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Clinical Implication of Consistently Strict Phosphate Control for Coronary and Valvular Calcification in Incident
Mao Shimizu1, Hideki Fujii1, Keiji Kono1
1Division of Nephrology and Kidney Center, Kobe University Graduate School of Medicine.
Insights
Strict phosphate control in hemodialysis patients may slow vascular and valvular calcifications. Maintaining low serum phosphate levels (≤ 4.5 mg/dL) is associated with reduced calcification progression.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Biochemistry
Background:
- Serum phosphate levels are critical in managing vascular and valvular calcifications.
- Strict phosphate control is proposed, but evidence is limited.
- This study investigates its impact on incident hemodialysis patients.
Purpose of the Study:
- To evaluate the effect of strict phosphate control on vascular and valvular calcifications.
- To assess calcification progression in incident hemodialysis patients with varying phosphate control.
Main Methods:
- 64 incident hemodialysis patients from a prior RCT were analyzed.
- Coronary artery calcification score (CACS) and cardiac valvular calcification score (CVCS) were measured via CT and ultrasound.
- Phosphate control was assessed using area under the curve (AUC) for serum phosphate levels ≥ 4.5 mg/dL over 18 months.
Main Results:
- Lower AUC (better phosphate control) correlated with significantly lower CACS and CVCS progression (ΔCACS, %ΔCACS, ΔCVCS, %ΔCVCS).
- Patients consistently below 4.5 mg/dL showed a trend towards reduced calcification.
- AUC demonstrated a significant correlation with both coronary and valvular calcification changes.
Conclusions:
- Consistently strict phosphate control appears to mitigate the progression of coronary and valvular calcifications.
- This suggests a potential benefit of tight serum phosphate management in incident hemodialysis patients.
Aims:
Serum phosphate control is crucial for the progression of vascular and valvular calcifications. Strict phosphate control is recently suggested; however, there is a lack of convincing evidence. Therefore, we explored the effects of strict phosphate control on vascular and valvular calcifications in incident patients undergoing hemodialysis.
Methods:
A total of 64 patients undergoing hemodialysis from our previous randomized controlled trial were included in this study. Coronary artery calcification score (CACS) and cardiac valvular calcification score (CVCS) were evaluated using computed tomography and ultrasound cardiography at baseline and 18 months after the initiation of hemodialysis. The absolute changes in CACS (ΔCACS) and CVCS (ΔCVCS) and the percent change in CACS (%ΔCACS) and CVCS (%ΔCVCS) were calculated. Serum phosphate level was measured at 6, 12, and 18 months after the initiation of hemodialysis. Moreover, phosphate control status was evaluated using the area under the curve (AUC) by the amount of time spent with a serum phosphate level of ≥ 4.5 mg/dL and the extent to which this threshold exceeded over the observation period.
Results:
ΔCACS, %ΔCACS, ΔCVCS, and %ΔCVCS were significantly lower in the low AUC group than in the high AUC group. ΔCACS and %ΔCACS were also significantly lower. ΔCVCS and %ΔCVCS tended to be lower in patients whose serum phosphate level never exceeded 4.5 mg/dL than in those whose serum phosphate level continuously exceeded 4.5 mg/dL. AUC significantly correlated with ΔCACS and ΔCVCS.
Conclusion:
Consistently strict phosphate control may slow the progression of coronary and valvular calcifications in incident patients undergoing hemodialysis.
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