CAJ | 학술논문

目的：从IgA血管炎角度分析器官特异性IgA血管炎(IgA肾病)与系统性IgA血管炎(紫癜性肾炎)临床和病理的差异。方法回顾性分析1993年6月至2014年11月住院的IgA肾病和紫癜性肾炎患儿的临床、病理和转归。结果 IgA肾病患儿405例，男256例、女149例，男女比例为1.7：1，平均发病年龄(10.2±2.8)岁；临床类型以肾病综合征最多，占31.6%，其次为血尿和蛋白尿型占27.9%。紫癜性肾炎患儿548例，男329例、女219例，男女比例为1.5：1，平均发病年龄(10.2±3.1)岁，临床类型以血尿和蛋白尿型最多，占60.9%，肾病综合征占21.4%。未发现IgA肾病因病情加重或反复进展至系统性血管炎的病例。结论 IgA肾病和过敏性紫癜的起病诱因、发病年龄、临床表现多有一致或重叠，二者在发病机制上也有一定共性，但IgA肾病更可能还有肾脏局部免疫紊乱等参与发病。
목적：종IgA혈관염각도분석기관특이성IgA혈관염(IgA신병)여계통성IgA혈관염(자전성신염)림상화병리적차이。방법회고성분석1993년6월지2014년11월주원적IgA신병화자전성신염환인적림상、병리화전귀。결과 IgA신병환인405례，남256례、녀149례，남녀비례위1.7：1，평균발병년령(10.2±2.8)세；림상류형이신병종합정최다，점31.6%，기차위혈뇨화단백뇨형점27.9%。자전성신염환인548례，남329례、녀219례，남녀비례위1.5：1，평균발병년령(10.2±3.1)세，림상류형이혈뇨화단백뇨형최다，점60.9%，신병종합정점21.4%。미발현IgA신병인병정가중혹반복진전지계통성혈관염적병례。결론 IgA신병화과민성자전적기병유인、발병년령、림상표현다유일치혹중첩，이자재발병궤제상야유일정공성，단IgA신병경가능환유신장국부면역문란등삼여발병。
Objectives To analysis clinical pathology of organ speciifc IgA vasculitis (IgA nephropathy) and systemic IgA vasculitis (allergic purpura) of purpura nephritis in children. Methods Clinical and pathological data of hospitalized pediatric patients of IgA nephropathy and purpura nephritis were retrospectively analyzed from June 1993 to November 2014. Results There were 405 patients of IgA nephropathy (256 males and 149 females). The ratio of male to female was 1.7:1. The average age was 10.2±2.8 years. The nephrotic syndrome (31.6%) was the most common clinical type, followed by hematuria and proteinuria (27.9%). There were 548 patients of purpura nephritis, 329 males and 219 females. The ratio of male to female was 1.5:1. The average age was 10.2±3.1 years. The hematuria and proteinuria (61.6%) was the most common clinical type, followed by nephrotic syndrome (21.4%). None of the IgA nephropathy progressed to systemic vasculitis (allergic purpura). Conclusions The causes, onset ages and clinical manifestations of IgA nephropathy and allergic purpura may be consistent or overlap, but none of IgA nephropathy (organ speciifcity IgA vasculitis) progressed to allergic purpura (systemic IgA vasculi-tis). IgA nephropathy might have more renal immune disorder mechanisms involved in its pathogenesis.