Treatment of secondary hyperparathyroidism in chronic kidney disease, and its effect on the QT interval

Wilner Samson, Jonathan Winston, Jayapriya Krishnaswamy, Jaime Uribarri

Research output: Contribution to journalArticlepeer-review


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 values200 pg/mL. The mean QTc was 441 ± 41.9 msec. There was no signifi cant change in the QTc for treated and untreated patients. PTH had a signifi cant decrease in the treated patients, from 522 ± 379 to 312 ± 244 pg/mL. The mean PTH signifi cantly increased in the untreated patients from 227 ± 197 to 302 ± 322 pg/mL. The corrected calcium non-signifi cantly 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 signifi cant 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.

Original languageEnglish
Pages (from-to)92-96
Number of pages5
JournalDialysis and Transplantation
Issue number3
StatePublished - Mar 2010


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