Abstract
Chronic kidney disease-mineral and bone disorder (CKD-MBD) is frequently present in advanced stages of chronic kidney disease (CKD) patients with high risk of fracture and elevated socioeconomic burden. Denosumab, an injectable human monoclonal antibody with affinity for nuclear factor-kappa ligand (RANKL), is an effective treatment for osteoporosis in postmenopausal women and men. Unlike the bisphosphonates, the pharmacokinetics and pharmacodynamics of denosumab are not influenced by the renal function and are being increasingly used for patients having CKD-MBD with low bone mineral density (BMD) to reduce the risk of fragility fractures. Hypocalcemia is a known side effect of this drug along with compensatory increase in parathyroid hormone (PTH). However, limited information is available in the literature regarding this potentially life-threatening side effect with denosumab in end-stage renal disease (ESRD) patients on dialysis. We present a patient with ESRD on peritoneal dialysis who developed severe symptomatic hypocalcemia and dramatic increase in PTH following denosumab therapy. She was conservatively managed with calcium supplementation and appropriate adjustment in calcium dialysate. We have also reviewed the literature on the use of denosumab in dialysis patients and looked at additional factors that may precipitate severe hypocalcemia in these patients. We believe that denosumab should be used with caution in dialysis patients since it may lead to profound hypocalcemia. Clinicians should ensure special attention in recognizing patients at risk of developing this serious adverse effect, so that prompt treatment and preventive strategies can be implemented.
Highlights
Disorders of mineral and bone metabolism are common sequelae of chronic kidney disease (CKD) that are collectively termed as chronic kidney disease-mineral and bone disorder (CKD-MBD)
We present a patient with end-stage renal disease (ESRD) on peritoneal dialysis who developed severe symptomatic hypocalcemia and dramatic increase in parathyroid hormone (PTH) following denosumab therapy
CKD is characterized by spectrum of mineral and bone disorders (CKD-MBD) that worsen with progressive loss of kidney function and is associated with an increased risk of fragility fractures
Summary
Disorders of mineral and bone metabolism are common sequelae of chronic kidney disease (CKD) that are collectively termed as chronic kidney disease-mineral and bone disorder (CKD-MBD). More severe stages of CKD (stages 4–5D) are associated with progressively reduced bone mineral density (BMD), a higher prevalence of fracture [1], and a mortality rate after fracture about twice as high as that compared to those without severe CKD [2]. It has greater effectiveness in increasing bone mineral density (BMD) [4] and better pharmacologic profile especially in CKD patients and is being increasingly used for patients having CKD-MBD with low BMD to reduce the risk of fragility fractures. It is known to cause severe hypocalcemia in certain high-risk individuals along with compensatory increase in parathyroid hormone (PTH); there have been few reported cases in peritoneal dialysis patients [5]. We present a patient with ESRD on peritoneal dialysis who developed severe symptomatic hypocalcemia and dramatic increase in PTH following denosumab therapy. 8.4 – 10.2 2.5 – 5.0 150 – 300 (Caucasian Dialysis patients) 34- 104 30 - 100 patients and looked at additional factors that may precipitate severe hypocalcemia in them
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