A case of amantadine intoxication in a patient with nephrotic syndrome and an acute kidney injury

Abstract

Amantadine is widely used to treat Parkinson’s disease. However, it should not be used in patients with impaired renal function since it is almost exclusively metabolized through renal excretion. We experienced a rare case of amantadine intoxication in a patient with Parkinson’s disease and nephrotic syndrome. A 71-year-old patient initially had normal renal function (eGFR: 62 mL/min/1.73 m²) and received the optimal dose of amantadine (150 mg/day). The patient then developed new-onset nephrotic syndrome with severe hypoalbuminemia (1.6 g/dL), which was complicated by an acute kidney injury. This resulted in amantadine intoxication. Treatment with both direct hemoperfusion (DHP) and hemodiafiltration (HDF) effectively reduced the patient’s serum amantadine concentration; however, this caused neuroleptic malignant syndrome, which manifested as disturbed consciousness, dyskinesia, and elevated serum creatine kinase levels. This case is noteworthy because nephrotic syndrome frequently causes acute kidney injury, which will lead to amantadine intoxication in patients taking the drug. Furthermore, hypoalbuminemia results in reduced binding of amantadine to serum albumin, and hence, an increase in the level of free amantadine, which promotes the accumulation of amantadine in target organs. However, it is also expected to result in amantadine being eliminated more efficiently via DHP/HDF. Thus, decreased serum albumin levels might constitute a critical determinant of the pharmacokinetics of amantadine with regard to the pathogenesis of amantadine intoxication and its responses to blood purification therapies.