher than that in NGR group (61.11% vs 20.93%, P<0.05). Baseline levels of 25(OH)D in NGR group and IGR group were all significantly higher than that in SDM group [(55.68 ± 13.09) nmol/L, (48.97 ± 9.91) nmol/L vs (40.91 ± 7.82) nmol/L, all P<0.05]. (3)Serum levels of 25(OH)D were positively correlated with serum albumin and serum calcium, and negatively correlated with BMI, urinary protein, cholesterol and the 2 hours postprandial blood glucose. (4)Logistic regression analysis indicated that 25(OH)D<50 nmol/L and HbA1c>5.6% increased the risk of developing steroid diabetes 5.586 and 5.197 times, respectively. Age increased 10 years or insulin resistance index increased one, the risk of occurred SDM increased 2.443 and 2.755 times, respectively. Conclusions Most glomerular disease patients are serum 25 (OH)D deficiency or insufficiency. Low level of serum 25(OH)D is one of the main risk factors of steroid diabetes in patients with glomerular disease when treated with glucocorticoid.
