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Parathormon, calcium, phosphorus, and left ventricular structure and function in normotensive hemodialysis patients
P Strózecki1, A Adamowicz, E Nartowicz
1Department of Nephrology, The Ludwik Rydygier Medical University, Bydgoszcz, Poland.
Insights
Parathyroid hormone (PTH) and mineral imbalances contribute to left ventricular hypertrophy and diastolic dysfunction in hemodialysis patients. These factors impact heart structure and function, even in normotensive individuals.
Area of Science:
- Nephrology
- Cardiology
- Endocrinology
Background:
- Clinical data link Parathormone (PTH), calcium, and phosphorus to left ventricular hypertrophy (LVH) and myocardial contractility issues in end-stage renal disease.
- Cellular calcium overload and fibrosis from PTH may impair left ventricular diastolic function.
- Hyperphosphatemia is an independent cardiovascular mortality risk in dialysis patients.
Purpose of the Study:
- To assess the impact of PTH and calcium-phosphorus metabolism on left ventricular structure and function.
- To compare echocardiographic findings between normotensive and hypertensive hemodialysis (HD) patients.
- To evaluate relationships between PTH, mineral metabolism, and echocardiographic parameters in normotensive HD patients.
Main Methods:
- Echocardiography was used to compare 22 normotensive HD patients with 43 hypertensive HD patients.
- Relationships between PTH, calcium-phosphorus metabolism, and echocardiographic parameters were analyzed in the normotensive group.
- Statistical analysis (correlation) was performed to identify significant associations.
Main Results:
- Normotensive HD patients had lower left ventricular mass index (LVMI) and LVH prevalence than hypertensive patients.
- Significant correlations were found between PTH and LVMI, calcium and posterior wall thickness, and phosphorus and LVMI in normotensive patients.
- Phosphorus, calcium x phosphorus product, and E/A ratio showed significant correlations with diastolic function parameters.
Conclusions:
- Disturbances in calcium-phosphorus metabolism and secondary hyperparathyroidism contribute to LVH.
- These metabolic derangements also lead to impaired left ventricular diastolic function in normotensive HD patients.
- PTH and mineral imbalances are critical factors affecting cardiac structure and function in HD patients.
Abstract:
Clinical and experimental data suggest that Parathormon (PTH), calcium, and phosphorus participate in left ventricular hypertrophy (LVH) and affect myocardial contractility in end-stage renal disease. Cellular calcium overload and interstitial fibrosis induced by PTH may lead to impairment of left ventricular diastolic function. Hyperphosphatemia is an independent risk of cardiovascular mortality in dialysis patients. The aim of the study was to estimate the influence of PTH and calcium-phosphorus metabolism on left ventricular structure and function in hemodialysis patients, without hypertension and antihypertensive drug therapy (SBP = 126.2 +/- 11.1 DBP = 75.8 +/- 6.5 mmHg). Echocardiographic findings in a group of 22 normotensive HD patients had been compared to 43 hypertensive HD patients. Relationships between PTH, calcium-phosphorus metabolism and echocardiography in normotensive group were then evaluated. Left ventricular mass index (LVMI) was lower in normotensive patients: 128.3 +/- 46.2 versus 165.8 +/- 46.7 (p < 0.01). The prevalence of LVH was 55% in normotensive HD patients compared to 86% in hypertensive group (p < 0.01). In normotensive group we found correlation between PTH and LVMI (r = 0.44; p < 0.05). There were also significant relationships between calcium and posterior wall thickness (r = -0.44; p < 0.05), phosphorus and LVMI (r = 0.47; p < 0.05). A significant correlation was observed between both phosphorus, calcium x phosphorus product and E/A ratio: r = -0.47 and r = -0.43, respectively (p < 0.05 both). Disturbances of calcium-phosphorus metabolism and secondary hyperparathyroidism contributes to left ventricular hypertrophy, and impaired left ventricular diastolic function in normotensive hemodialysis patients.