Myoclonus in a Patient with Acute Kidney Injury: A Rare Presentation of Gabapentin Toxicity

Muzammil Khan,Salah Aldergash,Shaza Khalid,Medha Joshi, Varun Malhotra,Asghar Marwat

doi:10.12691/ajmcr-5-8-8

Abstract

Gabapentin, an anti-epileptic drug (AED) is commonly used off label for management of neuropathic pain and psychiatric disorders. Dosing of gabapentin requires taking into consideration the renal function as it is entirely cleared by the kidneys. Acute kidney injury and end stage renal disease increase the risk of developing myoclonic activity, an infrequent manifestation of gabapentin toxicity. We report a case of confusion and myoclonic activity related to gabapentin toxicity coincident with acute kidney injury that resolved with discontinuation of gabapentin and treatment with intravenous fluid hydration. As gabapentin is commonly used off label across multiple specialties, clinician recognition of the significance of renal dosing and understanding of the potential association with myoclonus and neurotoxicity is important.

Highlights

Gabapentin is a widely used medicine in clinical practice to treat neuropathy and musculoskeletal pain [1]
Urinalysis revealed 2+ white blood cell, nitrite positive and a serum gabapentin level 35.4 ug/mL, normal serum gabapentin reference ranges from 4.0 - 16.0 ug/mL
Patient was discharged with normal renal function, blood urea nitrogen (BUN) 20 mg/dL, creatinine 0.7 mg/dL and resolved myoclonus

Summary

Introduction

Gabapentin is a widely used medicine in clinical practice to treat neuropathy and musculoskeletal pain [1]. Serious neurological toxicity may result in patients with impaired kidney function. The patient had no history of renal disease. Her medications on admission included acetaminophen, clonazepam, gabapentin 1500 mg/day, hydrocodone, lisinopril, hydrochlorothiazide, quetiapine, omeprazole, sumatriptan, and simvastatin. Abnormal lab results on admission included sodium level of 132 mmol/L, blood urea nitrogen (BUN) 73 mg/dL, creatinine (Cr) 3.7 mg/dL as compared to BUN 17 mg/dL and Cr 0.7 mg/dL at baseline 8 weeks ago, and white blood cell count 1.34x10 3/uL. CT scan of head without contrast was normal, EEG showed generalized mild–moderate slowing and generalized discharges with triphasic morphology, consistent with a diffuse disturbance of cerebral function or encephalopathy secondary to metabolic, toxic, inflammatory, or other systemic processes. Patient was discharged with normal renal function, BUN 20 mg/dL, creatinine 0.7 mg/dL and resolved myoclonus.

Discussion

Conclusion