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Heart valve calcifications in patients with end‐stage renal disease: Analysis for risk factors
36
Citations
15
References
2006
Year
Phosphate MetabolismHeart FailureRenal PathologyRenal FunctionMaintenance HdValve DiseaseChronic Kidney DiseaseCardiologyMineral MetabolismHealth SciencesHemodialysisRenal CareCardiorenal SyndromesKidney FailureClinical NutritionRenal PathophysiologyEnd‐stage Renal DiseaseRisk FactorsEnd-stage Renal DiseaseHeart Valve CalcificationsUrologyCardiovascular DiseaseValve CalcificationValvular Heart DiseaseMedicineNephrology
SUMMARY: Background: The prevalence of valve calcification (VC) in end‐stage renal disease patients is high and information regarding risk factors is scarce. Our aims were to determine the prevalence of VC in our maintenance haemodialysis (HD) population and to examine some possible aetiologic factors for its occurrence. Methods: We studied 90 patients (47 women) on maintenance HD for more than 12 months. An M‐mode two‐dimensional echocardiogram was carried out to evaluate mitral, aortic VC and ventricular geometry. We calculated mean daily calcium intake for the phosphate intestinal chelaing in the previous year to echocardiogram date and also mean values from previous year of Ca, PO4, Ca × PO4, parathyroid hormone, lipide profile, nutritional and inflammatory marquers. Finally consumption of calcium and alfacalcidol was also noted. Results: Thirty‐six patients (40%) presented with VC. Patients with VC were older and showed higher levels of serum calcium (92.00 ± 7.54 vs 89.27 ± 6.86 mg/L, P = 0.04), phosphorus (69.70 ± 18.33 vs 44.90 ± 12.43 mg/L, P < 0.0001), Ca × P product (6164.97 ± 1797.64 vs 4024.70 ± 1066.40 mg 2 /L 2 , P < 0.0001) and poor ventricular geometry, as compared with patients without VC. Moreover, they required higher doses of alfacalcidol for treating secondary hyperparathyroidism (0.43 ± 0.60 vs 0.11 ± 0.46 µg/day, P < 0.0001). Conclusion: Findings of the present study are consistent with a role of altered calcium and phosphate metabolism in the pathogenesis of VC in HD patients.
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