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Published on: June 2, 2022
Circulating CTRP9 correlates with the prevention of aortic calcification in renal allograft recipients
Nobuhiko Miyatake1, Hiroki Adachi1, Kanae Nomura-Nakayama1
1Department of Nephrology, Kanazawa Medical University School of Medicine, Daigaku, Uchinada, Ishikawa, Japan.
Insights
Cardiovascular disease (CVD) risk in kidney transplant patients may be reduced by C1q/TNF-α related protein-9 (CTRP9) and high-molecular-weight adiponectin (HMW-ADPN). Increased CTRP9 levels were associated with reduced aortic calcification progression in these patients.
Area of Science:
- Cardiovascular Research
- Nephrology
- Endocrinology
Background:
- Cardiovascular disease (CVD) is a leading cause of mortality in renal allograft recipients, primarily due to atherosclerosis.
- C1q/TNF-α related protein-9 (CTRP9), an adiponectin paralog, is implicated in atherosclerosis prevention, but its role in kidney transplant recipients is unclear.
Purpose of the Study:
- To investigate the relationship between serum CTRP9 concentration, serum adiponectin (ADPN) concentration, and vascular calcification in kidney transplant recipients.
- To evaluate the long-term changes in CTRP9, ADPN, and aortic calcification area index (ACAI) over 8 years.
Main Methods:
- Studied 50 kidney transplant recipients, measuring serum CTRP9, high-molecular-weight ADPN (HMW-ADPN), and ACAI from CT scans.
- Examined CTRP9, ADPN, and their receptors (AdipoR1, AdipoR2) expression in renal artery tissue via immunofluorescence.
- Analyzed correlations between serum concentrations, ACAI changes, and long-term trends.
Main Results:
- Initial CTRP9 levels did not correlate with eGFR or HMW-ADPN.
- Changes in CTRP9 positively correlated with HMW-ADPN changes and negatively with ACAI changes.
- Increased CTRP9 was linked to reduced ACAI progression, while aging exacerbated calcification.
Conclusions:
- CTRP9 and HMW-ADPN may prevent aortic calcification progression in renal allograft recipients, potentially via AdipoR1.
- CTRP9 emerges as a potential protective factor against vascular calcification in this patient group.
Background:
Cardiovascular disease (CVD) due to atherosclerosis is a major cause of death in renal allograft recipients. Recently, C1q/TNF-α related protein-9 (CTRP9), which is a paralog of adiponectin (ADPN), has been suggested to be related to the prevention of atherosclerosis and the occurrence of CVD, but this relationship has not been confirmed in renal allograft recipients.
Subjects And Methods:
The relationships among the serum CTRP9 concentration, serum ADPN concentration, and vascular calcification were investigated in 50 kidney transplantation recipients at our hospital. Calcification of the abdominal aorta was evaluated according to the aortic calcification area index (ACAI) calculated from CT images. Changes in the serum CTRP9 and ADPN fractions and ACAI were examined for 8 years. In addition, the expression of CTRP9 and ADPN and their respective receptors AdipoR1 and R2 in muscular arteries of the kidney was examined by immunofluorescence.
Results:
In renal allograft recipients, the serum CTRP9 concentration at the start of the observation was not significant correlated with eGFR or serum high-molecular-weight (HMW)-ADPN concentration (rS = -0.009, p = 0.950; rS = -0.226, p = 0.114, respectively). However, the change in the serum CTRP9 concentration was positively correlated with the change in the serum HMW-ADPN concentration (rS = 0.315, p = 0.026) and negatively correlated with the change in ACAI (rS = -0.367, p = 0.009). Multiple regression analysis revealed that the serum HMW-ADPN concentration was a significant positive factor for the change in the serum CTRP9 concentration. Moreover, for ACAI, an increase in the serum CTRP9 concentration was an improving factor, but aging was an exacerbating factor. Furthermore, colocalization of CTRP9 and AdipoR1 was noted in the luminal side of intra-renal arterial intima.
Conclusion:
In renal allograft recipients, both CTRP9 and HMW-ADPN were suggested to prevent the progression of aortic calcification through AdipoR1.
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