Denosumab-Induced Severe Hypocalcaemia in Chronic Kidney Disease

Background. Hypocalcaemia is increasingly recognized as a complication of denosumab use in Chronic Kidney Disease (CKD) patients with osteoporosis. Despite Therapeutic Goods Administration (TGA) notifications in 2013, we have subsequently encountered several cases of denosumab-induced hypocalcaemia,...

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Main Authors: Ryan Jalleh, Gopal Basu, Richard Le Leu, Shilpanjali Jesudason
Format: Article
Language:English
Published: Hindawi Limited 2018-01-01
Series:Case Reports in Nephrology
Online Access:http://dx.doi.org/10.1155/2018/7384763
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spelling doaj-4e4e1406b28246059560f4393077ff022020-11-24T22:03:06ZengHindawi LimitedCase Reports in Nephrology2090-66412090-665X2018-01-01201810.1155/2018/73847637384763Denosumab-Induced Severe Hypocalcaemia in Chronic Kidney DiseaseRyan Jalleh0Gopal Basu1Richard Le Leu2Shilpanjali Jesudason3Central and Northern Adelaide Renal and Transplantation Service, Royal Adelaide Hospital, Adelaide, South Australia, AustraliaCentral and Northern Adelaide Renal and Transplantation Service, Royal Adelaide Hospital, Adelaide, South Australia, AustraliaCentral and Northern Adelaide Renal and Transplantation Service, Royal Adelaide Hospital, Adelaide, South Australia, AustraliaCentral and Northern Adelaide Renal and Transplantation Service, Royal Adelaide Hospital, Adelaide, South Australia, AustraliaBackground. Hypocalcaemia is increasingly recognized as a complication of denosumab use in Chronic Kidney Disease (CKD) patients with osteoporosis. Despite Therapeutic Goods Administration (TGA) notifications in 2013, we have subsequently encountered several cases of denosumab-induced hypocalcaemia, raising concern about lack of widespread awareness among prescribing practitioners. Aims. We reviewed the morbidity and healthcare intervention needs of CKD patients with hypocalcaemia attributed to denosumab. Methods. A retrospective case series of CKD patients with clinically significant hypocalcaemia after exposure to denosumab, encountered at the tertiary care referral hospital from December 2013 to February 2017, was undertaken. Results. Eight patients (52-85 years of age) with stage 4-5 CKD developed clinically significant hypocalcaemia (corrected calcium 1.45±0.21mmol/L) following denosumab therapy for osteoporosis. Seven of the eight patients required inpatient management with three patients requiring intravenous calcium replacement and cardiac monitoring in a high dependency unit. Our study also identified additional factors that could potentially contribute to hypocalcaemia such as lack of calcium supplementation, use of noncalcium based phosphate binders, absence of or use of lower doses of calcitriol supplementation, low vitamin D levels, concomitant treatment with loop diuretics, history of parathyroidectomy, or presence of acute medical illness. Conclusion. Multiple cases of severe hypocalcaemia in CKD patients following denosumab exposure were encountered after TGA warnings, resulting in considerable morbidity and intensive healthcare interventions in CKD patients. We advocate greater awareness amongst the medical profession, careful consideration before using denosumab in CKD patients, and close follow-up after administration to prevent morbidity.http://dx.doi.org/10.1155/2018/7384763
collection DOAJ
language English
format Article
sources DOAJ
author Ryan Jalleh
Gopal Basu
Richard Le Leu
Shilpanjali Jesudason
spellingShingle Ryan Jalleh
Gopal Basu
Richard Le Leu
Shilpanjali Jesudason
Denosumab-Induced Severe Hypocalcaemia in Chronic Kidney Disease
Case Reports in Nephrology
author_facet Ryan Jalleh
Gopal Basu
Richard Le Leu
Shilpanjali Jesudason
author_sort Ryan Jalleh
title Denosumab-Induced Severe Hypocalcaemia in Chronic Kidney Disease
title_short Denosumab-Induced Severe Hypocalcaemia in Chronic Kidney Disease
title_full Denosumab-Induced Severe Hypocalcaemia in Chronic Kidney Disease
title_fullStr Denosumab-Induced Severe Hypocalcaemia in Chronic Kidney Disease
title_full_unstemmed Denosumab-Induced Severe Hypocalcaemia in Chronic Kidney Disease
title_sort denosumab-induced severe hypocalcaemia in chronic kidney disease
publisher Hindawi Limited
series Case Reports in Nephrology
issn 2090-6641
2090-665X
publishDate 2018-01-01
description Background. Hypocalcaemia is increasingly recognized as a complication of denosumab use in Chronic Kidney Disease (CKD) patients with osteoporosis. Despite Therapeutic Goods Administration (TGA) notifications in 2013, we have subsequently encountered several cases of denosumab-induced hypocalcaemia, raising concern about lack of widespread awareness among prescribing practitioners. Aims. We reviewed the morbidity and healthcare intervention needs of CKD patients with hypocalcaemia attributed to denosumab. Methods. A retrospective case series of CKD patients with clinically significant hypocalcaemia after exposure to denosumab, encountered at the tertiary care referral hospital from December 2013 to February 2017, was undertaken. Results. Eight patients (52-85 years of age) with stage 4-5 CKD developed clinically significant hypocalcaemia (corrected calcium 1.45±0.21mmol/L) following denosumab therapy for osteoporosis. Seven of the eight patients required inpatient management with three patients requiring intravenous calcium replacement and cardiac monitoring in a high dependency unit. Our study also identified additional factors that could potentially contribute to hypocalcaemia such as lack of calcium supplementation, use of noncalcium based phosphate binders, absence of or use of lower doses of calcitriol supplementation, low vitamin D levels, concomitant treatment with loop diuretics, history of parathyroidectomy, or presence of acute medical illness. Conclusion. Multiple cases of severe hypocalcaemia in CKD patients following denosumab exposure were encountered after TGA warnings, resulting in considerable morbidity and intensive healthcare interventions in CKD patients. We advocate greater awareness amongst the medical profession, careful consideration before using denosumab in CKD patients, and close follow-up after administration to prevent morbidity.
url http://dx.doi.org/10.1155/2018/7384763
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