Letters to the Editor
Memantine-associated renal impairment in a patient with Alzheimer's disease
Article first published online: 25 FEB 2013
© 2013 The Authors. Psychiatry and Clinical Neurosciences © 2013 Japanese Society of Psychiatry and Neurology
Psychiatry and Clinical Neurosciences
Volume 67, Issue 2, page 126, February 2013
How to Cite
Horikawa, N., Yamada, H. and Uchimura, N. (2013), Memantine-associated renal impairment in a patient with Alzheimer's disease. Psychiatry and Clinical Neurosciences, 67: 126. doi: 10.1111/pcn.12020
- Issue published online: 25 FEB 2013
- Article first published online: 25 FEB 2013
- Manuscript Accepted: 12 DEC 2012
- Manuscript Revised: 3 AUG 2012
- Manuscript Received: 3 MAY 2012
MEMANTINE, AN N-methyl-d-aspartate glutamate receptor antagonist, is used in many countries mainly for the treatment of Alzheimer's disease (AD). Because it is predominantly excreted unchanged via the kidneys, patients with decreased creatinine clearance (CCr) must be treated at lower dose of memantine. It is unclear, however, whether memantine itself causes renal dysfunction. We report herein a patient with AD and impaired renal function associated with memantine.
The patient, a 68-year-old man, was admitted for dyspnea and edematous legs and we were consulted for his cognitive impairment and behavioral problems, such as excitement. His friend reported that he had had memory impairment and anomia starting a few years earlier, followed by difficulty in conceptual thinking, driving and shopping. Mini-Mental State Exam score was 13 and functional assessment staging was 6d (severe cognitive decline). Computed tomography showed diffuse and moderate cerebral atrophy. He was diagnosed with AD and prescribed memantine (5 mg/day initial dosage, 10 mg/day 7 days later). According to laboratory examinations at the beginning of memantine use, serum creatinine (Cr) and blood urea nitrogen (BUN) levels were in the normal range (1.1 mg/dL and 21.8 mg/dL, respectively), then increased gradually up to 1.5 mg/dL and 35.9 mg/dL, respectively, 14 days after induction of treatment. The patient had been diagnosed with diabetes mellitus at the age of 35, although serum fasting blood sugar and glycohemoglobin were in the normal range. Due to all these findings, we concluded that memantine treatment had worsened his renal function and it was discontinued. After memantine cessation, his renal function returned to normal.
The most striking finding in this patient was that memantine itself had the potential to worsen renal impairment. In general, the normal dose for daily treatment of this drug is 20 mg, and 10 mg is recommended in patients with severe renal impairment, although no dosage adjustments are needed for patients with mild or moderate renal impairment. It should be taken into account that the presents renal dysfunction may have been caused by other factors such as dehydration. In fact, the present patient's serum Cr and BUN were slightly elevated at the time of admission (1.2 mg/dL and 29.3 mg/dL, respectively) and then normalized after he was given i.v. fluids. Because we could not completely exclude the possibility of chronic renal impairment, we used the lower dose of memantine (10 mg/day maximum). Nevertheless, memory impairment and behavioral and psychological symptoms of dementia had partially improved at the time of discontinuation of memantine therapy, which suggests that the concentration of memantine was higher than expected due to decreased renal clearance. In conclusion, although memantine is one of the most potent therapeutic agents for patients with AD and its potential side-effect requires further deliberation, renal function should be carefully monitored, especially in patients with complications.