Background: COVID-19 is characterized by severe inflammation during the acute phase and increased aortic stiffness in the early postacute phase. In other models, aortic stiffness is improved after the reduction of inflammation. We aimed to evaluate the mid- and long-term effects of COVID-19 on vascular and cardiac autonomic function. The primary outcome was aortic pulse wave velocity (aPWV). Methods: The cross-sectional Study-1 included 90 individuals with a history of COVID-19 and 180 matched controls. The longitudinal Study-2 included 41 patients with COVID-19 randomly selected from Study-1 who were followed-up for 27 weeks. Results: Study-1: Compared with controls, patients with COVID-19 had higher aPWV and brachial PWV 12 to 24 (but not 25–48) weeks after COVID-19 onset, and they had higher carotid Young’s elastic modulus and lower distensibility 12 to 48 weeks after COVID-19 onset. In partial least squares structural equation modeling, the higher the hs-CRP (high-sensitivity C-reactive protein) at hospitalization was, the higher the aPWV 12 to 48 weeks from COVID-19 onset (path coefficient: 0.184; P =0.04). Moreover, aPWV (path coefficient: −0.186; P =0.003) decreased with time. Study-2: mean blood pressure and carotid intima-media thickness were comparable at the end of follow-up, whereas aPWV (−9%; P =0.01), incremental Young’s elastic modulus (−17%; P =0.03), baroreflex sensitivity (+28%; P =0.049), heart rate variability triangular index (+15%; P =0.01), and subendocardial viability ratio (+12%; P =0.01×10 ⁻⁴ ) were significantly improved. There was a trend toward improvement in brachial PWV (−6%; P =0.14) and carotid distensibility (+18%; P =0.05). Finally, at the end of follow-up (48 weeks after the onset of COVID-19) aPWV (+6%; P =0.04) remained significantly higher in patients with COVID-19 than in control subjects. Conclusions: COVID-19-related arterial stiffening involves several arterial tree portions and is partially resolved in the long-term.

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.

This articles reviews the pathophysiology of membranous nephropathy (MN), the mechanism of action of obinutuzumab, clinical data supporting its use and discusses its potential as a game changer in MN treatment.

Surgically created native arteriovenous fistulas (AVFs) remain the preferred vascular access for chronic hemodialysis, yet they are limited by substantial early failure and progressive consumption of venous capital. Endovascular arteriovenous fistulas (endoAVFs, also referred to as percutaneous AVFs) have become a catheter-based alternative to surgical AVF (sAVF). We conduct an updated narrative, practice-oriented review of the literature on endoAVF creation, and we qualitatively synthesize evidence. Two devices are currently available in contemporary clinical practice: a dual 4 Fr-catheter, fluoroscopy-guided radiofrequency system (WavelinQ) and a single 6 Fr-catheter, ultrasound-guided thermal resistance system (Ellipsys). Across prospective studies and real-world series, endoAVF creation is consistently reported to have high technical success, with low major complication and infection rates. Clinical usability can often be achieved within weeks when ultrasound-based surveillance and protocol-driven maturation assistance are implemented; however, adjunctive procedures are frequently required and should be anticipated in program planning and informed consent. Observational comparisons and pooled analyses indicate broadly comparable functional outcomes versus surgery in selected cohorts, while estimates of primary patency and maintenance burden vary substantially across studies. Overall, endoAVFs represent a feasible, minimally invasive, vessel-sparing option that can be integrated into multidisciplinary access pathways in anatomically suitable candidates and experienced centers, complementing rather than replacing surgical strategies within a distal-first plan. Recent society practice guidance further emphasizes standardized mapping, expectation setting, troubleshooting algorithms for non-maturation, and dialysis-unit cannulation training to support consistent implementation. Pragmatic comparative studies and long-term registries using standardized endpoints, paired with healthcare-system-specific economic analyses, are needed to better define durability, resource use, and patient-centered outcomes over the full-access life cycle.

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.

In this editorial, we comment on the article by Muñoz-Serrano et al published in the World Journal of Transplantation . Chronic kidney disease (CKD) is one of the most frequent and severe complications after liver transplantation (LT), threatening long-term survival beyond graft-related issues. Its pathogenesis is multifactorial, combining calcineurin inhibitor (CNI) nephrotoxicity with pre- and perioperative renal insults and metabolic comorbidities. We reviewed recent evidence from clinical trials, meta-analyses, and practice guidelines evaluating risk factors and management of CKD after LT, with a focus on immunosuppression strategies, perioperative care, and prognostic determinants. CKD develops in approximately 30% of LT recipients at 1 year and exceeds 40% at 5 years, with stage G3 predominating. Key predictors of post-LT CKD include high pre-LT creatinine [odds ratio (OR) = 7.74], early post-LT acute kidney injury (OR = 2.72), hypertension (OR = 4.833), and metabolic dysfunction-associated steatotic liver disease, including non-alcoholic steatohepatitis, as the underlying etiology. Tacrolimus remains superior to cyclosporine in overall survival and hypertension control, though hypomagnesemia and diabetogenicity are clinically relevant toxicities. CNI minimization - through basiliximab induction, low-dose tacrolimus with mycophenolate, or everolimus conversion - improves renal outcomes without compromising graft survival, despite trade-offs such as mild acute rejection or higher malignancy rates. CKD at 1 year confers a 4.48-fold increase in mortality risk, underscoring the prognostic weight of renal preservation. Renal protection after LT requires systematic preoperative risk stratification, perioperative CNI minimization, individualized immunosuppression, and aggressive metabolic management. Future integration of non-invasive biomarkers, including kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin, together with standardized simultaneous liver-kidney transplantation criteria, may further refine patient-tailored nephroprotection strategies. Muñoz-Serrano et al retrospectively analyzed 594 liver transplant recipients over three decades to identify risk factors for CKD at one year post-transplant. The authors identified older age, female sex, pre-transplant renal dysfunction, and treatment with cyclosporine A as independent risk factors.