Fracture risk is a serious yet underrecognized complication among patients with chronic kidney disease (CKD), especially in those with stages G3-G5D. The overlap between CKD-Mineral and Bone Disorder (CKD-MBD) and osteoporosis leads to complex bone changes that increase the likelihood of fragility fractures. Studies show that 18% to 32% of CKD patients also have osteoporosis, and these individuals are more than 2.5 times as likely to suffer from fractures compared to those without CKD. In the advanced stages of the disease, fracture risk is up to four times higher than in the general population, with the femur, forearm, and humerus being the most commonly affected sites. Hip fractures are of particular concern as they are linked to longer hospital stays and higher rates of morbidity and mortality. Furthermore, dialysis patients who experience hip fractures have a mortality rate 2.4 times higher than those in the general population with similar fractures. This increased risk underscores the need for proactive bone health maintenance in CKD patients to prevent fractures and related complications. This review explores the underlying pathophysiological mechanisms, diagnostic challenges, and treatment options related to bone fragility in CKD. Diagnostic tools, such as bone mineral density (BMD) assessments, the trabecular bone score (TBS), and biochemical markers, remain underused, especially in advanced CKD stages. Recent treatment strategies emphasize a multidisciplinary, stage-specific approach, incorporating calcium and vitamin D supplements, anti-resorptive agents like denosumab, and anabolic therapies such as teriparatide and romosozumab. Effective management needs to be tailored to the patient’s bone turnover status and stage of CKD. Despite progress in understanding bone fragility in CKD, significant gaps remain in both diagnosis and treatment. Personalized care, guided by updated KDIGO recommendations and based on an interdisciplinary approach, is essential to reduce fracture risk and improve outcomes in this vulnerable population. Further research is needed to validate risk assessment tools and refine therapeutic protocols.

Background/Objectives: Chronic kidney disease (CKD) and diabetic kidney disease (DKD) are growing public health challenges. While diet and body composition influence metabolic and renal health, their combined role remains underexplored. This study investigates the association between the Planetary Health Diet Index (PHDI), body mass distribution, and the prevalence of CKD and DKD in U.S. adults. Methods: We analyzed data from 8093 adults aged ≥40 years from NHANES 2003–2018. PHDI was computed using two 24 h dietary recalls. Body composition was assessed using dual-energy X-ray absorptiometry (DXA), focusing on the android-to-gynoid fat ratio (AGFR) and lean mass ratio (AGLR). Survey-weighted linear and logistic regressions evaluated cross-sectional associations between PHDI score, body composition indices, and prevalence of CKD and DKD. Mediation analyses explored AGLR, AGFR, and body mass index (BMI) as potential mediators of the association between PHDI score and either CKD or DKD. Results: Higher PHDI scores were mildly associated with lower odds of CKD (OR per 10-point increase: 0.91; 95% CI: 0.83–0.99) and DKD (OR: 0.86; 95% CI: 0.76–0.97). Greater PHDI scores correlated with lower BMI, AGFR, and AGLR. Among participants with diabetes, AGLR mediated 17% of the relationship between a 10-point increase in PHDI score and decreased DKD prevalence, suggesting central lean mass distribution as a relevant pathway. No significant mediation was observed for AGFR, BMI, or for CKD. Conclusions: Adherence to PHD is associated with healthier body composition and lower prevalence of CKD and DKD. These findings support the promotion of dietary strategies that enhance metabolic and renal health in middle-aged and older individuals.

Aging is the major risk factor for several chronic conditions, including cognitive decline and dementia. It is accompanied by profound immune alterations characterized by a progressive decline in immune competence, a process known as immunosenescence. The resulting dysregulation of immune function leads to the overproduction of proinflammatory cytokines and fuels a persistent, low-grade inflammatory state termed inflammaging. This chronic inflammation contributes to dysfunction across the central and peripheral nervous systems, promoting neuronal damage and accelerating neurodegenerative processes such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and other age-related cognitive disorders. Within this framework, prolonged activation of inflammatory pathways can trigger regulated forms of cell death. Among these, necroptosis has recently emerged as a potential mediator linking inflammaging to neurodegeneration. Its core molecular effectors, including the receptor-interacting protein kinases RIPK1 and RIPK3 and the mixed-lineage kinase domain-like protein (MLKL), are increasingly expressed in aged neural tissues, promoting the release of damage-associated molecular patterns (DAMPs) that amplify glial activation, oxidative stress, and blood-brain barrier disruption. Growing evidence suggests that necroptotic signaling may be upregulated in the aging brain and in neurodegenerative disorders, where it could contribute to neuronal loss and cognitive impairment. This review discusses the potential role of necroptosis in the continuum between inflammation and neurodegeneration, highlighting emerging diagnostic and therapeutic perspectives. Epigenetic and circulating biomarkers, such as phosphorylated MLKL and specific microRNAs, may support early detection, while pharmacological and nutraceutical strategies targeting necroptosis show promising neuroprotective effects in preclinical studies.

Cryptococcosis, an opportunistic fungal infection predominantly caused by Cryptococcus neoformans, is the third most common invasive fungal disease in solid organ transplant recipients. While well-characterized in adult kidney transplant (KT) patients, pediatric data remain sparse. This article compares clinical presentation, immune response, renal involvement, and management strategies of cryptococcosis between adult and pediatric KT recipients. In adults, the disease typically presents as cryptococcal meningitis or pulmonary infection, often complicated by delayed diagnosis and high mortality. In contrast, children frequently exhibit non-specific respiratory symptoms or disseminated disease, reflecting immune immaturity and increased susceptibility to hematogenous spread. Key immunopathological differences include impaired Th1 type responses, macrophage dysfunction, and variable complement activity across age groups. Management involves similar antifungal regimens such as liposomal amphotericin B, flucytosine, and fluconazole, but requires weight-based dosing and careful toxicity monitoring in pediatric patients. Early diagnosis through serum cryptococcal antigen screening, appropriate adjustment of immunosuppressive therapy, and coordinated multidisciplinary care are essential. The findings underscore the need for pediatric specific research and clinical vigilance, emphasizing tailored antifungal dosing and individualized immune management to improve outcomes in this vulnerable population.

West Nile Virus (WNV) is becoming a significant and enduring public health menace in Europe, propelled by climate changes and accelerated population aging. Most infections are asymptomatic but older adults are more prone to develop neuroinvasive disease, which is characterized by high morbidity and mortality, as well as long-term neurological disturbances and disability. To date, there is still no licensed human vaccine or specific antiviral treatment, and management is mostly supportive. This review brings together the most recent information about WNV epidemiology, pathogenesis, and clinical manifestations, with a special focus on older people in Europe. We critically analyze current and novel pharmaceutical strategies, encompassing drug repurposing, nucleoside analogues, interferon-based therapies, peptides, monoclonal antibodies, and host-directed agents, emphasizing their therapeutic potential alongside the challenges presented by age-related pharmacokinetic and immunological alterations. We also discuss some important gaps in the current evidence base, such as the frequent exclusion of older adults from clinical studies and the lack of a coordinated clinical trial infrastructure that can be quickly activated during seasonal outbreaks. Lastly, we suggest a framework that combines systematic antiviral screening with the creation of a Europe-wide network of clinical trial readiness that is built into current One Health surveillance systems.