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Cyclosporine Neurotoxicity in a Renal-Transplant Recipient
Author(s) -
Rajinder Kumar Sharma,
Pardeep Kumar,
Praveer Rai,
Vijay Kher,
Arun Gupta,
A. Kumar,
M Bhandari
Publication year - 1995
Publication title -
˜the œnephron journals/nephron journals
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.951
H-Index - 72
eISSN - 2235-3186
pISSN - 1660-8151
DOI - 10.1159/000188601
Subject(s) - medicine , nephrology , urology , library science , computer science
Dr. Raj Kumar Sharma, Department of Nephrology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Raebareli Raod, Lucknow 226014 (India) Dear Sir, Cyclosporine A (CsA) has decreased the rate of allograft rejection, but its use is associated with multiple side effects [1]. CsA-induced neurotoxicity is often mild, and complex neurotoxicity manifesting as cerebellar syndrome and spinal motor dysfunction is rarely reported in bone marrow and liver transplant recipients. In this report, we wish to emphasize that severe cerebellar syndrome and psychiatric manifestations can occur due to CsA toxicity in renal-transplant patients who are profoundly immunosup-pressed. A 32-year-old male received a living-related renal allograft and was on conventional immunosuppression (Azoran 2.5 mg/ kg + 10 mg prednisolone). He was also receiving antitubercular treatment (Isonex, ethambutol and pyrazinamide) for pulmonary tuberculosis. Eight months after transplantation, he had a rise in serum creatinine, oliguria and was detected to have acute cellular rejection on renal-allograft biopsy. He received antirejection treatment with 80 mg i.v. dexamethasone for 3 days but did not show satisfactory response. He was put on CsA (5 mg/kg body weight orally daily). His serum creatinine level was 3.0 mg%. After 2 days of CsA therapy, he complained of instability of gait, slurring of speech and inability to use his hands. On examination he was normotensive (blood pressure 130/80 mm Hg) and cooperative. He had cerebellar signs in terms of cerebellar gait, scanning speech, dysdiadochokinesia and titubation. Motor power and deep tendon reflexes in all four limbs were normal. CT scan and CSF examination did not show any abnormality. The fundus was normal. CsA was withdrawn as a presumptive diagnosis of CsA-induced neurotoxicity was made. This cerebellar syndrome lasted for 8 h. Similar symptoms developed 4 days latter, when CsA was reintro-duced (dose 3 mg/kg + 30 mg prednisolone) as he was leukopenic and was not able to take Azoran. The patient required intravenous halo-peridol and diazepam to control psychosis followed by depression which persisted for 1 week. Blood biochemistry revealed serum creatinine 3 mg%, normal serum calcium, phosphorus, serum sodium and potassium and liver enzymes. Serum

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