CAJ | 학술논문

目的：研究单纯激素和激素联合不同免疫抑制剂（他克莫司、CTX等）对原发性IgA肾病伴轻中度肾功能损伤患者的疗效及安全性。方法纳入原发性IgA肾病患者36例。入组条件：30 ml·min-1·(1.73 m2)-1≤eGFR＜90 ml·min-1·(1.73 m2)-1、蛋白尿＞1.0 g/24 h。随机分成单纯激素组、激素+环磷酰胺组（CTX组）和激素+他克莫司组（他克莫司组）。结果单纯激素组、CTX组和他克莫司组24 h尿蛋白定量在治疗3个月[（0.90±0.75）g/24 h、（1.40±1.24）g/24 h、（1.10±1.33）g/24 h]、6个月[（0.76±0.73）g/24 h、（0.87±0.83）g/24 h、（0.78±0.69）g/24 h]、12个月[（0.35±0.35） g/24 h、（0.68±0.70） g/24 h、（0.69±0.82） g/24 h]时，均较基线值[（1.91±0.81）g/24 h，（2.42±1.46）g/24 h，（2.57±1.87）g/24 h，均P＜0.05]，且随着治疗时间的加长整体呈下降趋势。治疗6个月时，激素组和CTX组Scr与基线相比降低，差异无统计学意义[（111.72±31.23）μmol/L比（121.17±36.51）μmol/L ，（111.33±22.76）μmol/L比（124.33±35.51）μmol/L ，均P＜0.05]；他克莫司组血肌酐无变化。12个月时各治疗组Scr与基线相比差异无统计学意义（均P＞0.05）。各治疗组eGFR（CKD?EPI公式）与基线相比差异无统计学意义。不良反应：单纯激素组血糖升高1例，肝损1例；他克莫司组血糖升高2例、糖耐量异常1例，肝损1例。结论单纯激素、激素联合他克莫司或联合CTX在治疗伴轻中度肾功能不全的IgA肾病中有较好的控制蛋白尿作用，且未发现血肌酐明显上升；部分激素联合他克莫司治疗的患者可出现血糖升高，注意检测血药浓度很关键。
목적：연구단순격소화격소연합불동면역억제제（타극막사、CTX등）대원발성IgA신병반경중도신공능손상환자적료효급안전성。방법납입원발성IgA신병환자36례。입조조건：30 ml·min-1·(1.73 m2)-1≤eGFR＜90 ml·min-1·(1.73 m2)-1、단백뇨＞1.0 g/24 h。수궤분성단순격소조、격소+배린선알조（CTX조）화격소+타극막사조（타극막사조）。결과단순격소조、CTX조화타극막사조24 h뇨단백정량재치료3개월[（0.90±0.75）g/24 h、（1.40±1.24）g/24 h、（1.10±1.33）g/24 h]、6개월[（0.76±0.73）g/24 h、（0.87±0.83）g/24 h、（0.78±0.69）g/24 h]、12개월[（0.35±0.35） g/24 h、（0.68±0.70） g/24 h、（0.69±0.82） g/24 h]시，균교기선치[（1.91±0.81）g/24 h，（2.42±1.46）g/24 h，（2.57±1.87）g/24 h，균P＜0.05]，차수착치료시간적가장정체정하강추세。치료6개월시，격소조화CTX조Scr여기선상비강저，차이무통계학의의[（111.72±31.23）μmol/L비（121.17±36.51）μmol/L ，（111.33±22.76）μmol/L비（124.33±35.51）μmol/L ，균P＜0.05]；타극막사조혈기항무변화。12개월시각치료조Scr여기선상비차이무통계학의의（균P＞0.05）。각치료조eGFR（CKD?EPI공식）여기선상비차이무통계학의의。불량반응：단순격소조혈당승고1례，간손1례；타극막사조혈당승고2례、당내량이상1례，간손1례。결론단순격소、격소연합타극막사혹연합CTX재치료반경중도신공능불전적IgA신병중유교호적공제단백뇨작용，차미발현혈기항명현상승；부분격소연합타극막사치료적환자가출현혈당승고，주의검측혈약농도흔관건。
Objective To investigate the efficacy and safety of immunosuppressive therapy (Tacrolimus or CTX) in primary IgA nephropathy (IgAN) with mild or moderate renal dysfunction. Methods Thirty?six primary IgAN patients diagnosed by renal biopsy, with mild or moderate renal dysfunction[30 ml·min-1·(1.73 m2)-1≤eGFR<90 ml·min-1·(1.73 m2)-1, proteinuria>1.0 g/24 h] were recruited in this randomized controlled trial. All the patients were assigned into steroid therapy alone, steroid combined with CTX (CTX group) and steroid combined with tacrolimus (tacrolimus group). Results The 24?hour proteinuria at baseline were (1.91±0.81) g/24 h, (2.42±1.46) g/24 h, (2.57±1.87) g/24 h in steroid group, CTX group and tacrolimus group respectively. Compared with baseline, it was significantly decreased in steroid group at 3 months [(0.90 ± 0.75) g/24 h, P<0.05], 6 months [(0.76 ±0.73) g/24 h, P<0.05] and 12 months [(0.35±0.35) g/24 h, P<0.05], in CTX group at 3 months [(1.40± 1.24) g/24 h, P<0.05], 6 months [(0.87 ± 0.83) g/24 h, P<0.05] and 12 months [(0.68 ± 0.70) g/24 h, P<0.05], and in FK506 group at 3 months [(1.10±1.33) g/24 h, P<0.05], 6 months [(0.78±0.69) g/24 h, P<0.05] and 12 months [(0.69±0.82) g/24 h, P<0.05]. At 6 months, serum creatinine were decreased in steroid alone [(111.72 ± 31.23) μmol/L vs (121.17 ± 36.51) μmol/L, P<0.05] and in CTX group [(111.33 ± 22.76) μmol/L vs (124.33 ± 35.51) μmol/L, P<0.05], while no significant difference was detected in tacrolimus group. At 12 months, there was no significant difference in terms of serum creatinine in all three groups. Besides, there was no significant difference in terms of eGFR (CKD?EPI) in all three groups. One case presented hyperglycemia and one case had liver dysfunction during the treatment in steroid group. Two cases had hyperglycemia, one case had impaired glucose tolerance and one case had liver dysfunction in the tacrolimus group. Conclusions Steroid along, steroid combined with tacrolimus or combined with CTX are efficient in reducing urine protein in the treatment of primary IgAN with mild or moderate renal dysfunction without inducing increased serum creatinine. Given the occurrence of hyperglycemia during the treatment with steroid combined with tacrolimus, it is important to monitor tacrolimus concentration during the treatment.