Search Results (4,442)

Polygonatum cyrtonema Hua, a plant with a long history of consumption in China, serves both medicinal and edible purposes, and it exhibits numerous pharmacological effects, including promoting kidney health and enhancing immune function. However, the effect and molecular mechanism of Polygonatum cyrtonema polysaccharides (PCPs) on hyperuricemia have not yet been reported. The hyperuricemic mice model was induced by the intraperitoneal injection of potassium oxonate (PO, 300 mg/kg), combined with the intragastric administration of hypoxanthine (HX, 300 mg/kg). Biochemical assays in mice revealed that PCPs markedly lowered high serum uric acid levels, suppressed xanthine oxidase (XOD) activity, and reduced the expression of inflammatory cytokines, including interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α). Western blot analysis demonstrated that PCPs downregulated urate transporter 1 (URAT1), while H&E staining showed that PCPs effectively restored renal histological integrity. Here, we isolated and identified the PCPs, which consist mainly of rhamnose, glucuronic acid, galacturonic acid, glucose, galactose, and arabinose, with a molar mass ratio of 0.5:2.15:0.47:16.58:3.66:1.09. Furthermore, the galactose residue that docked with both XOD and URAT1 molecules forms more hydrogen bonds and exhibits a lower binding energy, which enables the improved regulation of both targets. We have demonstrated for the first time the improving effect of PCPs on hyperuricemia, and revealed their regulatory mechanisms by modulating xanthine oxidase, inflammatory factors, and uric acid transporters. This study not only provides new insights into the anti-hyperuricemic activity of PCPs in mice, but also lays a foundation for its potential application in the functional foods of anti-hyperuricemia. Full article

Vitamin D, long recognized for its essential role in calcium–phosphate balance and bone health, has increasingly been identified as a pleiotropic regulator of metabolic, cardiovascular, and renal function. Deficiency of vitamin D is widespread worldwide and has been linked to a higher risk of insulin resistance, type 2 diabetes, atherosclerosis, hypertension, and chronic kidney disease. Meta-analyses suggest that each 10 nmol/L (≈4 ng/mL) increase in serum 25-hydroxyvitamin D [25(OH)D] is associated with about a 4% lower risk of type 2 diabetes, whereas other analyses indicate an approximately 10% reduction in cardiovascular event risk per 10 ng/mL (≈25 nmol/L) increment in circulating 25(OH)D concentration. Clinical and epidemiological studies suggest that optimal 25(OH)D concentrations may protect against cardiometabolic and renal complications, though supplementation trials show heterogeneous outcomes depending on baseline vitamin D status, genetic background, and dosage. By synthesizing current knowledge, this work highlights vitamin D status as a potentially modifiable determinant of global disease burden and a target for preventive and therapeutic strategies. Full article

Living kidney transplantation offers the best results for end-stage renal disease patients, but concerns about cardiovascular risk after nephrectomy for kidney donors have been raised. We aimed to estimate the contribution of renal function to endothelial dysfunction (ED) and subclinical inflammation in a non-interventional, prospective, multicenter, longitudinal study with two cohorts: living kidney donors and their transplant recipients (registered clinical trial NCT02515643). The measured glomerular filtration rate (mGFR) by iohexol clearance, estimated GFR according to the CKD-EPI and MDRD-4 formulas, and levels of endothelial dysfunction (sVCAM-1, sICAM-1, E-selectin, von Willebrand Factor, pentraxin, and urinary albumin-to-creatinine ratio) and subclinical inflammation biomarkers (sIL-6, sTNF-R1, sTNF-R2, sTWEAK, and high-sensitivity C-reactive protein) were determined at baseline and 1-year follow-up. Fifty pairs of donors and recipients were recruited between 2015 and 2018. Among the endothelial dysfunction biomarkers, sVCAM-1 increased in donors and decreased in recipients (p < 0.01) while, among the inflammation biomarkers, sTNFR1 and sTNFR2 significantly increased in donors and decreased in recipients (p < 0.001). After transplantation, parallel increases and decreases in ED and subclinical inflammation biomarkers were observed in the donor and recipient cohorts, respectively. Long-term follow-up is needed to characterize the cardiovascular risk associated with these changes. Full article

Grass carp (Ctenopharyngodon idella), a key species in freshwater aquaculture, is particularly vulnerable to opportunistic pathogens, including Aeromonas hydrophila and Aeromonas veronii. While the pathogenic mechanisms of individual infections have been extensively characterized, the host immune responses during co-infection remain poorly understood. This research explored the renal pathological alterations and transcriptomic shifts in grass carp subjected to simultaneous infection by A. hydrophila and A. veronii. Mortality occurred as early as 24 h post-challenge, ultimately reaching a cumulative death rate of 65%. Quantitative analysis of renal bacterial burden revealed a marked increase in colonization at 3 days post-infection (dpi). The histopathological assessment showed progressive kidney damage, including tubular collapse, epithelial necrosis, interstitial edema, and widespread epithelial desquamation, with the most severe lesions observed at 5 dpi and partial signs of recovery by 7 dpi. A total of 1106 and 472 genes were found to be differentially expressed at 1 and 5 dpi, respectively, based on transcriptome profiling. The functional enrichment analysis indicated that the differentially expressed genes (DEGs) were mainly involved in the complement and coagulation cascade pathways. Notably, the immune-related genes exhibited a biphasic trend, with predominant downregulation at 1 dpi followed by marked upregulation by 5 dpi, indicating dynamic changes in immune modulation during co-infection. These results provide new insights into host responses during dual bacterial infections in fish and may inform disease prevention strategies in aquaculture. Full article

Hypophosphatemia, defined as serum phosphate levels below 2.5 mg/dL, is a common yet underrecognized electrolyte disturbance in critically ill patients, with prevalence estimates reaching up to 80%. This review explores the intricate bidirectional relationship between hypophosphatemia and hyperventilation, emphasizing its profound implications for respiratory function and critical care management. Hypophosphatemia impairs oxygen delivery by depleting 2,3-diphosphoglycerate (2,3-DPG), disrupts central respiratory drive, and weakens respiratory muscles, leading to hyperventilation, ventilatory failure, and prolonged mechanical ventilation. Conversely, hyperventilation exacerbates hypophosphatemia through respiratory alkalosis, triggering intracellular phosphate shifts and metabolic cascades that rapidly deplete serum levels. This cycle creates significant challenges for ventilator weaning and increases morbidity and mortality. Underlying mechanisms include impaired ATP synthesis, altered chemoreceptor sensitivity, and systemic inflammatory responses. Hypophosphatemia-induced hyperventilation manifests as unexplained tachypnea and respiratory alkalosis, often misdiagnosed as anxiety or pain, while hyperventilation-induced hypophosphatemia contributes to diaphragmatic dysfunction and poor ventilatory performance. Common precipitating factors include refeeding syndrome, diabetic ketoacidosis, continuous renal replacement therapy, and malnutrition. Complications extend beyond respiratory dysfunction to include cardiac depression, immune dysfunction, prolonged ICU stays, and increased healthcare costs. Current diagnostic approaches rely on serum phosphate measurements, which poorly reflect total body stores due to significant intracellular shifts. Emerging biomarkers such as fibroblast growth factor 23 (FGF23) and advanced monitoring technologies, including continuous phosphate tracking, may enhance recognition. Treatment strategies emphasize targeted phosphate repletion based on severity, with intravenous supplementation and ventilatory support tailored to minimize complications. Preventive measures, including risk stratification, prophylactic supplementation, and ventilator management, are critical for high-risk populations. Despite advances, knowledge gaps persist in optimizing monitoring and repletion protocols, understanding genetic variations, and identifying ideal phosphate targets for improved respiratory outcomes. This review provides a comprehensive framework for recognizing and managing hypophosphatemia’s impact on respiratory dysfunction in critically ill patients. Adopting evidence-based interventions and leveraging emerging technologies can significantly improve clinical outcomes, reduce ICU complications, and enhance recovery in this vulnerable population. Full article

Background: Alpiniae oxyphyllae-Saposhnikovia divaricata (AS), a traditional Chinese dietary supplement, exhibits potential therapeutic effects against diabetic kidney disease (DKD), though its active compounds and mechanisms require elucidation. Methods: Animal experiments integrated with UHPLC-QE-MS, bioinformatics, and experimental validation were employed to investigate AS’s pharmacodynamic basis against DKD. Results: Thirty-nine compounds were identified in AS, including four key flavonoids (daidzein, kaempferol, tectoridin, baicalin). Bioinformatics screening revealed 516 potential AS targets from PubChem/TCMSP/ETCM databases. Analysis of the GEO dataset (GSE30529) identified 482 DKD-related differentially expressed genes (DEGs). Venny 2.1 analysis yielded 42 co-DEGs and 6 co-core DEGs. Functional enrichment (GO/KEGG/GSEA) demonstrated AS’s modulation of apoptosis and extracellular matrix (ECM) pathways via these DEGs. ROC profiling and renal single-cell sequencing highlighted FOS as a specific regulator of podocyte apoptosis in DKD. Molecular docking confirmed stable binding between the four flavonoids and FOS. Experimentally, AS significantly suppressed expression of ECM-related proteins (Col-IV, LN, IL-6, IL-17) and pro-apoptotic proteins (Bax, Caspase-3), while restoring anti-apoptotic Bcl-2 levels and inhibiting phosphorylation of MEK4, JNK1, c-Jun, and FOS in DKD mice. Conclusion: This study elucidates that AS alleviates DKD by inhibiting the MAPK/FOS pathway, thereby attenuating podocyte apoptosis and ECM accumulation. These findings establish a foundation for targeted AS therapy in DKD. Full article

Medicinal plants remain central to traditional healthcare, yet their increasing integration into modern pharmacology necessitates robust toxicological evaluation. Origanum majorana L. (sweet marjoram), widely used in culinary and folk medicine, contains diverse secondary metabolites with both therapeutic and potential genotoxic activities. Despite its popularity, systematic in vivo and in vitro safety assessments remain limited. This study aimed to comprehensively evaluate the acute oral toxicity, cytotoxicity, and genotoxicity of O. majorana methanolic extract, providing baseline toxicological data to support its safe traditional use and potential pharmaceutical applications. The methanol extract of O. majorana leaves was tested in NIH-3T3 fibroblasts for cytotoxicity and genotoxicity. In vivo acute oral toxicity was assessed in rats according to OECD Guideline 420, with animals monitored over 14 days for clinical signs, hematological and biochemical alterations, and histopathological changes. The extract preserved fibroblast viability above 90% across all tested concentrations (10–200 µg/mL), indicating absence of cytotoxicity. However, comet and micronucleus assays revealed dose-dependent DNA damage, suggesting genotoxic potential at higher exposures. In vivo, no mortality or overt systemic toxicity was observed at doses up to 2000 mg/kg. Hematological analyses showed immunomodulatory shifts (increased neutrophils and monocytes, reduced eosinophils), while biochemical profiles indicated hepatoprotective and cardioprotective effects, with reduced ALT, AST, and LDH levels. Histopathological evaluation revealed only mild, focal changes consistent with adaptive rather than irreversible responses. O. majorana extract demonstrates a favorable acute safety profile with preserved hepatic and renal function, hematological modulation, and absence of in vitro cytotoxicity. Nevertheless, dose-dependent genotoxicity warrants caution for concentrated formulations. According to GHS classification, the extract aligns with Category 5 (acute oral toxicity, lowest hazard) and Category 2 (germ cell mutagenicity). These findings underscore the importance of dose management and further long-term genotoxicity studies before translational applications in nutraceutical or biomedical fields. Full article

Background/Objectives: Chronic kidney disease (CKD) progression is strongly influenced by systemic inflammation. The neutrophil-to-lymphocyte ratio (NLR), derived from routine blood counts, reflects the balance between innate and adaptive immunity and has been proposed as a marker of adverse renal outcomes. We hypothesized that elevated baseline NLR is associated with reduced kidney function and increased risk of progression to end-stage kidney disease (ESKD) in adults with non-dialysis CKD. Methods: Following PRISMA guidelines, we systematically searched MEDLINE, Embase, and Scopus for studies enrolling adults with CKD stages 1–4 that reported renal outcomes according to baseline NLR. The primary outcome was progression to ESKD or renal replacement therapy (RRT) initiation. Results: Six eligible studies were identified, of which four provided sufficient data for meta-analysis. Across cohorts, elevated baseline NLR was consistently associated with adverse renal outcomes. In pooled analyses, high NLR nearly doubled the risk of ESKD or RRT (RR 1.96, 95% CI 1.30–2.97). Leave-one-out sensitivity analysis strengthened the association while reducing heterogeneity. For kidney function, higher NLR was associated with lower baseline eGFR (SMD −1.59, 95% CI −2.38 to −0.80). Conclusions: Elevated NLR is a robust prognostic marker of renal function decline and progression to ESKD or RRT in non-dialysis CKD. As a simple and inexpensive biomarker, NLR offers additional predictive value beyond eGFR and albuminuria. Incorporating NLR into risk models may refine stratification, guide follow-up, and enable earlier therapeutic optimization. Prospective large studies are warranted to establish thresholds and validate its role in clinical practice. Full article

Background/Objective: Malnutrition and sarcopenia are common complications after ischemic stroke and have a negative impact on prognosis. The C-reactive protein/albumin ratio (CAR) reflects both inflammation and nutritional status, but its predictive role in this setting has not been widely studied. This study aimed to investigate the predictive value of CAR (C-reactive protein/albumin ratio) for malnutrition risk and probable sarcopenia in patients with ischemic stroke. Methods: In this prospective observational study, 197 patients with acute ischemic stroke were evaluated. Patients with chronic renal or hepatic failure, malignancy, active infection, and hand disability preventing grip strength measurement were excluded. Demographic data (age, sex), vascular risk factors, the NIHSS score, and laboratory parameters were recorded. The nutritional status of patients was assessed using the Nutritional Risk Screening-2002 (NRS-2002), and sarcopenia risk was evaluated with the SARC-F questionnaire. Handgrip strength was measured in patients with high SARC-F scores to define probable sarcopenia. CAR was calculated from serum CRP and albumin levels. Logistic regression was applied to identify independent predictors, and receiver operating characteristic (ROC) analyses were performed to determine the discriminatory ability and cut-off values of CAR. The nutritional status of patients admitted to the neurology clinic with acute ischemic stroke was assessed using the Nutritional Risk Screening-2002 (NRS-2002), and sarcopenia risk was evaluated with the SARC-F questionnaire. Handgrip strength was measured in patients with high SARC-F scores to define probable sarcopenia. CAR was calculated from serum CRP and albumin levels. Logistic regression and receiver operating characteristic (ROC) analyses were performed. Results: Malnutrition risk was identified in 32.5% of patients, and probable sarcopenia was identified in 19.3% of patients. ROC analysis showed that CAR had acceptable discriminatory power for both conditions. In multivariate analysis, CAR was consistently identified as an independent predictor of malnutrition risk and possible sarcopenia. ROC analysis for malnutrition risk showed an AUC of 0.750 (cut-off: 0.306; sensitivity 68.8%; specificity 75.2%). In regression analysis, CAR (OR = 2.13; 95% CI: 1.39–3.26; p < 0.001), age (OR = 1.05; 95% CI: 1.02–1.09; p = 0.003), and NIHSS (OR = 1.11; 95% CI: 1.01–1.23; p = 0.026) were independent predictors. For probable sarcopenia, ROC analysis revealed an AUC of 0.814 (cut-off: 0.320; sensitivity 81.6%; specificity 71.7%). Multivariate analysis identified CAR (OR = 1.73; 95% CI: 1.19–2.52; p = 0.004), age (OR = 1.11; 95% CI: 1.05–1.18; p < 0.001), and NIHSS (OR = 1.19; 95% CI: 1.05–1.35; p = 0.007) as independent predictors. Conclusions: CAR was identified as an independent predictor of both malnutrition risk and probable sarcopenia in ischemic stroke patients. CAR may serve as a reliable biomarker for early nutritional and functional risk stratification in clinical practice. Full article

Neuromuscular diseases (NMDs) like Duchenne muscular dystrophy (DMD), limb–girdle muscular dystrophy (LGMD), and amyotrophic lateral sclerosis (ALS) are rare, progressive disorders with complex molecular mechanisms. Traditional transcriptomic analyses often struggle to capture systems-level dysregulation, especially given the small sample sizes typical of rare disease studies. Our differential expression analysis of eight public RNA-seq datasets from various cell types in DMD, LGMD, and ALS revealed not only disease-relevant pathways but also unexpected enrichments, such as renal development, suggesting systemic impacts beyond muscle tissue. To address limitations in capturing broader molecular mechanisms, we applied an integrative systems biology approach combining differential expression data, protein–protein interaction (PPI) networks, and network embedding techniques. Comparative functional enrichment revealed shared pathways, including glycosaminoglycan binding in both DMD and FUS-related ALS, implicating extracellular matrix–protein interactions in FUS mutation effects. Mapping DEGs onto the human PPI network and assessing their proximity to causal genes uncovered dysregulated non-coding RNAs, such as PAX8-AS1, SBF2-AS1, and NEAT1, potentially indicating common regulatory roles. We also found candidate genes within disease-proximal clusters, like HS3ST3A1, which may contribute to pathogenesis. Overall, this integrative approach reveals shared transcriptional programs and novel targets, advancing our understanding and potential treatment strategies for NMDs. Full article

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has impacted global health. Remdesivir was approved based on clinical trials demonstrating improved outcomes in hospitalized patients. The ReEs-COVID19 study provides real-world evidence on its effectiveness and safety across two periods: Pre-Omicron and Omicron. This retrospective, observational cohort study included 1610 patients hospitalized with COVID-19, treated with remdesivir during Pre-Omicron (September 2020–February 2021; n = 606) and Omicron (June 2022–March 2023; n = 1004) periods. Primary endpoint: time to discharge; Hepatic/renal function abnormalities were also investigated. In the Omicron period patients were older and had more comorbidities but remdesivir was initiated earlier (median: 2 days from symptom onset) compared to the Pre-Omicron period (8 days). ICU admissions rates and direct COVID-19-related deaths were significantly lower, but overall 30-day mortality was higher during the Omicron period. Earlier remdesivir administration was associated with faster discharge. Abnormal liver tests and acute kidney injury were rare across both periods. ReEs-COVID19 confirmed remdesivir’s effectiveness and safety in real-world clinical settings during both periods, underscoring its importance in treatment of hospitalized COVID-19 patients, especially when initiated earlier in the disease course. Further research is needed to evaluate its utility in specific subgroups (e.g., immuno-compromised) and in combination with other treatments. Full article

Hemodialysis is the most commonly used renal replacement therapy worldwide, and arteriovenous fistulas (AVFs) are the preferred vascular access. The functional patency of AVFs directly determines the dialysis efficiency and quality of life of patients with end-stage renal disease (ESRD). However, in clinical practice, the failure of AVFs seriously affects the treatment prognosis of these patients. Vascular smooth muscle cells (VSMCs), as the main component of the vascular media, not only maintain the integrity and tension of the vascular wall under physiological conditions but also play a crucial role in the failure of AVF maturation and post-maturation dysfunction. VSMCs undergo metabolic reprogramming along with adaptive structural and functional alterations, driven by persistent stimulation from hyperphosphatemia, uremic toxins, oxidative stress, and inflammatory factors, as well as hemodynamic disturbances induced by AVF creation and surgical trauma. This review summarizes the roles of VSMC metabolic and phenotypic shifts in outward remodeling, inward remodeling, and medial calcification during AVF failure, elaborates on the metabolic crosstalk between VSMCs and endothelial cells, and discusses potential therapeutic targets targeting VSMC metabolism. Full article

Acute kidney injury (AKI) is a frequent and severe complication in trauma patients, affecting up to 28% of intensive care unit (ICU) admissions and contributing significantly to morbidity, mortality, and long-term renal impairment. Trauma-related AKI (TRAKI) arises from diverse mechanisms, including hemorrhagic shock, ischemia–reperfusion injury, systemic inflammation, rhabdomyolysis, nephrotoxicity, and complex organ crosstalk involving the brain, lungs, and abdomen. Pathophysiologically, TRAKI involves early disruption of the glomerular filtration barrier, tubular epithelial injury, and renal microvascular dysfunction. Inflammatory cascades, oxidative stress, immune thrombosis, and maladaptive repair mechanisms mediate these injuries. Trauma-related rhabdomyolysis and exposure to contrast agents or nephrotoxic drugs further exacerbate renal stress, particularly in patients with pre-existing comorbidities. Traditional markers such as serum creatinine (sCr) are late indicators of kidney damage and lack specificity. Emerging structural and stress response biomarkers—such as neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule 1 (KIM-1), liver-type fatty acid-binding protein (L-FABP), interleukin-18 (IL-18), C-C motif chemokine ligand 14 (CCL14), Dickkopf-3 (DKK3), and the U.S. Food and Drug Administration (FDA)-approved tissue inhibitor of metalloproteinases-2 × insulin-like growth factor-binding protein 7 (TIMP-2 × IGFBP-7)—allow earlier detection of subclinical AKI and better predict progression and the need for renal replacement therapy. Together, functional indices like urinary sodium and fractional potassium excretion reflect early microcirculatory stress and add clinical value. In parallel, risk stratification tools, including the Renal Angina Index (RAI), the McMahon score, and the Haines model, enable the early identification of high-risk patients and help tailor nephroprotective strategies. Together, these biomarkers and risk models shift from passive AKI recognition to proactive, personalized management. A new paradigm that integrates biomarker-guided diagnostics and dynamic clinical scoring into trauma care promises to reduce AKI burden and improve renal outcomes in this critically ill population. Full article

Chronic kidney disease (CKD) poses a global burden affecting over 10% of the adult population worldwide. Acute kidney injury (AKI) is an important cause of CKD, especially following severe and repeated episodes. However, the processes underpinning progressive and chronic renal deterioration after AKI are only incompletely understood. Thus, models reproducing this scenario are needed to study the pathophysiological mechanisms involved and identify biomarkers and molecular targets for diagnostic and therapeutic purposes. In this study, we developed a rat model of 3 serial AKIs leading to CKD, in which renal function, kidney structure and fibrosis, and urinary injury biomarkers were studied over a period of 9 months, alongside a traditional model of CKD caused by renal mass reduction. Our results show that consecutive AKIs eventually develop key features of CKD including progressive fibrosis and albuminuria. Renal injury biomarkers neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule 1 (KIM-1), and retinol binding protein 4 (RBP4) show distinct evolution patterns suggestive of specific but undetermined damages with different time courses. The chronic evolution of renal tissue degeneration and dysfunction following serial AKIs closely resembles those observed after extensive renal mass reduction, which indicates chronic degeneration. Finally, a clear dissociation in the evolution of interstitial fibrosis (progressively increasing) and of glomerular filtration (mainly stable) was observed in both models. This questions the consuetudinary paradigm ascribing an etiological role to fibrosis in progressive renal dysfunction. Full article

Background and Objectives: Partial nephrectomy is the standard treatment for small renal tumors, balancing cancer control with renal function preservation. Robot-assisted partial nephrectomy (RAPN) has improved surgical precision and reduced morbidity. Near-infrared fluorescence (NIRF) imaging with indocyanine green (ICG) improves intraoperative visualization of renal vasculature and tissue perfusion, potentially enabling selective arterial clamping to reduce ischemic injury. This study updates contemporary evidence on NIRF/ICG-guided RAPN, focusing on intraoperative, perioperative, and renal function outcomes. Materials and Methods: We systematically queried PubMed, Scopus, and Web of Science databases up to June 2025 for controlled prospective and retrospective studies comparing NIRF/ICG-guided RAPN (selective clamping or zero-ischemia) versus conventional RAPN with main artery clamping in adults with renal masses. Data were synthesized narratively, and random-effects meta-analyses were performed on warm ischemia time (WIT), operative time, estimated blood loss, transfusion rate, length of hospital stay, complication rate, positive surgical margins, and variation in renal function. Results: Eleven studies (10 full-text and one abstract), including two randomized controlled trials, encompassing a patient population of 893 patients (403 NIRF/ICG-guided RAPN and 490 conventional RAPN), were included. Ischemia strategies varied between no clamping, selective or super-selective clamping for NIRF/ICG, and main artery clamping for controls. ICG doses ranging from 3 to 7.5 mg or 0.5–7 mL. Most evidence was classified as level 2b or 3b, indicating a moderate to serious risk of bias. Meta-analysis showed that compared to conventional RAPN, NIRF/ICG-guided RAPN was associated with a shorter WIT (MD: −1.30 min, 95% CI: −2.51 to −0.09; p = 0.039), with no differences in other outcomes. Renal function favored NIRF/ICG at discharge and short-term follow-up, although the difference was not statistically significant. Conclusions: NIRF/ICG reduces WIT during RAPN without increasing perioperative risks. The technique shows promise for better preserving functional outcomes. However, further well-designed, large-scale trials with longer follow-up are needed to confirm these benefits and define clinical indications. Full article