Introduction: Chronic inflammation plays a significant role in cardiovascular disease (CVD)–related mortality among patients with chronic kidney disease (CKD). The neutrophil‑to‑albumin percentage ratio (NPAR) has emerged as an indicator of an individual’s inflammatory status. This study aimed to investigate the association between elevated NPAR and the risk of CVD mortality in patients with CKD. Materials and Methods: The study was conducted in accordance with the PRISMA reporting guidelines. Comprehensive searches were performed across the Cochrane Library, Scopus, Web of Science, Embase, and PubMed databases, as well as the Google Scholar search engine, up to 30 January 2026. All statistical analyses were carried out using STATA version 14. Results: Compared with lower NPAR values, elevated NPAR was associated with a higher risk of cardiovascular mortality (OR = 1.54; 95% CI: 1.33–1.78) and all‑cause mortality (OR = 1.62; 95% CI: 1.40–1.89) in patients with CKD. In addition, higher NPAR increased the risk of CVD‑related death among patients undergoing hemodialysis (OR = 1.66; 95% CI: 1.29–2.15) and peritoneal dialysis (OR = 1.56; 95% CI: 1.25–1.94). Furthermore, the third quartile of NPAR (OR = 1.44; 95% CI: 1.16–1.78), the fourth quartile (OR = 1.92; 95% CI: 1.61–2.30), the second tertile (OR = 1.38; 95% CI: 1.07–1.80), and the third tertile (OR = 1.97; 95% CI: 1.61–2.41) were all associated with increased CVD mortality compared with the lowest category. Elevated NPAR also increased the risk of CVD‑related mortality in both men (OR = 1.23; 95% CI: 1.04–1.45) and women (OR = 1.16; 95% CI: 1.08–1.24) with CKD. Conclusion: Higher NPAR levels were associated with an increased likelihood of cardiovascular and all‑cause mortality among individuals with CKD. As NPAR values rose, the risk of CVD‑related death increased correspondingly when compared with lower levels. In addition, cardiovascular mortality risk was greater in men than in women, and higher among patients receiving hemodialysis than those undergoing peritoneal dialysis. Registration: This study has been compiled based on the PRISMA checklist, and its protocol was registered on the PROSPERO (ID: CRD420261304086) and Research Registry (UIN: reviewregistry2082) websites.
Dental implant therapy in dialysis-dependent chronic kidney disease (CKD) patients presents significant osseointegration challenges due to systemic metabolic disturbances inherent to end-stage renal disease. Renal osteodystrophy, characterized by abnormal bone turnover, mineralization defects, and secondary hyperparathyroidism, critically compromises alveolar bone quality and remodeling capacity essential for implant stability. Elevated parathyroid hormone levels induce excessive bone resorption, while hyperphosphatemia and hypocalcemia disrupt hydroxyapatite crystallization, impairing the bone-implant interface formation. Uremic toxins accumulate despite dialysis, inducing chronic inflammation and oxidative stress that suppress osteoblast activity and angiogenesis while promoting osteoclastogenesis. Additionally, frequent comorbidities, including diabetes, hypertension, and anemia further compromise microcirculation and tissue healing. Anticoagulant use during hemodialysis increases perioperative bleeding risks, potentially disrupting early clot formation and cellular migration at the surgical site. Although dental implants remain a viable rehabilitation option for edentulous CKD patients, success rates are generally lower compared to healthy populations, with higher incidences of marginal bone loss and late failures. Careful patient selection, optimized dialysis timing around surgery, stringent control of calcium-phosphate products and parathyroid hormone levels, and also extended healing periods are recommended clinical strategies. Limited long-term prospective studies specifically addressing implant outcomes in this population highlight an evidence gap requiring further investigation. Multidisciplinary coordination between nephrologists and implantologists is essential to mitigate risks. Though not an absolute contraindication, implant placement in dialysis-dependent patients demands thorough preoperative assessment of bone metabolism markers, individualized surgical protocols, and realistic patient counseling regarding potentially prolonged osseointegration timelines and guarded long-term prognosis compared to non-renal compromised individuals.
Artificial intelligence (AI) is rapidly transforming the field of nephrology by enhancing the diagnosis, prognosis, and management of kidney diseases through advanced data-driven techniques. AI-driven medical image analysis using deep learning and radiomics enables early detection of structural abnormalities in chronic kidney disease (CKD) and diabetic kidney disease (DKD), improving diagnostic accuracy and enabling standardized interpretation of ultrasound, computed tomography (CT), and magnetic resonance imaging (MRI). Machine learning (ML)models that integrate clinical, laboratory, and genetic data surpass traditional risk equations in predicting CKD progression, dialysis initiation, and mortality, facilitating personalized monitoring and intervention. In renal pathology, AI-powered digital pathology tools automate lesion detection, quantification, and classification from biopsy specimens, offering objective metrics that correlate with clinical outcomes. Within kidney transplantation, AI refines donor–recipient matching, predicts acute rejection and graft survival, and augments biopsy interpretation to optimize use of scarce donor organs. AI-enabled decision support systems and real-time monitoring algorithms in dialysis and continuous kidney replacement therapy personalize treatment parameters, enhance symptom control, and predict complications. Despite these advances, challenges related to data bias, model interpretability, ethical considerations, and clinical integration must be addressed. Prospects include the integration of multi-omics data, federated learning to protect patient privacy, explainable AI models for transparent decision-making, and telemedicine applications to extend nephrology expertise globally. Continued interdisciplinary collaboration and rigorous clinical validation will be essential to fully harness AI’s potential and usher in an era of precision nephrology.
Brain metastasis (BM) from renal cell carcinoma (RCC) represent a significant clinical challenge, associated with high morbidity and poor prognosis. The advent of targeted therapies and immune checkpoint inhibitors (ICIs) has transformed the management of metastatic RCC (mRCC), yet patients with brain metastasis remain underrepresented in clinical trials, and optimal management strategies are still evolving. The findings indicated that brain metastasis occur in approximately 5–15% of patients with mRCC, with clear cell histology and the presence of extracranial metastases as key risk factors. The pathophysiology involves complex molecular mechanisms, including hematogenous dissemination and genetic alterations. Clinical presentation is often symptomatic, with headaches, focal deficits, and seizures, but a substantial proportion of cases are detected incidentally. Magnetic resonance imaging (MRI) remains the gold standard for diagnosis, though screening is typically reserved for symptomatic or high-risk patients. Treatment is multimodal: surgery and stereotactic radiosurgery (SRS) are mainstays for local control, while systemic therapies, particularly cabozantinib and ICI-based regimens, have shown promising intracranial activity. Prognosis remains guarded, with median survival after BM diagnosis ranging from 10 to 18 months, but outcomes have improved in the ICI era. In conclusion, the management of RCC brain metastases requires a multidisciplinary, individualized approach. Advances in systemic and local therapies have improved survival, but significant challenges remain, including the risk of intracranial hemorrhage and the need for better screening and surveillance strategies. Ongoing research into molecular mechanisms and novel therapeutics holds promise for further progress in this high-risk population.
Malignancy-associated hypercalcemia represents a severe metabolic complication frequently observed in advanced renal cell carcinoma (RCC), often precipitating acute kidney injury (AKT) and limiting therapeutic options. Though systemic volume depletion and renal vasoconstriction contribute to renal disturbance, direct tubular toxicity mediated by intrinsic mitochondrial dysfunction remains underexplored. This review discusses on mechanistic framework linking excessive extracellular calcium load to renal tubular epithelial failure. Hypercalcemia induces profound intracellular calcium overload within proximal tubular cells, triggering mitochondrial calcium uniporter activation. Consequently, mitochondrial membrane potential collapses due to permeability transition pore opening, effectively uncoupling oxidative phosphorylation. This bioenergetic crisis generates excessive reactive oxygen species (ROS), promoting lipid peroxidation, protein oxidation and DNA damage. Simultaneously, cytochrome c release initiates apoptotic cascades, whereas severe ATP depletion triggers necrotic cell death. The resulting tubular obstruction, cast formation, and inflammation exacerbate glomerular filtration rate loss. Furthermore, tumor-derived factors like parathyroid hormone-related protein (PTHrP) may sensitize mitochondria to calcium-induced stress, amplifying injury. Dysregulated mitochondrial dynamics, including fission and fusion imbalance, further compromise cellular resilience against calcium stress. Identification this pathway highlights mitochondria as critical therapeutic targets beyond standard hydration and bisphosphonates. Interventions stabilizing mitochondrial integrity, modulating calcium handling, or scavenging ROS could mitigate tubular injury. Eventually, deciphering these molecular events offers novel strategies to preserve renal function in patients with advanced renal cancer suffering from hypercalcemic crises. Such approaches may significantly improve survival outcomes and enable continued systemic therapy, addressing a critical unmet need in oncology nephrology where renal preservation dictates treatment eligibility and quality of life during palliative care.
