Background The novel COVID-19 vaccines have side effects that require efficient and close monitoring. Aims of the Study To examine whether the Pfizer-BioNTech vaccine is associated with multiple cranial neuropathy. Methods We report the case of a 29-year-old male patient with no notable history who presented with left oculomotor, abducens, trigeminal and facial palsies 6 days after receiving the first dose of the Pfizer-BioNTech COVID-19 vaccine. Results Gadolinium-enhanced MRI of the brain revealed enhancement in the left facial, trigeminal and oculomotor nerves, which persisted upon repeated examination. The cerebrospinal fluid analysis showed no sign of inflammation, both initially and after 1 month from the start of the patient's symptoms. Other causes were excluded by laboratory tests. The patient received high doses of corticosteroids, with improvement of symptoms. Conclusions In our case, the most probable etiology of the patient's multiple cranial neuropathy is the Pfizer-BioNTech vaccine, which highlights the need for prolonged surveillance of COVID-19 vaccine neurological complications.

Diabetic nephropathy (DN) is a leading cause of kidney morbidity. Despite the multilayered complexity of the mechanisms involved in the pathogenesis of DN, the conventional treatment is limited to just a few drug classes fraught with the risk of adverse events, including the progression of renal dysfunction. Phytoceuticals offer a promising alternative as they act on the many-sidedness of DN pathophysiology, multitargeting its intricacies. This paper offers a review of the mechanisms underlying the protective action of these phytoagents, including boosting the antioxidant capabilities, suppression of inflammation, averting the proliferative and sclerosing/fibrosing events. The pathogenesis of DN is viewed as a continuum going from the original offense, high glucose, through the noxious products it generates (advanced glycation end-products, products of oxidative and nitrosative stress) and the signaling chains consequently brought into action, to the harmful mediators of inflammation, sclerosis, and proliferation that eventually lead to DN, despite the countervailing attempts of the protective mechanisms. Special attention was given to the various pathways involved, pointing out the ability of the phytoagents to hinder the deleterious ones (especially those leading to, driven by, or associated with TGF-β activation, SREBP, Smad, MAPK, PKC, NF-κB, NLRP3 inflammasome, and caspase), to promote the protective ones (PPAR-α, PPAR-γ, EP4/Gs/AC/cAMP, Nrf2, AMPK, and SIRT1), and to favorably modulate those with potentially dual effect (PI3K/Akt). Many phytomedicines have emerged as potentially useful out of in vitro and in vivo studies, but the scarcity of human trials seriously undermines their usage in the current clinical practice—an issue that stringently needs to be addressed.

Oxidative stress is a key component in the pathogenesis of a broad number of renal disorders, including acute kidney injury, chronic kidney disease, and various types of nephropathies. Moreover, oxidative stress seems to at least partly explain the intricate relationship the kidney has with other pathological entities, for instance with cardiovascular comorbidities. Renal replacement therapies give end-stage renal disease patients a fighting chance; however, even these interventions may carry the risk of enhancing existing oxidative stress. Even if nutritional components are not currently routinely used, many have shown promise in preclinical or even clinical studies and could counter some of the deleterious pathways that oxidative stress sets in place. This narrative review provides an update on how these natural nutrients could be beneficial to renal disease patients, and it also aims to give an incentive to future research in the field.

Background and Objectives: The main cause of morbidity and mortality in hemodialysis patients is cardiovascular disease, which is quite common. The main objective of our study was to investigate the relationship between oxidative stress, inflammation, and vascular and valvular calcifications in hemodialysis patients. Materials and Methods: This observational study had 54 hemodialysis patients, with an average age of 60.46 ± 13.18 years. Cardiovascular ultrasound was used to detect and/or measure aortic and mitral valve calcifications, carotid and femoral atheroma plaques, and common carotid intima-media thickness. The aortic calcification score was determined using a lateral abdomen plain radiograph. The inflammatory, oxidative, metabolic, and dietary statuses, as well as demographic characteristics, were identified. Results: There were significant correlations between the levels of IL-6 and carotid plaque number (p = 0.003), fibrinogen level and aortic valve calcifications (p = 0.05), intima-media thickness (p = 0.0007), carotid plaque number (p = 0.035), femoral plaque number (p = 0.00014), and aortic calcifications score (p = 0.0079). Aortic annulus calcifications (p = 0.03) and intima-media thickness (p = 0.038) were adversely linked with TNF-α. Nutrition parameters were negatively correlated with atherosclerosis markers: number of carotid plaques with albumin (p = 0.013), body mass index (p = 0.039), and triglycerides (p = 0.021); number of femoral plaques with phosphorus (0.013), aortic calcifications score with albumin (p = 0.051), intima-media thickness with LDL-cholesterol (p = 0.042). Age and the quantity of carotid plaques, femoral plaques, and aortic calcifications were linked with each other (p = 0.0022, 0.00011, and 0.036, respectively). Aortic annulus calcifications (p = 0.011), aortic valve calcifications (p = 0.023), and mitral valve calcifications (p = 0.018) were all associated with an increased risk of death. Conclusions: Imaging measures of atherosclerosis are adversely connected with dietary status and positively correlated with markers of inflammation and risk of mortality.

Background: Arterial stiffness is a crucial factor in the pathogenesis of cardiovascular disease, often associated with aging. However, the impact of smoking on arterial stiffness is frequently underestimated. This study aims to investigate the intricate relationship between smoking and arterial stiffness to advance our understanding of and therapeutic approaches to cardiovascular health. Methods: A prospective analysis was conducted from January to July 2024, focusing on arterial stiffness parameters in a cohort of students from the Carol Davila University of Medicine and Pharmacy. Participants were categorized as smokers or non-smokers based on self-reported smoking status. The study endpoints included correlations between high pulse wave velocity, elevated peripheral and central systolic blood pressure, increased peripheral and central pulse pressure, and smoking status. These markers were assessed using an arteriograph device measuring the time difference between the initial forward pulse wave and the reflected pulse wave in the brachial artery to indirectly estimate the PWV using oscillometric pulsations. Results: Our investigation, involving 102 young individuals aged 20 to 26 (69 females, 33 males), revealed that smokers exhibited significantly higher average values of arterial stiffness indicators compared to non-smokers. Current smokers had higher mean systolic blood pressure (130.65 vs. 123.05 mmHg), higher mean peripheral pulse pressure (53.19 vs. 45.64 mmHg), higher mean central pulse pressure (33.66 vs. 29.69 mmHg), and higher mean pulse wave velocity (5.27 vs. 5.03 m/s). Conclusions: The utilization of arterial stiffness markers as predictive tools offers opportunities for personalized treatment strategies, potentially enhancing cardiovascular health outcomes.

A complex interplay of factors reflecting the general biological, cardiovascular, neurological, renal, and metabolic status of patients influences the outcome of thrombolysis in stroke patients. This is a retrospective cohort observational study aimed to determine the importance of kidney dysfunction among these factors. Data (demographic, lifestyle, physical examination, laboratory, imaging, including metabolic and cardiovascular risk factors and comorbidities, neurological scores, and outcomes) of all stroke patients who underwent thrombolysis have been registered since January 1, 2016, in an online database. A total of 296 patients registered until December 31, 2020, were included in the study. The National Institutes of Health Stroke Scale, modified Rankin scale, Barthel index, percentage of hemorrhagic transformation, and in hospital death were used to evaluate the neurological status and outcomes of the patients. Regression analysis, Mann–Whitney test, Fisher exact test, logistic regression, and multivariate analysis were used for statistical analysis. Kidney dysfunction, as reflected by the estimated glomerular filtration rate, was associated with in hospital death and all but one of the neurological scores. Other risk factors most frequently associated with neurological scores were age, international normalized ratio, and cognitive decline. Multivariate analysis revealed estimated glomerular filtration rate (as determined by chronic kidney disease-EPI equation) as a determinant for all but one of these scores, and as the most important determinant for most of them, except for those reflecting the pre-intervention neurological status of the patient. Kidney dysfunction seems to be the most important determinant of the outcome of thrombolysed stroke patients, a result obtained by no other study.