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The cardiocyte as a target for parathyroid hormone in end-stage renal disease
1Department of Medicine, New York Medical College, Valhalla, New York.
Insights
Parathyroid hormone (PTH) may be a cardiotoxin contributing to cardiac dysfunction in end-stage renal disease (ESRD). Research suggests PTH receptors in heart cells could mediate these harmful effects in uremia.
Area of Science:
- Nephrology
- Cardiology
- Endocrinology
Background:
- Cardiovascular disease accounts for 50% of mortality in end-stage renal disease (ESRD) patients.
- Factors like volume overload, hypertension, and diabetes mellitus negatively impact cardiac function in ESRD.
- The role of parathyroid hormone (PTH) in uremic cardiomyopathy is under investigation.
Purpose of the Study:
- To propose that parathyroid hormone (PTH) acts as a cardiotoxin.
- To explore PTH as a potential mediator of cardiac dysfunction in uremia.
- To discuss the implications of PTH signaling in cardiac cells.
Main Methods:
- Review of recent scientific literature on PTH, its receptors, and cardiac function.
- Analysis of evidence for PTH binding sites and receptor cloning in cardiocytes.
- Discussion of potential effector pathways and PTH-related protein signaling in the heart.
Main Results:
- Cardiocytes possess specific binding sites for PTH.
- The PTH receptor has been identified and cloned.
- The PTH receptor may activate multiple intracellular signaling pathways.
Conclusions:
- Parathyroid hormone (PTH) is hypothesized to be a cardiotoxin in uremia.
- PTH signaling pathways in cardiac cells may contribute to cardiac dysfunction.
- Further research is warranted to elucidate the role of PTH in uremic heart disease.
Abstract:
Approximately 50% of the annual mortality in patients with end-stage renal disease (ESRD) is attributed to cardiovascular-related events. Multiple factors, including volume overload, hypertension, electrolyte abnormalities, and the presence of comorbid diseases, such as diabetes mellitus, may have an adverse effect on left ventricular function in ESRD. The purpose of this brief review is to advance the hypothesis that parathyroid hormone (PTH) is a cardiotoxin and a potential mediator of cardiac dysfunction in uremia. Recent studies have provided evidence that cardiocytes possess a distinct class of binding sites for PTH, and the PTH receptor has recently been cloned. Furthermore, the PTH receptor may be coupled to more than one effector pathway. Finally, the possibility that a PTH-related protein autocrine system may be present in cardiocytes and the implications of this signaling pathway on cardiocyte function are discussed.