Two cases of pregabalin neurotoxicity in chronic kidney disease patients

Two cases of pregabalin neurotoxicity in chronic kidney disease patients Sir We report two cases of newly presenting pregabalin neuro-toxicity in chronic kidney disease (CKD) patients. A 67-year-old man was referred to our nephrology department for consultation. He had been admitted to the department of orthopedics because of spinal stenosis and had undergone surgery 5 weeks earlier. He had started hemodialysis 3 months previously. Upon presentation, he was in a deep drowsy mental state. He was also suffering from generalized myoclonic jerk, aphasia and dysarthria of several days duration. We did not detect a brain lesion on magnetic resonance imaging or computed tomography. No medications were being given that could have induced his neurologic symptoms and signs. No laboratory abnormalities were detected that would explain his neurologic deficits. However, pregabalin had been started at a dosage of 300 mg/day 2 weeks before presentation, and the dosage had been increased to 450 mg/day 7 days previously. We concluded that his neurologic deficits were the result of pregabalin toxicity. Pregabalin was immediately withdrawn and an additional three hemodialysis sessions were performed, after which the patient became mentally alert and the generalized myoclonus, aphasia and dysarthria completely disappeared. The second case is that of a 43-year-old man who was admitted for evaluation of nausea, vomiting and general weakness. He was diagnosed with diabetes mellitus and CKD Stage 4. Three days after admission, he complained of pain around the posterior neck region and in both shoulders. He was diagnosed with fibromyalgia and commenced therapy with pregabalin. After receiving a 75 mg/day dose of pregabalin for 2 days, he developed a drowsy mental state and myoclonus of both upper extremities was detected. His calculated creatinine clearance (CCr) by Cockcroft–Gault formula was 25.7 mL/min. We suspected pregabalin toxicity and immediately withdrew it. Thereafter, he fully recovered from the drowsiness, disorientation and myoclonus. Pregabalin is well absorbed orally and has a bioavail-ability of >90%. It is completely excreted into the urine without hepatic metabolism. It is usually suggested that pregabalin doses be decreased by ~50% for each 50% decline in CCr to achieve similar plasma drug concentrations in patients with impaired renal function [1]. Pregabalin toxicity in CKD patients has very rarely been reported [2–4]. Two cases have occurred in hemodialysis patients, whereas one case occurred in a patient undergoing perito-neal dialysis. Our first patient was also undergoing hemo-dialysis, whereas the second one was a CKD Stage …