Effect of pharmacological suppression of secondary hyperparathyroidism on cardiovascular hemodynamics in predialysis CKD patients: A preliminary observation.

Cardiovascular events are the principal cause of mortality in patients with chronic kidney disease (CKD). Secondary hyperparathyroidism (SHPT), a common complication of CKD, contributes to cardiac dysfunction. This study is an attempt to demonstrate the effects of parathyroid hormone suppression with oral calcitriol on cardiovascular hemodynamics. Twenty predialysis CKD patients with SHPT were given calcitriol therapy for 12 weeks. Ten similar patients received placebo. Echocardiographic assessment of cardiac function was performed at baseline and after 12 weeks of treatment. Calcitriol therapy effectively suppressed SHPT. Baseline left ventricular (LV) end diastolic diameter and LV end systolic diameter were 4.86+/-0.48 and 2.86+/-0.33 cm, and the mean FS was 41.02+/-4.79%. Left ventricular end systolic and end diastolic volumes were normal (42.30+/-9.07 and 91.40+/-19.68 mL). The ejection fraction was slightly reduced (53.54+/-3.57%). Pretreatment Doppler indices including E velocity (0.816+/-0.087 m/s), A velocity (0.696+/-0.089 m/s), and E/A ratio (1.193+/-0.210) were significantly impaired. After 12 weeks of calcitriol therapy, there was no significant change in the LV dimensions or ejection fraction, but there was a significant improvement in the diastolic parameters, namely the A velocity (0.680+/-0.084) and E/A ratio (1.238+/-0.180). Secondary hyperparathyroidism is an important factor in the pathogenesis of cardiovascular complications in CKD. There is evidence to support that correction of hyperparathyroidism can improve the systolic dysfunction seen in advanced kidney disease. This study shows that diastolic dysfunction seen in predialysis CKD patients may also be possibly improved with calcitriol therapy.

RCT Entities:   Population Interventions Outcomes