Elsevier

Pediatric Neurology

Volume 23, Issue 4, October 2000, Pages 353-356
Pediatric Neurology

Case report
Cyclosporine A neurotoxicity in a patient with idiopathic renal magnesium wasting

https://doi.org/10.1016/S0887-8994(00)00198-3Get rights and content

Abstract

We report a female child who had idiopathic renal magnesium wasting secondary to suspected Gitleman syndrome and cyclosporine A neurotoxicity after a heart transplant. The child had acute, progressive encephalopathy, intractable seizures, quadriparesis, and extensive, bilateral cortical involvement on neuroimaging. Two days after discontinuation of the cyclosporine, the child’s condition improved dramatically, including an improved level of consciousness, and she became seizure free. By 6 weeks, she was fully ambulatory. Follow-up magnetic resonance imaging and electroencephalograms demonstrated significant improvement. This patient had drug-induced neurotoxicity, exacerbated by hypomagnesemia. Cyclosporine should be used cautiously in transplant patients with Gitelman syndrome or other acquired magnesium homeostasis disorders because of the possible increased risk of neurotoxicity. This report is the first case of a patient with both cyclosporine neurotoxicity and magnesium-wasting nephropathy.

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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