ECE2019 Guided Posters Interdisciplinary Endocrinology 1 (11 abstracts)
1Shire Human Genetic Therapies, Inc., a member of the Takeda group of companies, Cambridge, MA, USA; 2Brigham and Womens Hospital, Boston, MA, USA; 3Stratton VA Medical Center and Albany Medical College, Albany, NY, USA; 4Aarhus University and Aarhus University Hospital, Aarhus, Denmark; 5Analysis Group Inc., Boston, MA, USA; 6Klinikum Coburg GmbH, Coburg, Germany.
Background: Little is known about the risk of developing nephrolithiasis and nephrocalcinosis in patients with chronic HypoPT treated with conventional therapy (ie, oral calcium and active vitamin D). This study evaluated whether HypoPT is associated with increased risk of these conditions.
Methods: This retrospective cohort study, based on a large US commercial claims database (Q1 2007Q2 2017), was conducted to compare the risk of nephrolithiasis and nephrocalcinosis between chronic HypoPT patients (excluding those receiving parathyroid hormone) and randomly selected non-HypoPT patients over 5 years of follow-up. For HypoPT patients, the first date of follow-up (ie, index date) was the earliest HypoPT diagnosis date ≥6 months after the initial HypoPT diagnosis; for non-HypoPT patients, it was the date of a randomly selected medical claim. Patient characteristics at baseline (the 6 months before index date) and risk of nephrolithiasis (identified by diagnosis and procedure codes) were compared between cohorts, the latter using Kaplan-Meier analysis and Cox proportional hazards models adjusting for baseline demographic (age, sex, race, region, and index year) and clinical (nephrolithiasis, gout, hypercalciuria, hypertension, diabetes, and thiazide diuretic use) characteristics. Similar analyses, adjusting for demographics and hypercalciuria, were conducted on the risk of nephrocalcinosis (based on diagnosis codes) among those without the condition at baseline. A sensitivity analysis for nephrocalcinosis was conducted among those with study period kidney imaging.
Results: The study included 8097 chronic HypoPT patients and 40,485 non-HypoPT patients. At baseline, HypoPT patients were older than non-HypoPT patients (58.6 years vs 47.3 years), a higher proportion were female (76.2% vs 54.4%), and higher proportions had nephrolithiasis (3.3% vs 1.3%), nephrocalcinosis (0.6% vs <0.1%), gout (3.0% vs 1.2%), hypercalciuria (23.8% vs 0.5%), type 2 diabetes (20.6% vs 10.8%), and hypertension (43.7% vs 25.2%) (all P<0.001). Over 5 years of follow-up, HypoPT patients had an increased risk of nephrolithiasis and nephrocalcinosis compared with non-HypoPT patients (P<0.001 based on Kaplan-Meier analyses). The adjusted hazard ratios (95% CIs) associated with HypoPT vs non-HypoPT were 1.81 (1.602.04) for nephrolithiasis and 6.94 (4.4110.92) for nephrocalcinosis (both P<0.001). In the sensitivity analysis, 2.6% of HypoPT and 0.5% of non-HypoPT patients (P<0.001) had nephrocalcinosis during the study.
Conclusions: Chronic HypoPT was associated with increased risks of nephrolithiasis and nephrocalcinosis. Further research is warranted to understand the potential mechanisms for the relationship of chronic HypoPT and its management with the observed risk of these conditions.