Is parathormone a cardiac toxin in uremia?

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.