MO354PRELIMINARY EVIDENCE OF RIVASTIGMINE EFFICACY IN CKD RELATED MILD COGNITIVE IMPAIRMENT. (29th May 2021)

• Record Type: Journal Article
• Authors: Mone, Pasquale; Pansini, Antonella; Capasso, Giovambattista; Viggiano, Davide
• Is Part Of: Nephrology dialysis transplantation. Volume 36(2021)Supplement 1
• Publication Date: 2021-05-29
• Subjects: Nephrology -- Periodicals; Hemodialysis -- Periodicals; Kidneys -- Transplantation -- Periodicals; Hemodialysis; Kidneys -- Transplantation; Nephrology; Periodicals; 616.61
• DOI: 10.1093/ndt/gfab082.008
• Languages: English
• ISSNs: 0931-0509

Abstract

Abstract: Background and Aims: Mild Cognitive Impairment (MCI) is a common finding in chronic kidney disease (CKD) patients. Indeed, CKD represents a relevant risk factor for developing dementia and MCI. Cholinesterase inhibitors, such as rivastigmine, are among the few drugs approved for the treatment of dementia and MCI. Rivastigmine is also used to treat vascular dementia because it protects subcortical brain structures. Data are scanty regarding the use of rivastigmine in CKD patients with MCI and are much needed to guide the therapy for MCI in this cohort of patients. Method: This retrospective case-control study compared the effects of rivastigmine on cognitive functions in MCI patients with CKD (stage III-IV; n= 20) and without CKD (n=21, control group), comparable for the extent of cognitive impairment (indexed by Montreal Cognitive Assessment, MoCA), age (range 18-65 years), gender, weight, and comorbidities. Patients under treatment with rivastigmine and with a baseline MoCA score available were included in the study. Exclusion criteria were ictus, psychiatric or other neurological conditions, heart failure, liver failure, severe obesity, anemia, electrolyte disorders, cancer, dialysis, and other severe comorbidities. Laboratory test data (glycemia, cholesterol, hemoglobin, proteinuria, creatinine) were used to characterize the two populations. MCI was defined as a MoCA score between 21-26. The cognitive screening was available at baseline (before treatment) and during a follow-up in a range of three-six months after the start of the treatment. CKD was defined by eGFR < 60 mL/min/1.73m 2 . Results: The follow-up timing for cognitive screening was not statistically different between the two cohorts. The control group (MCI without CKD) showed a small, significant improvement in the MoCA score after treatment (baseline MoCA: 22.9±0.5, follow-up MoCA: 23.5±0.5, p=0.02, t-test for paired data). At variance, the MCI-CKD group showed a significant improvement in the MoCA score (baseline MoCA=23±0.4, follow-up MoCA=24.3±0.4, p<0.05). Accordingly, the extent of improvement of MoCA score after rivastigmine was inversely correlated to the eGFR (r = -0.23). Conclusion: A significant improvement in MoCA score accompanied treatment with rivastigmine in the CKD group. More extensive population studies are needed to verify the greater efficacy of Acetylcholinesterase inhibitors in this population.