PDF(Pubmed)
Abstract：
UNASSIGNED: The aim of this study was to investigate the potential importance of complement system activation, with particular emphasis on the complement alternative pathway (AP), in the pathogenesis of hypertensive renal damage.
UNASSIGNED: Serum complement C3, complement Factor H (CFH) and AP activation were assessed in 66 participants with established essential hypertension with renal damage (RD). Fifty-nine patients with age- and sex-matched essential hypertension without renal damage (NRD) and 58 healthy participants (normal) were selected.
UNASSIGNED: Our study revealed that C3 and AP50 continuously increased from normal to NRD to RD (p < 0.05, respectively), while CFH was significantly lower than that in NRD and healthy participants (p < 0.05, respectively). After multifactorial logistic regression analysis corrected for confounders, elevated serum C3 (p = 0.001) and decreased CFH (p < 0.001) were found to be independent risk factors for hypertension in healthy participants; elevated serum C3 (p = 0.034), elevated AP50 (p < 0.001), decreased CFH (p < 0.001), increased age (p = 0.011) and increased BMI (p = 0.013) were found to be independent risk factors for the progression of hypertension to hypertensive renal damage; elevated serum C3 (p = 0.017), elevated AP50 (p = 0.023), decreased CFH (p = 0.005) and increased age (p = 0.041) were found to be independent risk factors for the development of hypertensive renal damage in healthy participants.
UNASSIGNED: Abnormal activation of complement, particularly complement AP, may be a risk factor for the development and progression of hypertensive renal damage.
UNASSIGNED: Serum complement C3, complement Factor H (CFH) and AP activation were assessed in 66 participants with established essential hypertension with renal damage (RD). Fifty-nine patients with age- and sex-matched essential hypertension without renal damage (NRD) and 58 healthy participants (normal) were selected.
UNASSIGNED: Our study revealed that C3 and AP50 continuously increased from normal to NRD to RD (p < 0.05, respectively), while CFH was significantly lower than that in NRD and healthy participants (p < 0.05, respectively). After multifactorial logistic regression analysis corrected for confounders, elevated serum C3 (p = 0.001) and decreased CFH (p < 0.001) were found to be independent risk factors for hypertension in healthy participants; elevated serum C3 (p = 0.034), elevated AP50 (p < 0.001), decreased CFH (p < 0.001), increased age (p = 0.011) and increased BMI (p = 0.013) were found to be independent risk factors for the progression of hypertension to hypertensive renal damage; elevated serum C3 (p = 0.017), elevated AP50 (p = 0.023), decreased CFH (p = 0.005) and increased age (p = 0.041) were found to be independent risk factors for the development of hypertensive renal damage in healthy participants.
UNASSIGNED: Abnormal activation of complement, particularly complement AP, may be a risk factor for the development and progression of hypertensive renal damage.
摘要：
■这项研究的目的是调查补体系统激活的潜在重要性，特别强调补体旁路(AP)，在高血压肾损害的发病机制中。
■对66例原发性高血压合并肾损害(RD)患者进行血清补体C3、补体因子H(CFH)和AP激活评估。选择59例年龄和性别匹配的原发性高血压患者，无肾损害（NRD）和58例健康参与者（正常）。
■我们的研究表明，C3和AP50从正常到NRD再到RD连续增加（分别为p<0.05），而CFH显著低于NRD和健康参与者(p<0.05)。在校正了混杂因素的多因素逻辑回归分析后，血清C3升高（p=0.001）和CFH降低（p<0.001）是健康参与者高血压的独立危险因素；血清C3升高（p=0.034），AP50升高（p<0.001），CFH降低（p<0.001），年龄增加(p=0.011)和BMI增加(p=0.013)是高血压进展为高血压肾损害的独立危险因素;血清C3升高(p=0.017),AP50升高（p=0.023），CFH降低(p=0.005)和年龄增加(p=0.041)是健康参与者发生高血压肾损害的独立危险因素.
■补体异常激活，特别是补充AP，可能是高血压肾损害发展和进展的危险因素。
■对66例原发性高血压合并肾损害(RD)患者进行血清补体C3、补体因子H(CFH)和AP激活评估。选择59例年龄和性别匹配的原发性高血压患者，无肾损害（NRD）和58例健康参与者（正常）。
■我们的研究表明，C3和AP50从正常到NRD再到RD连续增加（分别为p<0.05），而CFH显著低于NRD和健康参与者(p<0.05)。在校正了混杂因素的多因素逻辑回归分析后，血清C3升高（p=0.001）和CFH降低（p<0.001）是健康参与者高血压的独立危险因素；血清C3升高（p=0.034），AP50升高（p<0.001），CFH降低（p<0.001），年龄增加(p=0.011)和BMI增加(p=0.013)是高血压进展为高血压肾损害的独立危险因素;血清C3升高(p=0.017),AP50升高（p=0.023），CFH降低(p=0.005)和年龄增加(p=0.041)是健康参与者发生高血压肾损害的独立危险因素.
■补体异常激活，特别是补充AP，可能是高血压肾损害发展和进展的危险因素。
