中国综合临床
中國綜閤臨床
중국종합림상
CLINICAL MEDICINE OF CHINA
2011年
1期
5-8
,共4页
李丽娟%朱彩侠%于欣%杨震
李麗娟%硃綵俠%于訢%楊震
리려연%주채협%우흔%양진
高血压肾损害%肿瘤坏死因子-α%白细胞介素-10
高血壓腎損害%腫瘤壞死因子-α%白細胞介素-10
고혈압신손해%종류배사인자-α%백세포개소-10
Hypertensive renal damage%Tumor necrosis factor-α%Interleukin 10
目的 探讨肿瘤坏死因子-α(TNF-α)和白细胞介素-10(IL-10)在高血压肾损害患者中的变化及其相关性.方法 将73例原发性高血压患者(原发性高血压组)根据其尿蛋白排泄率不同又分为2个亚组:单纯高血压组37例,高血压肾损害组36例;采用放射免疫法检测血清TNF-α、IL-10浓度.同期选择30名健康体检者作为正常对照组.结果 原发性高血压组TNF-α高于正常对照组[(2.91±0.94)μg/L与(0.98±0.35)μg/L,P＜0.01],其中高血压肾损害组TNF-α高于单纯高血压组[(3.75±0.88)μg/L与(1.87±0.58)μg/L,P＜0.01].原发性高血压组IL-10低于正常对照组[(19.2±5.8)μg/L与(28.6±5.7)μg/L,P＜0.01],其中高血压肾损害组IL-10又低于单纯高血压组[(15.4±4.3)μg/L与(22.5±5.9)μg/L,P＜0.01].原发性高血压组TNF-α、IL-10与尿蛋白排泄率有相关性(r=0.703,P＜0.001 ;r=-0.613,P＜0.001),而与血压水平无相关性.结论 高血压肾损害患者TNF-α升高,IL-10水平降低,细胞因子系统的失衡可能参与了高血压肾损害的进展.
目的 探討腫瘤壞死因子-α(TNF-α)和白細胞介素-10(IL-10)在高血壓腎損害患者中的變化及其相關性.方法 將73例原髮性高血壓患者(原髮性高血壓組)根據其尿蛋白排洩率不同又分為2箇亞組:單純高血壓組37例,高血壓腎損害組36例;採用放射免疫法檢測血清TNF-α、IL-10濃度.同期選擇30名健康體檢者作為正常對照組.結果 原髮性高血壓組TNF-α高于正常對照組[(2.91±0.94)μg/L與(0.98±0.35)μg/L,P＜0.01],其中高血壓腎損害組TNF-α高于單純高血壓組[(3.75±0.88)μg/L與(1.87±0.58)μg/L,P＜0.01].原髮性高血壓組IL-10低于正常對照組[(19.2±5.8)μg/L與(28.6±5.7)μg/L,P＜0.01],其中高血壓腎損害組IL-10又低于單純高血壓組[(15.4±4.3)μg/L與(22.5±5.9)μg/L,P＜0.01].原髮性高血壓組TNF-α、IL-10與尿蛋白排洩率有相關性(r=0.703,P＜0.001 ;r=-0.613,P＜0.001),而與血壓水平無相關性.結論 高血壓腎損害患者TNF-α升高,IL-10水平降低,細胞因子繫統的失衡可能參與瞭高血壓腎損害的進展.
목적 탐토종류배사인자-α(TNF-α)화백세포개소-10(IL-10)재고혈압신손해환자중적변화급기상관성.방법 장73례원발성고혈압환자(원발성고혈압조)근거기뇨단백배설솔불동우분위2개아조:단순고혈압조37례,고혈압신손해조36례;채용방사면역법검측혈청TNF-α、IL-10농도.동기선택30명건강체검자작위정상대조조.결과 원발성고혈압조TNF-α고우정상대조조[(2.91±0.94)μg/L여(0.98±0.35)μg/L,P＜0.01],기중고혈압신손해조TNF-α고우단순고혈압조[(3.75±0.88)μg/L여(1.87±0.58)μg/L,P＜0.01].원발성고혈압조IL-10저우정상대조조[(19.2±5.8)μg/L여(28.6±5.7)μg/L,P＜0.01],기중고혈압신손해조IL-10우저우단순고혈압조[(15.4±4.3)μg/L여(22.5±5.9)μg/L,P＜0.01].원발성고혈압조TNF-α、IL-10여뇨단백배설솔유상관성(r=0.703,P＜0.001 ;r=-0.613,P＜0.001),이여혈압수평무상관성.결론 고혈압신손해환자TNF-α승고,IL-10수평강저,세포인자계통적실형가능삼여료고혈압신손해적진전.
Objective To investigate the changes of the serum levels of necrosis alpha (TNF-o)and interleukin 10( IL-10 )in patients with hypertensive renal damage,and to study the correlation of TNF-α and IL-10 with the hypertensive renal damage. Methods Seventy three patients with primary hypertension were divided into two groups according to their urinary albumin excretion rate(UAER): simple hypertensive group( n = 37 ),hypertensive renal damage group(n =36). TNF-α and IL-10 were measured using radioimmune assay. Thirty normotensive healthy persons were selected as normotensive control group. Results TNF-α were significantly higher and IL-10 significantly lower in patients with essential hypertension than those in normotensive control group(TNF-α: [2.91 ±0.94]μg/L vs [0.98 ±0.35]μg/L,P＜0. 05;IL-10:[ 19.2 ±5.8]μg/L vs [28.6±5. 7] μg/L,P ＜0. 01 ) ,and in patients with hypertension,those with renal damage had higher TNF-α and lower IL-10 than those without( TNF-α: [ 3.75 ± 0. 88 ] μg/L vs [ 1.87 ± 0. 58 ] μg/L, P ＜ 0. 01; IL-10: [ 15. 4 ± 4. 3 ]μg/L vs [ 22. 5 ± 5.9 ] μg/L, P ＜ 0. 01 ), with statistically significant difference between groups ( P ＜ 0. 01 ).TN F-α and IL- 10 were found to have correlations with UAER ( r = 0. 703, P ＜ 0. 001; r = - 0. 613, P ＜ 0. 001 ),but no correlation with the level of blood pressure. Conclusion TNF-α increased and IL-10 decreased significantly in patients with hypertensive renal damage, which indicates that the imbalanced cytokine network may play a role in the pathological mechanisms of hypertensive renal damage.
