Is parathormone a cardiac toxin in uremia?
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Published on: March 14, 2017
R B Himelman1, C A Helms, N B Schiller
1John Henry Mills Echocardiography Laboratory, University of California, San Francisco.
Insights
Parathyroid hormone (PTH) in uremia is linked to hypertension but not directly to left ventricular hypertrophy or mitral annular calcification (MAC). Renal transplantation improves cardiac structure but does not resolve MAC.
Area of Science:
- Nephrology
- Cardiology
- Endocrinology
Background:
- Uremia is associated with elevated parathyroid hormone (PTH), which may contribute to cardiovascular complications.
- Left ventricular hypertrophy (LVH), cardiomyopathy, and mitral annular calcification (MAC) are common in patients with chronic kidney disease.
- The relationship between PTH, cardiac structure, and MAC in uremic patients undergoing renal transplantation requires further investigation.
Purpose of the Study:
- To investigate the association between serum PTH levels, electrolytes, and cardiovascular parameters in uremic patients before and after renal transplantation.
- To assess the impact of renal transplantation on left ventricular mass, wall thickness, ejection fraction, and MAC.
- To determine if PTH levels correlate with cardiac abnormalities or MAC in end-stage renal disease.
Main Methods:
- Echocardiography was used to measure left ventricular wall thickness, mass index, and ejection fraction.
- Mitral annular calcification (MAC) presence and extent were assessed by echocardiography.
- Serum levels of PTH, calcium, phosphate, and magnesium were measured before and after renal transplantation in 44 patients.
Main Results:
- Pre-transplant, 41% of patients had MAC. Elevated PTH (>1000 mcl eq/ml) was associated with higher pre-transplant systolic blood pressure.
- Post-transplant, significant reductions in left ventricular mass index and diastolic wall thickness were observed (p<0.05).
- No significant correlation was found between PTH or electrolyte levels and cardiac parameters or MAC, either pre- or post-transplant. MAC did not resolve after transplantation.
Conclusions:
- While PTH does not directly correlate with LVH, cardiac function, or MAC in uremia, elevated pre-transplant levels are linked to hypertension.
- Renal transplantation improves cardiac structural parameters but does not reverse established MAC.
- PTH may act as a mild pressor agent in some patients with end-stage renal failure.
Abstract:
In uremia, parathormone (PTH) has been associated with inadequate left ventricular hypertrophy, cardiomyopathy, and mitral anular calcification (MAC). We related levels of serum PTH, calcium, phosphate, magnesium, calcium-phosphate product, and systolic blood pressure to average left ventricular wall thickness, left ventricular mass index, ejection fraction, and presence and extent of MAC by echocardiography in 44 patients before and after renal transplantation. Pre-transplant, 18 patients (41%) had MAC; these and the 26 others had similar values for serum PTH, calcium-phosphate product, systolic blood pressure, age, and years of hemodialysis. The patients with PTH levels greater than 1000 mcl eq/ml had higher systolic blood pressures pre-transplant (157 +/- 21 vs 147 +/- 17 mm Hg, p less than 0.05), but not post-transplant as PTH levels normalized. Post-transplant, there were significant decreases in left ventricular mass index (140 +/- 35 to 103 +/- 25 g/m2) and average diastolic left ventricular wall thickness (1.4 +/- 0.2 to 1.2 +/- 0.2 cm, both p less than 0.05); however, ejection fraction and extent of MAC did not change. Left ventricular mass index, average diastolic left ventricular wall thickness, and ejection fraction did not correlate with serum PTH or electrolyte levels before or after renal transplantation. MAC is present in more than one third of uremic pts and does not resolve after renal transplantation. Although PTH does not correlate with left ventricular hypertrophy, cardiac function, or MAC before or after transplantation, elevated levels pre-transplant are associated with a slightly greater degree of hypertension. Thus PTH may be a mild vasoactive pressor in some patients with end-stage renal failure.
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