南方医科大学学报
南方醫科大學學報
남방의과대학학보
JOURNAL OF SOUTHERN MEDICAL UNIVERSITY
2010年
1期
133-136
,共4页
李申恒%史伟%夏运风%梁馨苓%王文健%马建超%邬丹
李申恆%史偉%夏運風%樑馨苓%王文健%馬建超%鄔丹
리신항%사위%하운풍%량형령%왕문건%마건초%오단
尿酸%高血压%IgA%肾小球肾炎
尿痠%高血壓%IgA%腎小毬腎炎
뇨산%고혈압%IgA%신소구신염
uric acid%hypertension%IgA%glomerulonephritis
目的 探讨尿酸升高IgA肾病临床病理特征变化的差异.方法 选取肾活检确诊时的IgA肾病患者171例,分为3组:①尿酸正常血压正常组58例,②尿酸升高血压正常组57例,③尿酸升高高血压组56例,比较各组临床病理变化的差异.结果 从尿酸正常血压正常组到尿酸升高血压止常组,再到尿酸升高高血压组,IgA肾病患者病程延长,体质量增加,收缩压、舒张压升高,血尿素氮、肌酐升高,肾小球滤过率下降,24 h尿蛋白增多,载脂蛋白A、高密度脂蛋白、白蛋白水平下降,载脂蛋白B100、甘油三酯、胆固醇、低街度脂蛋白升高.肾小球损伤加重,小管明显萎缩,间质纤维化加剧,血管壁进一步增厚,病理Lee氏分级①组以Ⅲ级为主,②组以Ⅲ、Ⅳ级为主,③组则Ⅲ、Ⅳ、Ⅴ级的患者显著增加.①、②组以系膜增生性肾炎为主要病理类型,③组则多为局灶节段硬化或硬化性肾炎多见.结论 尿酸升高IgA肾病患者的临床病理损伤重于尿酸正常的IgA肾病患者,高血压使尿酸升高IgA肾病患者的临床病理损伤进一步加重.
目的 探討尿痠升高IgA腎病臨床病理特徵變化的差異.方法 選取腎活檢確診時的IgA腎病患者171例,分為3組:①尿痠正常血壓正常組58例,②尿痠升高血壓正常組57例,③尿痠升高高血壓組56例,比較各組臨床病理變化的差異.結果 從尿痠正常血壓正常組到尿痠升高血壓止常組,再到尿痠升高高血壓組,IgA腎病患者病程延長,體質量增加,收縮壓、舒張壓升高,血尿素氮、肌酐升高,腎小毬濾過率下降,24 h尿蛋白增多,載脂蛋白A、高密度脂蛋白、白蛋白水平下降,載脂蛋白B100、甘油三酯、膽固醇、低街度脂蛋白升高.腎小毬損傷加重,小管明顯萎縮,間質纖維化加劇,血管壁進一步增厚,病理Lee氏分級①組以Ⅲ級為主,②組以Ⅲ、Ⅳ級為主,③組則Ⅲ、Ⅳ、Ⅴ級的患者顯著增加.①、②組以繫膜增生性腎炎為主要病理類型,③組則多為跼竈節段硬化或硬化性腎炎多見.結論 尿痠升高IgA腎病患者的臨床病理損傷重于尿痠正常的IgA腎病患者,高血壓使尿痠升高IgA腎病患者的臨床病理損傷進一步加重.
목적 탐토뇨산승고IgA신병림상병리특정변화적차이.방법 선취신활검학진시적IgA신병환자171례,분위3조:①뇨산정상혈압정상조58례,②뇨산승고혈압정상조57례,③뇨산승고고혈압조56례,비교각조림상병리변화적차이.결과 종뇨산정상혈압정상조도뇨산승고혈압지상조,재도뇨산승고고혈압조,IgA신병환자병정연장,체질량증가,수축압、서장압승고,혈뇨소담、기항승고,신소구려과솔하강,24 h뇨단백증다,재지단백A、고밀도지단백、백단백수평하강,재지단백B100、감유삼지、담고순、저가도지단백승고.신소구손상가중,소관명현위축,간질섬유화가극,혈관벽진일보증후,병리Lee씨분급①조이Ⅲ급위주,②조이Ⅲ、Ⅳ급위주,③조칙Ⅲ、Ⅳ、Ⅴ급적환자현저증가.①、②조이계막증생성신염위주요병리류형,③조칙다위국조절단경화혹경화성신염다견.결론 뇨산승고IgA신병환자적림상병리손상중우뇨산정상적IgA신병환자,고혈압사뇨산승고IgA신병환자적림상병리손상진일보가중.
Objective To explore the changes in the clinicopathological features of patients with IgA nephropathy with elevated uric acid level. Methods A total of 171 patients with IgA ncphropathy diagnosed at biopsy were classified into 3 groups, namely normotensive group with normal level uric acid (group 1), normotensive group with elevated uric acid level (group 2), and hypertensive group with elevated uric acid level (group 3). The clinicopathological features were compared between the 3 groups. Results From group 1 to group 3, the disease duration became elongated, body weight increased, systolic and diastolic pressures elevated, blood urea nitrogen and serum creatinine increased, glomerular filtration rate decreased, and 24-h urine protein increased; the apolipoprotein A, high-density lipoprotein and albumin levels decreased, while apolipoprotein B100, triglyceride, cholesterol and low-density lipoprotein increased. The glomerular damage, tubulointerstitial lesions and arteriole hypertrophy worsened, and Lee's grade Ⅲ changes were predominant in group 1, grade Ⅲ or Ⅳ in group 2 and grades Ⅲ-Ⅴ in group 3. Mesangial proliferative glomerulonephritis was the major pathological type in groups 1 and 2, as compared with focal segmental glomerulonephritis or sclerosing glomerulonephritis in group 3. Conclusion Patients with lgA nephropathy and elevated uric acid level have greater clinicopathological damage than those with normal uric acid level, and hypertension further aggravates such damages.