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Published on: November 7, 2017
Association between circulatory complement activation and hypertensive renal damage: a case-control study
Zhongli Wang1, Tingting Zhang2, Xinyu Wang3
1Department of Physical Examination Center, Hebei General Hospital, Shijiazhuang, Hebei, China.
Insights
Abnormal complement alternative pathway (AP) activation, indicated by elevated C3 and AP50 and reduced CFH, is linked to hypertensive renal damage. These complement factors are independent risk factors for developing and worsening kidney damage in hypertension.
Area of Science:
- Nephrology
- Immunology
- Cardiovascular Research
Background:
- Hypertensive renal damage is a significant complication of essential hypertension.
- The role of the complement system, particularly the alternative pathway (AP), in this damage is not fully understood.
Purpose of the Study:
- To investigate the potential role of complement system activation, specifically the AP, in the pathogenesis of hypertensive renal damage.
- To identify specific complement factors associated with hypertension and renal damage.
Main Methods:
- Serum levels of complement C3, complement Factor H (CFH), and AP activation (AP50) were measured.
- Participants included patients with essential hypertension and renal damage (RD), essential hypertension without renal damage (NRD), and healthy controls.
- Multifactorial logistic regression analysis was used to identify independent risk factors.
Main Results:
- Serum C3 and AP50 levels increased progressively from healthy controls to NRD to RD.
- CFH levels were significantly lower in patients with RD compared to NRD and healthy controls.
- Elevated C3, elevated AP50, and decreased CFH were identified as independent risk factors for the development and progression of hypertensive renal damage, alongside age and BMI.
Conclusions:
- Abnormal activation of the complement system, particularly the AP, is implicated in the pathogenesis of hypertensive renal damage.
- Complement factors C3, AP50, and CFH serve as potential biomarkers and therapeutic targets for managing hypertensive renal damage.
Objective:
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.
Methods:
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.
Results:
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.
Conclusion:
Abnormal activation of complement, particularly complement AP, may be a risk factor for the development and progression of hypertensive renal damage.
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