MON-524 Risk of Decline in Estimated Glomerular Filtration Rate (eGFR) in Patients with Chronic Hypoparathyroidism (HypoPT)

Background: Chronic hypoparathyroidism (HypoPT) managed with conventional therapy (i.e., oral calcium and active vitamin D) may potentially impact renal function. This study evaluated whether chronic HypoPT is associated with increased rate of estimated glomerular filtration rate (eGFR) decline. Methods: A retrospective cohort study was conducted to compare eGFR decline between chronic HypoPT patients (excluding those receiving parathyroid hormone) and randomly selected non-HypoPT patients over 5 years of follow-up using a large commercial claims database (Q1 2007 - Q2 2017). The first date of follow-up (i.e., index date) for HypoPT patients was the earliest HypoPT diagnosis date at least 6 months after the initial HypoPT diagnosis and for non-HypoPT patients was the date of a randomly selected medical claim. All patients were required to have eGFR values (calculated using the CKD-EPI formula) recorded during baseline (the six months prior to index date). The risk of eGFR decline ≥ 10 mL/min/1.73 m(2) was compared between cohorts using Kaplan-Meier analysis and adjusted Cox proportional hazards models. Adjusting parameters included demographic (age, sex, race, region, and index year) and clinical (eGFR, heart failure, hypertension, diabetes, and medication use) characteristics at baseline. Subgroup analyses were performed among patients with baseline eGFR ≥ 60 and < 60 mL/min/1.73 m(2). A sensitivity analysis was conducted among the subset of patients with ≥ 1 study period eGFR value in addition to baseline eGFR. Results: A total of 1,880 chronic HypoPT and 4,414 non-HypoPT patients met the study criteria. Compared to non-HypoPT patients, HypoPT patients were older (59.7 vs. 54.0 years) and a higher proportion were female (75.1 vs. 56.2%). At baseline, HypoPT patients had lower median eGFR (75.2 vs. 87.9 mL/min/1.73 m(2)) and a higher proportion had history of heart failure, hypertension, and type 2 diabetes compared to non-HypoPT patients. Kaplan-Meier analyses showed that, compared to non-HypoPT patients, HypoPT patients had an increased rate of eGFR decline among all patients, in the subgroups with baseline eGFR ≥ and < 60mL/min/1.73m(2), and among the sensitivity cohort with baseline and study period eGFR (all p<0.001). The adjusted hazard ratios (HRs) of eGFR decline ≥ 10mL/min/1.73 m(2) for HypoPT vs. non-HypoPT were 1.97 (95% confidence interval [CI]: 1.75, 2.21) among all patients, 2.10 (1.84, 2.38) among those with baseline eGFR ≥ 60, 1.74 (1.29, 2.34) among those with baseline eGFR < 60, and 1.51 (1.35, 1.70) among the sensitivity cohort (all p<0.001). Conclusions: Chronic HypoPT was associated with an increased rate of eGFR decline. Further research is warranted to understand the potential mechanisms for the relationship of chronic HypoPT and its management with the observed decline in eGFR. Funding: Shire