CAJ | 학술논문

目的探讨血清尿酸对IgA肾病临床、病理及预后的影响.方法回顾性分析我院2007年1月至2010年10月456例经肾穿刺活检病理确诊为原发性IgA肾病住院患者的临床和肾脏病理特点资料.采用t检验和x2检验进行统计学处理.结果 456例IgA肾病患者中高尿酸血症者127例,发生率为27.9％,高尿酸血症组平均年龄、男性所占比例、高血压发生率、血清胆固醇、甘油三酯、体质量指数、肌酐、尿蛋白定量(24h)水平显著高于血尿酸正常组(P＜0.05,P＜0.01)；高尿酸血症组肾组织病理病变程度显著重于血尿酸正常组(P＜0.01),分别为肾小球积分(8.1±0.8和5.3±0.9),肾小管间质积分(4.2±0.4和2.7±0.4),血管病变积分(1.43±0.60和0.76±0.29).结论高尿酸水平对IgA肾病有明显影响,积极降低血清尿酸,有效控制上述临床指标,可望减轻肾组织损害,延缓IgA肾病的进展.
목적 탐토혈청뇨산대IgA신병림상、병리급예후적영향.방법 회고성분석아원2007년1월지2010년10월456례경신천자활검병리학진위원발성IgA신병주원환자적림상화신장병리특점자료.채용t검험화x2검험진행통계학처리.결과 456례IgA신병환자중고뇨산혈증자127례,발생솔위27.9％,고뇨산혈증조평균년령、남성소점비례、고혈압발생솔、혈청담고순、감유삼지、체질량지수、기항、뇨단백정량(24h)수평현저고우혈뇨산정상조(P＜0.05,P＜0.01)；고뇨산혈증조신조직병리병변정도현저중우혈뇨산정상조(P＜0.01),분별위신소구적분(8.1±0.8화5.3±0.9),신소관간질적분(4.2±0.4화2.7±0.4),혈관병변적분(1.43±0.60화0.76±0.29).결론 고뇨산수평대IgA신병유명현영향,적겁강저혈청뇨산,유효공제상술림상지표,가망감경신조직손해,연완IgA신병적진전.
Objective To explore the effect of serum uric acid on the clinical manifestations,pathological characteristics and prognosis of IgA nephropathy.Methods Four hundred and fifty-six cases of primary IgA nephropathy confirmed by renal biopsy from Jan 2007 to Oct 2010 in the Ji'nan Military General Hospital were reviewed retrospectively.The clinical manifestations and pathological characteristics of all the patients were analyzed,x2-test and t-test were used for statistical analysis.Results There were 127 cases with hyperuricemia in 456 IgAN patients (27.9％).The mean age,percentage of male patients,number of patients with hypertension,the serum cholesterol and triglyceride level,body mass index (BMI),serum creatinine and 24 hour urine protein level in hyperuricemia group were significantly higher than those with normal serum uric acid (P＜0.01).The renal pathological changes,glomerular score (8.1 ±0.8 v 5.3t0.9 ),tubulointerstitial score (4.2±0.4 vs 2.7±0.4) and vasculopathy score ( 1.43±0.60 vs 0.76±0.29) in the hyperuricemia group were more severe than those with normal serum uric acid (P＜0.01).Conclusion High level of serum uric acid can affect IgA nephropathy significantly.It is effe-ctive to delay the kindey damage and progression of IgA nephropathy by decreasing the level of uric acid and control the clinical parameters listed above.