Session: SUN 234-256-Bone & Calcium Metabolism: Clinical Trials & Case Series
Poster Board SUN-253
Hyperparathyroidism has been associated with cardiovascular morbidity and mortality. Recently basic science models have shown a direct relationship of parathyroid hormone (PTH) with aldosterone. However it is not known if blocking aldosterone receptor leads to suppression of parathyroid hormone (PTH) in clinical setting and if it has clinical benefits.
This is a incidence case – control study where cases were all the consecutive patients with chronic kidney disease on aldosterone antagonists (AA). Controls were matched (1:1) on age, gender, race, estimated GFR and number of medications for hypertension from the insurance database >2 million patients not on AA that had PTH measured in the same year as that of the corresponding cases. PTH was measured within 1 year of starting AA and within 1 year after initiation of AA. Cox proportional hazard modeling was performed for outcomes; decrease in PTH, rates of new onset heart failure (HF), rates of heart failure related readmissions, and cardiovascular specific mortality. Analyses were adjusted for 25 OH vitamin D, hypertension, diabetes, smoking, and alkaline phosphatase. Time dependent covariate analysis was used to compare various levels of PTH in the year prior and after the initiation of aldosterone antagonist.
Out of 850 patients, 425 patients (mean age 67±13, women 60.2%) were started on AA. Compliance was >80% with a mean follow up of 4.6±3.2 years. Mean PTH prior to initiation of AA was 141±133ng/dL which decreased by a mean of 40±113ng/dL compared to a change of 0.1 ± 64 ng/dL in controls (p<0.0001). The decrease in PTH was associated with decreased cardiovascular mortality (HR 0.71;95% CI 0.53 – 0.97, p = 0.03). Increase in PTH was associated with risk of new onset HF (HR 1.93; 95% CI 1.32 – 2.83, p = 0.001) and heart failure related readmission (HR 1.73; 95% CI 1.15 – 2.60, p = 0.009) but not with non fatal myocardial infarctions (p = 0.88). Kaplan – Meier’s showed worse survival of patients that did not have a decrease in PTH by 30% within 2 years (log rank p – value = 0.03). On post hoc analysis, there was no interaction of outcomes with degree of chronic kidney disease and vitamin D supplements, phosphate binding, bisphosophonates or calcimimetic medications.
In conclusion, modulating PTH via AA may provide another therapeutic way to improve hormonal imbalance in the patients with secondary hyperparathyroidism from renal disease. This modulation has important clinical implications.
Nothing to Disclose: MH, LS, ML, DA, WQ
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