Background: Chronic kidney disease (CKD) presents a profound clinical challenge, not only affecting physical health but also significantly impacting mental well-being. The complex interplay between CKD and psychiatric morbidities remains understudied.
Aim: To address the existing gap by investigating the prevalence and patterns of psychiatric morbidity and cognitive dysfunction among CKD patients.
Materials And Methods: This study adopted a cross-sectional and hospital-based study design. It included 72 patients diagnosed with CKD who fulfilled the inclusion and exclusion criteria. Structured clinical interviews, validated assessment tools (GHQ-12, HAD-S, AUDIT, Addenbrooke's Cognitive Examination-III), and a proforma gathered data on socio-demographic factors, illness severity, treatment history, and psychiatric history.
Results: 70.1% of participants exhibited psychological distress, indicating a high prevalence of psychiatric morbidity. Anxiety disorders were prevalent, affecting 58.1% of participants, while depression affected 32.3% (12.9% mild, 20.8% moderate, 4.8% severe). Cognitive impairment varied with CKD severity, with Stage 3 showing better scores than Stage 4, and hemodialysis patients exhibiting the most significant decline.
Conclusion: This study underscores the substantial burden of psychiatric morbidity and cognitive dysfunction in CKD patients within a general hospital setting. Early identification and integrated interventions in mental health care are crucial for improving CKD patient outcomes and well-being.
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http://dx.doi.org/10.4103/ipj.ipj_62_24 | DOI Listing |
Alzheimers Dement (Amst)
January 2025
Neurochemistry Laboratory Department of Laboratory Medicine Amsterdam UMC Amsterdam The Netherlands.
Introduction: Blood-based glial fibrillary acidic protein (GFAP), neurofilament light chain (NfL), and phosphorylated tau (pTau) have shown promising prognostic potential in Alzheimer's disease (AD), but their applicability in clinical settings where comorbidities are prevalent remains uncertain.
Methods: Simoa assays quantified GFAP, NfL, and pTau181 in retrospectively retrieved prediagnostic serum samples from 102 AD patients and 21 non-AD controls.
Results: Higher serum GFAP levels predicted earlier clinical presentation and faster subsequent Mini-Mental State Examination decline in AD patients.
Neural Regen Res
January 2025
Laboratorio de Neurofisiología, Departamento de Fisiología, Universidad de Concepción, Concepción, Chile.
For many decades, Alzheimer's disease research has primarily focused on impairments within cortical and hippocampal regions, which are thought to be related to cognitive dysfunctions such as memory and language deficits. The exact cause of Alzheimer's disease is still under debate, making it challenging to establish an effective therapy or early diagnosis. It is widely accepted that the accumulation of amyloid-beta peptide in the brain parenchyma leads to synaptic dysfunction, a critical step in Alzheimer's disease development.
View Article and Find Full Text PDFJ Neuroinflammation
January 2025
Department of Translational Neuroscience, Barrow Neurological Institute, Phoenix, AZ, 85013, USA.
The ApoE ε4 allele (APOEε4) is a major genetic risk factor for sporadic Alzheimer's disease (AD) and is linked to demyelination and cognitive decline. However, its effects on the lipid transporters apolipoprotein E (ApoE) and fatty acid-binding protein 7 (Fabp7), which are crucial for the maintenance of myelin in white matter (WM) during the progression of AD remain underexplored. To evaluate the effects of APOEε4 on ApoE, Fabp7 and myelin in the WM of the frontal cortex (FC), we examined individuals carrying one ε4 allele that came to autopsy with a premortem clinical diagnosis of no cognitive impairment (NCI), mild cognitive impairment (MCI) and mild to moderate AD compared with non-carrier counterparts.
View Article and Find Full Text PDFSci Rep
January 2025
School of Medicine, Yan'an University, Yan'an, 716000, China.
The study aims to develop and validate an effective model for predicting frailty risk in individuals with mild cognitive impairment (MCI). The cross-sectional analysis employed nationally representative data from CHARLS 2013-2015. The sample was randomly divided into training (70%) and validation sets (30%).
View Article and Find Full Text PDFSci Rep
January 2025
Medical Genome Center, Research Institute, National Center for Geriatrics and Gerontology, 7-430 Morioka-cho, Obu, 474-8511, Aichi, Japan.
The prevalence of Alzheimer's disease (AD) is increasing as society ages. The details of AD pathogenesis have not been fully elucidated, and a comprehensive gene expression analysis of the process leading up to the onset of AD would be helpful for understanding the mechanism. We performed an RNA sequencing analysis on a cohort of 1227 Japanese blood samples, representing 424 AD patients, 543 individuals with mild cognitive impairment (MCI), and 260 cognitively normal (CN) individuals.
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