Background: Post-COVID-19 cognitive impairment, commonly referred to as “brain fog,” represents a significant clinical problem, yet its underlying mechanisms remain incompletely understood. New research indicates that long-term cognitive consequences of SARS-CoV-2 infection may result from chronic immunological dysregulation and neurometabolic changes. Objective: We aimed to assess the associations between cognitive performance, cerebral glucose metabolism, and inflammatory markers in patients with COVID-19 brain fog symptoms. Methods: This study included 47 patients with post-COVID-19 cognitive complaints enrolled in the COVMENT trial. Cognitive performance was assessed using the Montreal Cognitive Assessment (MoCA). Brain glucose metabolism was evaluated with FDG PET-CT, and inflammatory markers, including C-reactive protein (CRP), monocyte-to-lymphocyte ratio, neutrophil-to-lymphocyte ratio, eosinophil-to-lymphocyte ratio, and platelet-to-lymphocyte ratio (PLR), were measured. Correlation analyses, logistic regression, and ROC analysis were performed to explore relationships between these factors. Results: A lower score of the MoCA abstraction domain correlated significantly with lower FDG uptake in multiple brain regions, including inferior parietal lobules and precuneus. Among inflammatory markers, only PLR demonstrated significant associations with both brain metabolism and abstraction performance. Lower PLR values were associated with greater neurometabolic impairment, and PLR < 130.1 was associated with abnormal abstraction performance. Conclusions: Post-COVID-19 cognitive dysfunction can be associated with selective neurometabolic alterations in brain regions supporting abstract reasoning. PLR seems to be associated with both cognitive performance and regional brain metabolism, suggesting a potential link between chronic immune dysregulation and neurocognitive impairment in post-COVID-19.

Chronic kidney disease (CKD) affects more than 10% of the world’s population, increasing the risk of cardiovascular disease and mortality. Background: Nephroprotective interventions can reduce the risk of end-stage renal disease, delay the time to dialysis, and prolong life. However, there is ongoing debate about the effectiveness of combining amino acid ketoanalogues (KAA) with a low-protein diet (LPD) to slow CKD progression. This study aimed to retrospectively analyze kidney function outcomes after a 6-month KAA+LPD regimen in patients with CKD. Methods: The analysis included results from 38 non-dialyzed patients (12 F, 26 M; age 64.0 ± 13.6 years) with stable CKD in stages G4 to G5, who followed LPD with KAA (Ketosteril, Fresenius Kabi) treatment as part of the Polish National Health Fund Ketosteril Drug Program. Results: No significant change in estimated glomerular filtration rate (eGFR) was observed during 6 months of KAA+LPD therapy. However, eGFR increased or decreased in half of the patients (p < 0.001), and this change was associated only with initial protein intake and urinary phosphate excretion. Initial high phosphate excretion was independently associated with an increase in eGFR, and initial phosphaturia > 0.5 g/24 h identified eGFR improvement (sensitivity 84.2%; specificity 57.9%; AUC 0.712; p = 0.018) in CKD patients who started KAA+LPD treatment. Conclusions: Six-month treatment with KAA+LPD may be associated with stabilization of kidney function in patients with CKD stages G4-G5. The individual effect of KAA+LPD on renal function may be related to the initial protein intake level and urinary phosphate excretion. Further studies are needed to validate these findings across larger patient populations with a broader spectrum of symptoms.

Background: Antineutrophil cytoplasmic antibody-associated systemic vasculitis (AAV) most often involves the kidneys, upper airways and lungs, and peripheral and central nervous systems (PNS, CNS). However, in contrast to PNS, the involvement of the CNS is rarely taken into account in the recognition and assessment of systemic vasculitis, probably because of nonspecific symptoms such as headaches and dizziness, aphasia, memory disorders, or mood changes. In addition, it is not clear whether treatment of systemic vasculitides reduces cerebral vascular alterations. In this study, we aimed to evaluate the effects of AAV treatment on vascular and vasogenic alterations in the brain in patients with acute vasculitis onset with renal involvement. Methods: Twenty-nine patients (17F, 12M, age 60.4 ± 9.8) with AAV relapse with renal involvement were included in the study. The initial baseline assessment and the second evaluation, performed 12.6 ± 2.5 months after the beginning of immunosuppressive treatment, included clinical, neurological, and renal function assessments, along with a brain MRI. Results: Compared with baseline, improvement in clinical, neurological, and renal function was observed during the second clinical evaluation. A significant reduction in the occurrence of vascular dilatation and narrowing in secondary (37.9% vs. 17.2%; p = 0.031) and tertiary (37.9% vs. 10.3%; p = 0.008) cerebral vascular branches was observed. However, the number of vasogenic cerebral white matter lesions detected on the FLAIR sequence increased significantly (36.0 vs. 48.0%; p < 0.001). Conclusions: Intensive immunosuppressive treatment of acute-onset systemic AAV with renal involvement decreases disease activity, improves kidney function, and decreases central nervous system vascular but not vasogenic alterations.

Objective: The renal resistive index (RRI), measured by Doppler ultrasonography, is commonly used to assess renal vascular-interstitial damage. However, the RRI may be associated with cardiovascular and general hemodynamic factors, as well as with structural and functional changes within the kidney. These associations may be influenced by the measurement location of the RRI. This scoping review aimed to evaluate differences in RRI associations with hemodynamic or structural and functional alterations in the kidney across measurements at different sites along the renal arterial tree. Methods: A search of the PubMed database was conducted to identify studies evaluating the association between the RRI measured at different levels of the renal arterial tree. Separate search strategies were used for the main renal artery, segmental/interlobar arteries, and intraparenchymal cortical vessels. Studies were selected based on predefined inclusion and exclusion criteria. Results: A total of 888 publications were identified. After applying the exclusion criteria, the final analysis included 6 papers on main arteries, 30 on segmental arteries, and 7 on parenchymal arteries. All analyzed publications showed associations between the RRI and cardiovascular or renal factors, or both. Conclusions: Available data suggest that the relationship between the renal resistive index and systemic or local changes may vary by measurement site. However, reliable studies directly comparing RRI associations across measurement sites are lacking. Therefore, current evidence does not establish whether RRI measurements obtained at different sites can be used interchangeably.