Treatment of Secondary Hyperparathyroidism in Chronic Kidney Disease, and Its Effect on the Qt Interval

BACKGROUND Prolongation of corrected QT interval (QTcp) can result in arrhythmias, which may, in part, be responsible for the increased cardiovascular mortality in chronic kidney disease (CKD) patients. Since hypocalcemia can cause QTcp, we postulated a link between QTcp and disturbances in divalent ions seen in CKD patients with secondary hyperparathyroidism (sHPT). METHODS We prospectively determined the prevalence of sHPT, hypocalcemia, and QTcp in 97 CKD patients. Patients with a parathyroid hormone (PTH) level ≥200 pg/mL were initiated on a vitamin D protocol for 1 year. QTc was measured at baseline and follow-up using an electrocardiogram (ECG) recorder. RESULTS The initial mean value for PTH was 343 ± 334 pg/mL. Nearly two-thirds of the patients had PTH values >200 pg/mL. The mean QTc was 441 ± 41.9 msec. There was no significant change in the QTc for treated and untreated patients. PTH had a significant decrease in the treated patients, from 522 ± 379 to 312 ± 244 pg/mL. The mean PTH significantly increased in the untreated patients from 227 ± 197 to 302 ± 322 pg/mL. The corrected calcium non-significantly decreased from 9.4 ± 1.0 to 9.0 ± 2.2. At 5 years follow-up, nearly half of this cohort had died; however we did not observe any significant difference in mortality between treated and untreated patients. CONCLUSIONS We observed a 44.7% prevalence of prolonged QTc in an unselected population of CKD patients. This cohort had a high prevalence of sHPT. Treatment of sHPT did not appear to have an effect on QTc or mortality.