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Effects of phosphorus-restricted diet and phosphate-binding therapy on outcomes in patients with chronic kidney
Domenico Russo1, Antonio Bellasi, Andrea Pota
1Section of Nephrology and Hypertension, Department of Surgery, Nephrology, University of Naples "Federico II", Via Guglielmo Marconi, 80, 80024, Cardito, Naples, Italy, domenicorusso51@hotmail.com.
Insights
Combining a phosphorus-restricted diet with sevelamer significantly reduced mortality and dialysis initiation in chronic kidney disease (CKD) patients with moderate coronary artery calcification (CAC) progression. Accelerated CAC progression negated these benefits, highlighting the importance of managing calcification in CKD management.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Public Health
Background:
- Elevated phosphorus levels in chronic kidney disease (CKD) correlate with increased mortality, potentially via vascular calcification.
- Dietary phosphorus restriction alone may not halt vascular calcification progression in CKD patients.
- This study investigates a combined dietary and pharmacologic approach to mitigate risks in non-dialysis CKD.
Purpose of the Study:
- To assess if a phosphorus-restricted diet plus phosphate binders reduce mortality and dialysis initiation.
- To determine if this combined strategy attenuates coronary artery calcification (CAC) progression in CKD stages 3-4.
- To compare the efficacy of calcium carbonate versus sevelamer in this patient cohort.
Main Methods:
- Post hoc analysis of 113 CKD patients (stage 3-4) with existing CAC on a phosphorus-restricted diet.
- Randomization to calcium carbonate or sevelamer as add-on therapy for 36 months.
- Primary endpoints included all-cause mortality and dialysis initiation; CAC progression was a secondary measure.
Main Results:
- Calcium carbonate use was linked to increased CAC progression, mortality, and dialysis initiation.
- Sevelamer use independently predicted reduced risk of adverse outcomes, but only with absent or moderate CAC progression.
- Accelerated CAC progression independently increased mortality risk, irrespective of sevelamer use.
Conclusions:
- A combined phosphorus-restricted diet and sevelamer regimen significantly lowered mortality and dialysis risk in non-dialysis CKD patients with moderate CAC progression.
- The benefits were not observed in patients with accelerated CAC progression.
- Further research is needed on serum phosphorus targets and the role of dietary phosphorus restriction in CKD.
Background:
Phosphorus is associated with mortality in patients with chronic kidney disease (CKD) not on dialysis, possibly through phosphorus-dependent vascular calcification. Although a phosphorus-restricted diet reduces serum phosphorus, it is unlikely that it reduces vascular calcification progression in CKD. This study evaluated whether a combined strategy of phosphorus-restricted diet and phosphate-binding therapy can reduce the risk of all-cause mortality and/or dialysis initiation by attenuating coronary artery calcification (CAC) progression in non-dialysis CKD patients.
Methods:
This was a post hoc analysis of a subgroup of patients from a study that evaluated the impact of two phosphorus binder regimens on hard outcomes in CKD. Patients (n = 113) with stage 3-4 CKD and evidence of CAC on a phosphorus-restricted diet were randomized to receive either calcium carbonate or sevelamer added to their phosphorus-restricted diet. End-points were death for any cause and initiation of dialysis. Patients were monitored to the first event or to conclusion of the 36-month follow-up.
Results:
Overall, treatment with calcium carbonate was associated with increased CAC progression and occurrence of all-cause mortality, dialysis initiation, and the composite end-point. After adjustment for confounders, sevelamer use was the only independent predictive factor of reduced risk of each endpoint but only if CAC progression was either absent or moderate. Accelerated progression (annual CAC increase >75th percentile of the study cohort) increased the risk of all-cause mortality and composite end-point (p = 0.01) independently of the use of sevelamer.
Conclusions:
A significant reduction in all-cause mortality, dialysis initiation, and composite end-point risk was achieved by combining phosphorus-restricted diet and sevelamer in non-dialysis CKD patients with absent or moderate but not accelerated CAC progression. Future studies should investigate the role of serum phosphorus, the usefulness of a phosphorus-restricted diet, and the appropriateness of current normal ranges of serum phosphorus concentration in relation to events in non-dialyzed CKD patients.
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