Cyclosporine-A induced neurotoxicity after renal transplantation.
Cyclosporine-A is a highly potent immunosuppressive agent for solid organ transplantation, but has many side effects including nephrotoxicity, hypertension, gum hyperplasia, hepatotoxicity, and neurotoxicity. Neurotoxicity is a less known toxic effect. The pathogenesis of this effect is unclear. However, it has been postulated that hypomagnesemia, hypocholesterolemia, corticosteroids, and/or neurotoxic substances can induce this syndrome. Also, it has been suggested that the endothelial damage caused by Cyclosporine-A may contribute to neuropeptide-mediated ischemia in the brain and lead to the development of neurological symptoms. In this report, we present a case with reversible neurologic deficits whose symptoms returned to normal after the cessation of cyclosporine-A.
Derici
U
U
Department of Nephrology, Gazi University Hospital, Ankara, Turkey.
Arinsoy
T
T
Sindel
S
S
Tali
T
T
Leventoglu
A
A
Sert
S
S
D001929:Brain Edema / Q000139:chemically induced / Q000175:diagnosis; D016572:Cyclosporine / Q000009:adverse effects*; D005260:Female; D006084:Graft Rejection / Q000188:drug therapy; D006801:Humans; D007166:Immunosuppressive Agents / Q000009:adverse effects*; D016030:Kidney Transplantation / Q000009:adverse effects; D008875:Middle Aged; D009422:Nervous System Diseases / Q000139:chemically induced* / Q000175:diagnosis; D012640:Seizures / Q000139:chemically induced
D007166:Immunosuppressive Agents; D016572:Cyclosporine