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Published on: June 2, 2022
Valvular calcification and left ventricular modifying in peritoneal dialysis patients
Damir Rebić1, Senija Rašić1, Aida Hamzić-Mehmedbašić1
1a Clinic for Nephrology and.
Insights
Cardiac valve calcification (CVC) is common in end-stage renal disease (ESRD) patients undergoing peritoneal dialysis (PD). CVC is linked to left ventricular hypertrophy (LVH), suggesting a need for monitoring cardiovascular risks in these patients.
Area of Science:
- Nephrology
- Cardiology
- Biomarkers
Background:
- Cardiac valve calcification (CVC) and left ventricular (LV) alterations are common in end-stage renal disease (ESRD).
- Prevalence of CVC and LV hypertrophy (LVH) in ESRD patients before and after peritoneal dialysis (PD) was investigated.
Purpose of the Study:
- To determine the prevalence of CVC and LVH in ESRD patients before and 12 months after initiating PD.
- To explore the association between CVC and LVH in PD patients.
Main Methods:
- Prospective longitudinal study of 50 incident PD patients.
- Echocardiography used to assess CVC and LVH at baseline and after 1 year.
- Demographic, clinical data, and blood assays collected.
Main Results:
- CVC prevalence at baseline: mitral (30%), aortic (18%), both (10%).
- After 12 months of PD, CVC prevalence: aortic (20%), mitral (24%), both (8%).
- LVH was significantly higher in patients with CVC (62%) versus without CVC (36%) after 1 year (p<0.05).
- Endothelin-1 predicted CVC at baseline; nitric oxide predicted CVC at follow-up.
Conclusions:
- Cardiac valve calcification is associated with left ventricular hypertrophy in PD patients.
- Monitored biomarkers may aid in detecting and treating cardiovascular complications in PD patients.
Background:
Cardiac valve calcification (CVC) and left ventricular (LV) alterations are frequent complication in end-stage renal disease (ESRD). We determined the prevalence of CVC and LV hypertrophy (LVH) in ESRD patients before renal replacement therapy and 12 months after peritoneal dialysis (PD).
Methods:
A prospective longitudinal of 50 incident PD patients was studied. Demographic and clinical data were recorded and blood assayed at baseline and after 1-year of follow-up. CVC and LVH were evaluated by M-mode two-dimensional echocardiography.
Results:
CVC of the mitral and aortic valves and of both valves were noted in 30, 18 and 10% of patients, respectively. After 12 months of PD regimen, 20% patients had aortic, 24% mitral and 8% had calcification of both valves. After one year of PD, LVH was 62 and 36% in patients with and without CVC, respectively (p < 0.05). Endothelin-1 is an independent predictor of CVC at the baseline, while nitric oxide is inversely an independent predictor at the end of follow-up.
Conclusions:
CVC is associated with LVH in PD patients. These findings identified a potential role for monitored markers to be incorporated into therapeutic strategies aimed at detection and treatment of cardiovascular complications and prevention strategies.
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