论文部分内容阅读
目的观察IgA肾病(IgAN)的临床病理特征,探讨肾小管间质损害与小儿IgAN进展的关系。方法收集2004年1月-2008年12月经本院肾活检确诊为原发性IgAN的165例患儿(男107例,女58例;年龄3～17岁)的临床及病理资料,并进行回顾性分析。结果本组患儿肾脏受损的组织学特点为均存在肾小球系膜区病变,肾小球毛细血管襻的病变多为节段性分布;急性重症病变为血管襻纤维素样坏死、新月体形成;慢性化病变则为肾小球毛细血管襻瘢痕形成,导致球性硬化。而肾小管间质也有不同程度损害。肾小管间质无损害组占15.2%,肾小管间质轻度损害组占43.6%,中度损害组占33.9%,重度损害组占7.3%。不同肾小管间质损害程度组年龄、病程比较差异均无统计学意义(Pa>0.05)。随着肾小管间质损害程度的加重,患儿血压升高,尿蛋白定量增加,血肌酐升高;随着系膜增殖程度及新月体积分的增加,肾小管间质损害程度加重;肾小管间质损害程度与球性硬化呈正相关(r=0.461,P<0.01)。结论随着小管间质损害程度的加重,IgAN进行性加重。肾小管间质损害与蛋白尿、高血压、肾小球系膜增生、球性硬化、新月体形成密切相关。肾小管间质损害是IgAN进展的重要原因之一。
Objective To observe the clinicopathological features of IgA nephropathy (IgAN) and to explore the relationship between tubulointerstitial damage and the progress of IgAN in children. Methods The clinical and pathological data of 165 children (107 males and 58 females; aged 3-17 years) diagnosed as primary IgAN by renal biopsy in our hospital from January 2004 to December 2008 were collected and reviewed Sexual analysis. Results The histological features of kidney damage in this group of children were all the glomerular mesangial area lesions, the lesions of glomerular capillary loop were mostly segmental distribution; acute severe disease was vascular calcification fibrosis, new The formation of the body; chronic lesions of glomerular capillary scar formation, resulting in sclerosis. The tubulointerstitial damage to varying degrees. Tubulointerstitial injury group accounted for 15.2%, mild tubulointerstitial injury group accounted for 43.6%, moderate damage group accounted for 33.9%, severe injury group accounted for 7.3%. There was no significant difference in the age and course of tubulointerstitial injury among groups (Pa> 0.05). With the severity of tubulointerstitial damage, children with elevated blood pressure, urine protein increased, serum creatinine increased; with the mesangial proliferation and crescent volume increases, the degree of tubulointerstitial damage increased; kidney The degree of tubulointerstitial damage was positively correlated with the degree of sclerosis (r = 0.461, P <0.01). Conclusions As tubulointerstitial damage aggravates, IgAN progresses. Tubulointerstitial damage and proteinuria, hypertension, mesangial proliferation, ball sclerosis, crescent formation are closely related. Tubulointerstitial damage is one of the important reasons for the progress of IgAN.