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Parathyroid hormone and phosphorus overload in uremia: impact on cardiovascular system
Melani R Custódio1, Marcia K Koike, Katia R Neves
1Department of Internal Medicine, Universidade de São Paulo, São Paulo, Brazil.
Insights
Parathyroid hormone (PTH) and phosphorus overload independently worsen cardiac remodeling in uremia, leading to hypertrophy and fibrosis. Better control of these factors is crucial for managing chronic kidney disease patients.
Area of Science:
- Nephrology
- Cardiology
- Endocrinology
Background:
- Uremia causes cardiac remodeling, including left ventricular hypertrophy, fibrosis, and microvascular disease.
- Cardiovascular disease is a leading cause of death in uremic patients, with sudden death and heart failure being prevalent.
- The study investigates the specific roles of parathyroid hormone (PTH) and phosphorus in experimental uremia-induced cardiac remodeling.
Purpose of the Study:
- To evaluate the isolated effects of parathyroid hormone (PTH) and phosphorus on cardiac remodeling in experimental uremia.
- To assess the impact of varying PTH levels and phosphorus diets on myocardial structure and cardiovascular markers.
- To identify key molecular pathways involved in uremic cardiomyopathy.
Main Methods:
- Wistar rats underwent parathyroidectomy (PTx) and 5/6 nephrectomy (Nx), receiving different doses of PTH and phosphorus-rich or poor diets.
- Biochemical analyses, myocardial morphometry, and arteriolar morphological assessments were conducted after 8 weeks.
- Immunohistochemical analysis evaluated markers such as angiotensin II, TGF-β, FGF-23, and Runx-2.
Main Results:
- Nephrectomized animals showed higher creatinine and hypertension.
- Elevated PTH levels correlated with myocardial hypertrophy, fibrosis, and increased coronary lesions.
- Phosphorus overload was linked to higher FGF-23, Runx-2 expression, and myocardial hypertrophy.
Conclusions:
- Both PTH and phosphorus overload are independently associated with significant cardiac remodeling changes in uremia.
- These findings highlight the importance of controlling PTH and phosphorus levels in chronic kidney disease.
- Targeting these factors may mitigate cardiovascular complications in uremic patients.
Background:
Cardiac remodeling in uremia is characterized by left ventricular hypertrophy, interstitial fibrosis and microvascular disease. Cardiovascular disease is the leading cause of death in uremic patients, but coronary events alone are not the prevalent cause, sudden death and heart failure are. We studied the cardiac remodeling in experimental uremia, evaluating the isolated effect of parathyroid hormone (PTH) and phosphorus.
Methods:
Wistar rats were submitted to parathyroidectomy (PTx) and 5/6 nephrectomy (Nx); they also received vehicle (V) and PTH at normal (nPTH) or high (hPTH) doses. They were fed with a poor-phosphorus (pP) or rich-phosphorus (rP) diet and were divided into the following groups: 'Sham': G1 (V+normal-phosphorus diet (np)) and 'Nx+PTx': G2 (nPTH+pP), G3 (nPTH+rP), G4 (hPTH+pP) and G5 (hPTH+rP). After 8 weeks, biochemical analysis, myocardium morphometry and arteriolar morphological analysis were performed. In addition, using immunohistochemical analysis, we evaluated angiotensin II, α-actin, transforming growth factor-beta (TGF-β) and nitrotyrosine, as well as fibroblast growth factor-23 (FGF-23), fibroblast growth factor receptor-1 (FGFR-1) and runt-related transcription factor-2 (Runx-2) expression.
Results:
Nx animals presented higher serum creatinine levels as well as arterial hypertension. Higher PTH levels were associated with myocardial hypertrophy and fibrosis as well as a higher coronary lesion score. High PTH animals also presented a higher myocardial expression of TGF-β, angiotensin II, FGF-23 and nitrotyrosine and a lower expression of α-actin. Phosphorus overload was associated with higher serum FGF-23 levels and Runx-2, as well as myocardial hypertrophy. FGFR-1 was positive in the cardiomyocytes of all groups as well as in calcified coronaries of G4 and G5 whereas Runx-2 was positive in G3, G4 and G5.
Conclusion:
In uremia, PTH and phosphorus overload are both independently associated with major changes related to the cardiac remodeling process, emphasizing the need for a better control of these factors in chronic kidney disease.
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