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摘要: 目的：探讨恶性高血压患者是否存在补体活化及其与临床的相关性。方法：选取恶性高血压肾损害患者18例（恶高组），原发性高血压患者15例（原发组），同期健康查体的正常人18例（对照组）。采用双抗体夹心酶联免疫吸附（ELISA）法测定血清经典途径、旁路途径、凝集素途径各自激活标志物C1q、Bb、FCN2，经典及凝集素途径共同激活产物C4d、共同调节因子sCR1，旁路途径的调节因子补体H因子（CFH），以及3条途径共同的补体激活产物C3a、C5a、SC5b-9，同时收集研究对象血清生化、补体C3、C4及尿蛋白等临床指标。结果：恶高组血清Bb、C4d、CFH、C3a及SC5b-9水平明显高于原发组和对照组，差异有统计学意义（P<0.05），原发组与对照组比较差异无统计学意义；恶高组血清sCR1、C5a水平明显高于对照组，差异有统计学意义（P<0.05）；恶性高血压患者血清CFH水平与血清肌酐呈正相关（r=0.682，P=0.009），C4d与24 h尿蛋白定量呈正相关（r=0.804，P=0.002）。结论：恶性高血压患者补体系统被激活，且旁路途径活化并参与恶性高血压患者肾损伤。sCR1、C4d水平升高是否与经典和（或）凝集素途径相关有待于进一步探讨。Abstract: Objective: To investigate the presence of complement activation and its association with clinical feature in patients with malignant hypertension.Method: Double antibody sandwich enzyme linked immune sorbent assay (ELISA) was used to evaluate the serum levels of complement component(C1q, Bb, FCN2, C4d, sCR1, CFH, C3a, C5a, SC5b-9) in 18 patients with malignant hypertension, 15 patients with hypertension and 18 normal controls. At the same time, the indicators of clinical biochemistry, complement C3 and C4, and protein in the urine of the patients with malignant hypertension were collected.Result: The levels of serum Bb, C4d, CFH, C3a and SC5b-9 in patients with malignant hypertension were significantly higher than those in patients with hypertension and in normal controls(P<0.05) with no significant difference between the hypertension group and control group. The levels of serum sCR1 and C5a in patients with malignant hypertension were significantly higher than those in normal control group, the difference was statistically significant(P<0.05);The level of serum CFH was positively correlated with creatinine(r=0.682, P=0.009), and the level of serum C4d was positively correlated with 24-hour urine protein(r=0.804, P=0.002).Conclusion: The complement system is activated in patients with malignant hypertension, and the alternative pathway activation participates in the malignant hypertensive renal damage. Further study is needed for the correlation between the increase of sCR1/C4d and classical and/or the lectin pathway.
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Key words:
- malignant hypertension /
- complement
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