Case reportCyclosporine A neurotoxicity in a patient with idiopathic renal magnesium wasting
Introduction
Cyclosporine A neurotoxicity, although infrequently reported among children, is well documented [1], [2]. Most instances of this condition have been reported in patients after liver, kidney, or bone marrow transplantation [2]; its occurrence after heart transplantation has been infrequent [3], [4], [5]. This report documents an unusual presentation of cyclosporine neurotoxicity in a 10-year-old heart transplant patient who had renal magnesium wasting secondary to suspected Gitelman syndrome.
Section snippets
Case report
An 8-year-old female child had severe heart failure and idiopathic dilated cardiomyopathy confirmed by echocardiogram and endomyocardial biopsy. Her family history was unremarkable. During the initial hospital admission for evaluation of acute heart failure, she developed tetany because of low serum magnesium (0.31 mmol/L, normal range = 1.14-1.29), marginally low serum potassium (3.3 mmol, normal range = 3.5-5.2), and metabolic alkalosis. A 24-hour urine collection for magnesium revealed that
Discussion
Cyclosporine is a lipophilic, immunosuppressive peptide that selectively inhibits T-lymphocyte activation in response to antigen stimulation. Although it is the drug of choice in organ transplantation, its clinical use is hampered by its toxicity and unpredictable pharmacokinetics. The incidence of moderate and severe cyclosporine neurotoxicity during the early period after transplantation is reported to be up to 11% [7]. Most of the reported cases occur after bone marrow, liver, or kidney
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Acquired Disorders of Hypomagnesemia
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2021, Pharmacology Research and PerspectivesOrthotopic Heart Transplantation in a Patient With Gitelman Syndrome and Dilated Cardiomyopathy
2020, World Journal for Pediatric and Congenital Heart SurgeryOrgan transplant recipients and critical care seizures
2017, Current Clinical Neurology