ECEESPE2025 Poster Presentations Bone and Mineral Metabolism (112 abstracts)
1Ascendis Pharma, Inc., Palo Alto, United States; 2University Hospitals of Leicester NHS Trust, Leicestershire, United Kingdom; 3CorEvitas, Cheshire, United Kingdom; 4Cencora, London, United Kingdom
JOINT637
Hypoparathyroidism is an endocrine disease caused by insufficient levels of parathyroid hormone (PTH). Postsurgical hypoparathyroidism accounts for most cases; other etiologies include genetic, autoimmune, and idiopathic (non-surgical). Conventional therapy, active vitamin D and calcium, aims to alleviate hypocalcemia but does not address insufficient PTH levels and is associated with hypercalcemia which may increase chronic kidney disease (CKD) risk. We assessed CKD risk in patients with hypoparathyroidism compared to non-hypoparathyroid individuals using routinely collected healthcare data from England. English linked primary (Clinical Practice Research Datalink [CPRD] Aurum) and secondary care (Hospital Episode Statistics) data were used to identify patients aged ≥18 years with incident chronic postsurgical (n = 215) or prevalent chronic non-surgical (n = 730) hypoparathyroidism between 01/Apr/200822/Mar/2019. Patients were matched 1:10 to non-hypoparathyroid controls on 5-year age bands, gender, and ≥1 year overlap in CPRD registration periods. CKD progression was compared between patients with hypoparathyroidism and controls using Cox proportional hazards regression adjusted for age (at surgery for postsurgical and follow-up start for non-surgical), gender, and cardiovascular disease presence. Progressions of CKD1/2 to CKD3, CKD3 to CKD4, CKD4 to CKD5, and CKD4 to dialysis were determined from recorded diagnoses. Patients without CKD at hypoparathyroidism diagnosis were conservatively assumed as CKD1/2. Each progression comparison was limited to patients with the starting CKD stage at hypoparathyroidism diagnosis or during follow-up, and censored at earliest of CKD progression, death, end of CPRD registration, or 22/Mar/2020. Patients with postsurgical hypoparathyroidism had a 3-fold increase in CKD1/2 to CKD3 progression compared to matched controls (Table 1). Patients with non-surgical hypoparathyroidism had a 4-fold and 3-fold increase in CKD1/2 to CKD3 progression and CKD3 to CKD4 progression, respectively. Our results show increased risks of early-stage CKD progression amongst patients with hypoparathyroidism compared to non-hypoparathyroid individuals. The small sample size in this rare disease precludes definitive analysis of late-stage risk difference.
Outcome | Post-surgical hypoparathyroidism | Non-surgical hypoparathyroidism | ||||
N progressed (N considered) | HR (95%CI) | Adjusted HR (95%CI) | N progressed (N considered) | HR (95%CI) | Adjusted HR (95%CI) | |
CKD1/2 to CKD3 | 13 (144) | 2. 74 (1. 52-4. 94) | 3. 02 (1. 67-5. 47) | 56 (536) | 3. 06 (2. 30-4. 07) | 4. 05 (3. 03-5. 42) |
CKD3 to CKD4 | <5 (25) | 1. 53 (0. 44-5. 33) | 2. 21 (0. 59-8. 29) | 17 (158) | 2. 44 (1. 39-4. 29) | 2. 94 (1. 54-5. 63) |
CKD4 to CKD5 | <5 (9) | 2. 00 (0. 17-23. 18) | * | 14 (57) | 2. 30 (0. 99-5. 32) | 1. 80 (0. 71-4. 56) |
CKD4 to dialysis | <5 (9) | 3. 67 (0. 21-63. 87) | * | 6 (57) | 2. 92 (0. 73-11. 71) | 2. 13 (0. 45-10. 03) |
*Insufficient sample CI=confidence intervals; HR= hazard ratios |