Background: Chronic kidney disease (CKD) represents a state of persistent, sterile low-grade inflammation in which sustained innate immune activation accelerates renal decline and cardiovascular complications. Diet-induced gut dysbiosis and intestinal barrier dysfunction lower mucosal immune tolerance, promote metabolic endotoxemia, and position the gut as an upstream modulator of systemic inflammatory signaling along the gut–kidney axis. Scope: Most studies address microbiota-derived metabolites, food-derived bioactive peptides, or omega-3 fatty acids separately. This review integrates evidence across these domains and examines their convergent actions on epithelial barrier integrity, immune polarization, oxidative-inflammatory stress, and inflammasome-dependent pathways relevant to CKD progression. Key mechanisms: CKD-associated dysbiosis is characterized by reduced short-chain fatty acid (SCFA) production and increased generation and accumulation of uremic toxins and co-metabolites, including indoxyl sulfate, p-cresyl sulfate, trimethylamine N-oxide, and altered bile acids. Reduced SCFA availability weakens tight junction-dependent barrier function and regulatory immune programs, favoring Th17-skewed inflammation and endotoxin translocation. Bioactive peptides modulate inflammatory mediator networks and barrier-related pathways through effects on NF-κB/MAPK signaling and redox balance, while omega-3 fatty acids and specialized pro-resolving mediators support resolution-phase immune responses. Across these modalities, shared control points include barrier integrity, metabolic endotoxemia, oxidative stress, and NLRP3 inflammasome activation. Conclusions: Although evidence remains heterogeneous and largely preclinical, combined nutritional modulation targeting these convergent pathways may offer greater immunomodulatory benefit than isolated interventions. Future multi-omics-guided, factorial trials are required to define responder phenotypes and translate precision immunonutrition strategies into clinical CKD care.

Our paper aims to present three cases of committed suicide in SARS-CoV-2 infection during the quarantine period. We investigated if there is a role for the infection itself in triggering the suicidal act or if it is augmented by other risk factors such as fear, psychosocial stress, lifestyle changes, and social isolation. To this goal, we analyzed the clinical, paraclinical, histopathological, toxicological records, mental health conditions, psychological, social, cultural, and economic aspects in detail. One patient committed suicide at home, by hanging, while the other two during hospitalization in the red zone, within the Sibiu County Emergency Clinical Hospital, hanging and falling from a height, respectively. The autopsy was carried out within the restricted area for COVID-19 in Sibiu County Forensic Medicine Service. Patients’ medical histories were analyzed based on the available medical reports. Additionally, we interviewed a family member, applying the so-called psychological autopsy method, based on open-ended questions and standardized instruments (questionnaire) to point out the motives and behavioral changes that might explain the committed suicide. With this data, we could fulfill a design to elucidate and outline the reasons for the suicidal act. Our findings showed that the mental state deteriorated progressively, both in preexisting depressive and non-depressive backgrounds. Furthermore, we highlight the COVID-19 psychological impact in the suicidal acts. Further on, we reviewed the risk factors presented in the literature that are associated with mental health problems and behavioral changes such as stress, anxiety, depressions, sleep disorders, impulsivity, loneliness.

Von Hippel-Lindau (VHL) is a rare genetic disorder caused by mutations in the VHL gene on chromosome 3. The disease is associated with increased incidence of neoplasia. The most common manifestations of the disease are hemangioblastomas of the CNS and spinal cord, followed by renal cell carcinomas (RCC), pancreatic tumors, pheocromocytomas, endolymphatic sac tumors, and broad ligament or epididymal cystadenomas. Due to low incidence of the disease, information about its manifestation and genetic makeup has been slow to be gathered. Herein, we present three patients suffering from VHL, all part of the same family: patient one is the father; patient two is the daughter; and patient three is the nephew of the father, cousin to the daughter. Patients and their samples were investigated by magnetic resonance imaging, immunohistochemistry and genetic testing. Results show a tumor process in the left cerebellar hemisphere of the first patient which was successfully removed. The second patient presents with cervical medullary hemangioblastoma which was also successfully removed. The third patient had a tumor formation located at the craniospinal junction, at the level of the posterior bulb which was also treated. Genetic analysis showed patients one and two presented mutations in the VHL gene, confirming the VHL diagnosis. While the cases presented here follow the general lines for VHL disease, patients are related to each other, present tumors of the nervous system and mutations in the VHL gene, their particularities of presentation and manifestation bring new insights into this rare genetic disease.

Late-onset Alzheimer’s disease (LOAD) is increasingly recognized as a complex, multifactorial disorder driven by the convergence of genetic susceptibility and interconnected molecular pathways, rather than a single linear pathogenic cascade. In this review, we integrate evidence from genome-wide association studies, sequencing analyses, and experimental research to map disease-associated single-nucleotide polymorphisms (SNPs) onto key biological processes underlying LOAD pathogenesis. Converging data consistently implicate a limited number of core domains, including amyloid-β metabolism, tau pathology, neuroinflammation, lipid homeostasis, endosomal–lysosomal trafficking, mitochondrial dysfunction, and synaptic impairment. Importantly, genetic risk variants are not randomly distributed, but cluster within these pathways, exerting coordinated effects across multiple biological systems and supporting a network-based organization of disease. We further examine how these pathways interact at a systems level, highlighting key interfaces such as the amyloid–tau, lipid–immune, inflammation–proteostasis, and mitochondria–synaptic dysfunction axes. These interconnected processes form self-reinforcing feedback loops that amplify neurodegeneration and contribute to disease progression. From a translational perspective, this integrated framework provides a mechanistic basis for the limited efficacy of single-target therapies and supports the development of multi-target and pathway-oriented strategies, as well as precision medicine approaches based on genetic and biomarker integration. Collectively, this review supports a unified model of LOAD as a polygenic network disorder and underscores the importance of pathway convergence in understanding disease heterogeneity and guiding future therapeutic development.

Background: Acute kidney injury (AKI) is a dynamic clinical syndrome, and a single serum creatinine measurement may not adequately reflect the severity or progression of renal dysfunction. The aim of this study was to assess whether early changes in serum creatinine provide better discrimination for renal replacement therapy (RRT) requirement than admission creatinine alone and to identify clinical factors associated with RRT and short-term renal outcomes. Methods: This retrospective observational cohort study included 115 adults with AKI admitted to the Nephrology Department or Intensive Care Unit of Sibiu County Clinical Emergency Hospital between January 2018 and December 2025. Clinical, biochemical, hemodynamic, fluid-balance and nephrotoxic exposure data were analyzed. Serum creatinine was assessed at admission or transfer to the Nephrology Department or Intensive Care Unit (time zero) and at 24 and 48 h thereafter. Multivariable logistic regression and receiver operating characteristic analyses were used to evaluate factors associated with RRT requirement and an eGFR below 60 mL/min/1.73 m² at 30 days. Creatinine change was defined as the absolute difference from the value measured at study entry. Results: Fifty-two patients required RRT. The 48 h change in serum creatinine showed better discrimination for RRT requirement than admission creatinine (AUC 0.758 vs. 0.634; DeLong p = 0.012). An exploratory, cohort-derived 48 h creatinine-change threshold of 0.79 mg/dL showed a sensitivity of 90.4% and a specificity of 52.4% for distinguishing RRT status. In multivariable analysis, vasopressor requirement, maximum serum potassium and positive 24 h fluid balance were independently associated with RRT, while the overall model showed high apparent discrimination (AUC 0.925). RRT requirement was also associated with an eGFR below 60 mL/min/1.73 m² at 30 days (adjusted OR 2.84, 95% CI 1.02–7.91). Conclusions: The 48 h creatinine change showed modest apparent discrimination of RRT status, but these findings are exploratory and do not establish prospective prediction. Patients requiring RRT also had greater hemodynamic instability, hyperkalemia and positive fluid balance and were more likely to have an eGFR below 60 mL/min/1.73 m² at 30 days. Serial assessment of renal function, together with the patient’s clinical and metabolic status, may therefore be more informative than a single creatinine measurement.

Background: Type 2 diabetes mellitus (T2DM) is common in patients with gastrointestinal malignancies, yet its relationship with functional status at cancer diagnosis remains poorly defined. Because both diabetes and cancer are characterized by systemic inflammatory activation, inflammation may be associated with the relationship between diabetes and functional impairment. Methods: We performed a retrospective observational study of 344 patients with colon or pancreatic cancer diagnosed between January 2019 and December 2025, including 172 patients with T2DM and 172 without diabetes, frequency-matched by tumor site. Clinical characteristics, The Eastern Cooperative Oncology Group - ECOG performance status (ECOG-PS) and laboratory parameters were assessed at diagnosis before oncological treatment. Associations between T2DM and ECOG-PS were examined using multinomial and ordinal logistic regression adjusted for age, cancer stage, tumor site, and sex. Multivariable linear regression was used to assess associations with log-transformed C-reactive protein (CRP) and lactate dehydrogenase (LDH). An exploratory analysis evaluated the indirect statistical association through a composite inflammatory score derived from standardized CRP, LDH, and neutrophil count values using 5000 bootstrap samples. Results: T2DM was independently associated with a higher ECOG-PS category in the ordinal model (OR = 1.78; 95% CI 1.14–2.76; p = 0.010). In the multinomial model, T2DM was associated with ECOG 2 versus ECOG 0 (OR = 2.84; 95% CI 1.22–6.63; p = 0.016), whereas the association with ECOG 1 versus ECOG 0 was not statistically significant. After multivariable adjustment, T2DM was associated with 56.4% higher CRP and 34.7% higher LDH levels. A significant indirect statistical association through the composite inflammatory score was observed (β = 0.147; 95% bootstrap CI 0.083–0.216; p < 0.001), whereas the direct association after inclusion of the inflammatory score was not significant (β = 0.020; 95% CI −0.119 to 0.158; p = 0.780). Conclusions: In this selected sample assessed cross-sectionally at cancer diagnosis, T2DM was associated with poorer ECOG performance status and higher systemic inflammatory markers. The observed indirect statistical association through the composite inflammatory score should be interpreted as exploratory because the concurrent assessment of inflammatory markers and ECOG-PS precludes temporal or causal inference. Prospective longitudinal studies are required to clarify these relationships.