Abstract: SA-PO659
Denosumab: Is It Safe to Use in CKD?
Session Information
- Bone and Mineral Metabolism: Clinical - II
October 27, 2018 | Location: Exhibit Hall, San Diego Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Bone and Mineral Metabolism
- 402 Bone and Mineral Metabolism: Clinical
Author
- Mckenna, Eimear, Altnagelvin Area Hospital, Derry, United Kingdom
Background
Denosumab is a monoclonal antibody directed against receptor activator of RANK ligand used to treat osteoporosis. It has been promoted as safe to use in Chronic Kidney Disease (CKD) as it does not appear to accumulate in kidney failure and because of the experience in a small number of patients with CKD 3-4 enrolled in RCTs. There is no evidence for use in CKD 5. Case reports show patients with severe CKD are at higher risk of developing hypocalcemia following Denosumab. This may be due to hyperparathyroidism and vitamin D deficiency. In this case series we have examined the incidence of hypocalcemia following Denosumab treatment and tried to identify any risk factors.
Methods
Patients with CKD stages 3-5 attending our service treated with Denosumab in the last 5 years were included. Retrospective data was collected using an electronic patient database. Data collected included Corrected calcium levels prior to and after dosing, vitamin D and Parathormone (PTH) levels prior to dosing.
Results
14 patients were identified; 9 had a functioning renal transplant and 1 patient was on hemodialysis. 4 patients were male and 10 female. Mean duration of treatment was 2.2 years. Average eGFR was 27 ml/min/1.73m2. Mean patient age was 60 years (range 44-84). Mean BMI was 25 (range 19-36). 11 patients were on oral steroids. The average calcium prior to dosing was 2.35 mmol/l (2.12 to 2.54) falling to 1.98mmol/l (1.58-2.22) after dosing. 9 patients achieved their lowest calcium at 1 week, 2 at 4 weeks and 3 at 8 weeks. Average PTH level prior to dosing was 153ng/l (42-371) and after was 888ng/l (155-1990). 5 patients developed severe hypocalcemia (corrected calcium less than1.9mmol/l), average prior calcium in this group was 2.39mmol/l (2.22 – 2.54) falling to 1.77mmol/l (range 1.58 – 1.86). The average prior PTH was 206ng/l, rising to 1171ng/l after denosumab. Four patients did not have Vitamin D checked before dosing.
Conclusion
Denosumab will cause a small but not clinically significant reduction in serum Calcium in most patients with CKD. Severe hypocalcaemia can result if Vitamin D levels are unknown or in higher PTH levels. eGFR does not seem to correlate with the risk of hypocalcaemia. The biochemical abnormalities associated with CKD should be corrected, specifically, calcium, phosphate, PTH and vitamin D. Densoumab is the preferred treatment in CKD 4/5 however its use should be avoided in severe hyperparathyroidism and vitamin D deficiency.