Glial fibrillary acidic protein (GFAP) is a type III intermediate filament protein primarily produced by cells in the central nervous system (CNS) and other major organs such as the kidneys. This study investigated whether serum GFAP could be used to estimate cross-sectional vasculitis activity presented via the Birmingham vasculitis activity score (BVAS) in patients with antineutrophil cytoplasmic antibody-associated vasculitis (AAV). This study included 74 patients with AAV. Clinical and laboratory data at diagnosis including BVAS and C-reactive protein (CRP) were reviewed. During follow-up, all-cause mortality and end-stage kidney disease (ESKD) were considered poor outcomes. Serum GFAP was measured from sera collected and stored at diagnosis. The median age of the 74 patients was 63.5 years. Serum GFAP was inversely correlated with the cross-sectional BVAS (r = -0.373) and CRP (r = -0.320). It was also significantly correlated with general (r = -0.237) and renal (r = -0.335) manifestations among BVAS systemic items, and furthermore, among minor items of renal manifestation, correlating with sum scores for proteinuria (r = -0.409) and haematuria (r = -0.305). Additionally, compared with patients with serum GFAP > 194.9 pg/mL, those with serum GFAP ≤ 194.9 pg/mL showed a higher risk for progression to ESKD (relative risk 3.150) and a significantly lower cumulative ESKD-free survival rate. This study demonstrated the clinical potential of serum GFAP at diagnosis for predicting not only cross-sectional vasculitis activity through the anticipation of the extent of renal involvement but also future progression to ESKD in patients with AAV.
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http://dx.doi.org/10.3390/medicina60101639 | DOI Listing |
Alzheimers Dement
December 2024
University of North Dakota, Grand Forks, ND, USA.
Background: Alzheimer's disease (AD) is an age-related neurodegenerative disorder affecting nearly 50 million individuals worldwide. Besides aging, various comorbidities can increase the risk of AD, such as asthma. However, the molecular mechanism(s) underlying this asthma-associated AD exacerbation is unknown.
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December 2024
Brigham and Women's Hospital; Harvard Medical School, Boston, MA, USA.
Background: Previously, we found that germline C3 deletion protected cognition and hippocampal synapses in aged APP/PS1dE9 mice, despite increasing Aß plaques. Here, we crossed our C3 inducible conditional mouse model to APP knockin mice to determine whether global C3 lowering in an adult amyloid mouse model would be protective.
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Alzheimers Dement
December 2024
Aging Research Center, Karolinska Institutet and Stockholm University, Stockholm, Sweden.
Background: Alzheimer's disease (AD)-related biomarkers assessed in blood have proved to be useful for detecting dementia and cognitive impairment in the memory clinic. However, less is known about their predictive value in the long-term and in a community-based setting.
Method: We examined six common serum-derived biomarkers of AD (P-tau181, T-tau, Aβ42/Aβ40 ratio, P-tau181/Aβ42 ratio, Nfl, and GFAP) from the baseline assessment of the population-based Swedish National Study on Aging and Care in Kungsholmen (SNAC-K; n = 2071, mean age at baseline = 72 years).
Alzheimers Dement
December 2024
Amsterdam Neuroscience, Neurodegeneration, Amsterdam, Noord-Holland, Netherlands.
Background: Sporadic bvFTD is often misdiagnosed as a primary psychiatric disorder (PPD) due to overlapping clinical features and lack of reliable biomarkers. The multi-centre study DIPPA-FTD aims to develop diagnostic- and prognostic-algorithms that can distinguish sporadic bvFTD from late-onset PPD. The aim of the retrospective DIPPA-FTD study was to identify the strongest clinical discriminators.
View Article and Find Full Text PDFMol Neurobiol
December 2024
Department of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Virus encephalitis (VE), recognized as one of the common kinds of central nervous system (CNS) diseases after virus infection, has a surprising correlation with autoimmune encephalitis (AE) when autoimmune antibodies emerge in cerebrospinal fluid (CSF) or serum. Herpes simplex virus and Epstein-Barr virus are the most critical agents worldwide. By molecular mimicry, herpes viruses can invade the brain directly or indirectly.
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