Introduction: Systemic congestion and pulmonary congestion (PC) are common in hemodialysis (HD) patients. However, the relationship between these two entities is not quite clear. We study this relationship and attempt to uncover the factors that may affect it considering different inter-dialytic intervals.Methods: A prospective pilot observational and interventional study including 18 HD patients was conducted. The following were obtained: i) B-line score (BLS) by lung ultrasound (LUS) (reflecting significant pulmonary congestion if BLS > 5), ii) echocardiography, iii) bioelectrical impedance analysis (BIA) (reflecting global volume status), and iv) inferior vena cava (IVC) dynamics (reflecting systemic congestion) before and after the first two consecutive HD sessions of the week, with different inter-dialytic intervals (68 hours and 44 hours). Serum N-terminal pro-brain natriuretic peptide type B (NT-proBNP) levels were obtained before each session. Then, patients were randomized into two groups: the active group, where dry weight was reduced according to BLS + standard of care, and the control group, where dry weight was modified according to standard of care. All the measures were repeated on day 30.Results: We found no correlation between pulmonary congestion represented by BLS and IVC dimensions and dynamics reflecting systemic congestion, independent of different inter-dialytic intervals. Pulmonary congestion was quite prevalent, as mean pre- and post-dialysis BLSs were quite elevated (16 ± 5.53 and 15.3 ± 6.63, respectively) in the first session compared with the second session (16.3 ± 5.26 and 13.6 ± 5.83, respectively). Systolic (left ventricular ejection fraction) and diastolic cardiac function (e/è ratio) parameters from one side and pulmonary congestion (BLS) from the other were not always correlated. BLS was correlated to e/è ratio before HD (session 1) (R² = 0.476, p = 0.002) and after HD (session 2) (R² = 0.193, p = 0.034). Pulmonary congestion reflected by BLS was correlated to the global volume state reflected by BIA only in the second HD session (HD2) (R² = 0.374, p = 0.007). NT-proBNP levels and BLS were correlated before both sessions (R² = 0.421, p = 0.004, and R² = 0.505, p = 0.001, respectively). Systemic congestion was quite prevalent, as mean pre- and post-dialysis IVC dimensions and dynamics were quite elevated in both sessions, with a higher level of systemic congestion in the first HD session (diameter and collapsibility of 2.1 cm and 23%, and 2.01 cm and 19%, respectively) compared with the second session (1.98 cm and 17.5%, and 1.9 cm and 22%, respectively) without reaching statistical significance. IVC dimensions and global volume status measured by BIA were correlated in the second dialysis session (R² = 0.260, p = 0.031). No correlation was found between IVC dimensions and diastolic cardiac function (e/è ratio) parameters or with NT-proBNP levels. On day 30, BLS was significantly reduced in the active group, whereas no difference was found in the control group. However, no real impact was observed on IVC dimensions and dynamics or in total volume status by BIA.Conclusion: Pulmonary congestion is common in HD patients even after reaching their dry weight at the end of two consecutive sessions, and it is not correlated to systemic congestion, suggesting a complex multifactorial pathophysiology origin. Global volume status reflected by BIA and cardiac function are not always related to either systemic congestion represented by IVC dimensions or pulmonary congestion represented by BLS. Fluid redistribution anomalies may allow pulmonary congestion accumulation independently from systemic congestion and global volume status (non-cardiogenic pulmonary congestion). We recommend a personalised approach when managing HD patients by integrating systemic and pulmonary congestion parameters. Dry weight modification guided by repeat LUS may safely reduce pulmonary congestion. However, no impact was observed on systemic congestion or global volume status.

Background: Arteriovenous fistula (AVF) is the preferred vascular access option for hemodialysis (HD). The latter requires a remodeling process called maturation that can take up to 3 months. Maturation failure is a frequent complication associated with significant morbidity. The prevalence of antiphospholipid antibody (aPL) positivity in HD patients is high and may result in thrombosis of the vascular access. Recently, aPL persistent positivity has been associated with AVF maturation failure in a retrospective study including 116 patients. Methods: We are conducting an observational prospective cohort study aiming to evaluate this association. Included patients are planned for AVF creation, aged over 18 years old, and have an interpretable aPL assay confirmed at 12 weeks and without any other innate or acquired thrombophilia or inflammatory disease. Primary endpoints will be the evaluation of AVF maturation clinically and by ultrasound. Secondary endpoints will focus on clinical outcomes other than AVF maturation (i.e., primary patency, thrombosis or stenosis, bleeding and hemodialysis adequacy parameters). Conclusions: This prospective observational cohort study aims to examine the possibly causative link between aPL persistent positivity and AVF maturation failure. This study was registered on ClinicalTrials.gov (ID number: NCT06112821).

Introduction: Uremic toxins have been shown to cause adverse pulmonary effects by inducing endothelial and epithelial dysfunction, disrupting the alveolar-capillary barrier, and increasing inflammation and oxidative stress. This article reviews these effects with a specific focus on chronic kidney disease and the mechanisms by which uremic toxins affect lung tissue. Methods: A narrative review was conducted using keywords related to uremic toxins and lung injury to search the PubMed database. An advanced literature review was conducted in PubMed to identify studies explaining the mechanisms underlying lung pathophysiology in chronic kidney disease (CKD), with particular focus on CKD-induced pulmonary epithelial and endothelial dysfunction. Additionally, to highlight the pathological processes of lung congestion in CKD, studies on CKD-induced dysfunction of the alveolar-capillary barrier were retrieved. Studies published up to November 2025 were evaluated. Results: A total of 148 articles were reviewed in full text. Uremic toxins negatively impact lung tissue structure and function through multiple mechanisms, including oxidative stress, inflammation, and direct effects. Uremic toxins appear to share signaling pathways in endothelial cells, including those linked to Mitogen-activated protein kinases (MAPK), the Aryl Hydrocarbon Receptor (AhR), the receptor for advanced glycation end products (RAGE), and pro-inflammatory transcription factors such as nuclear factor κB (NF-κB). Additionally, oxidative stress acts as a pro-inflammatory signal shared by several uremic toxins. The mechanisms behind the harmful interactions between CKD and lung disease are mostly unknown, although more evidence exists for acute kidney injury (AKI). Conclusions: Chronic kidney disease, which leads to the buildup of uremic toxins, negatively affects the lungs. Overall, the accumulation of uremic toxins in CKD impairs endothelial and epithelial cells and the alveolar capillary barrier. Further research is needed to understand the specific mechanisms underlying these effects and to identify therapeutic options to protect the lungs in these patients.

Background: Kidney involvement is frequent in antineutrophil cytoplasmic antibody-associated vasculitis (AAV), with a proportion of 70% in granulomatosis with polyangiitis (GPA) and almost 100% in microscopic polyangiitis (MPA). Renal prognosis is still unfavorable, even with newer induction and maintenance regimens. Indeed, up to 25% of affected individuals will experience end-stage kidney disease within a few years of diagnosis. It remains cumbersome to adequately predict renal outcome in those patients. Because of limited data supporting rituximab and glucocorticoids in patients presenting with reduced glomerular filtration rate (GFR < 30 mL/min,), a cyclophosphamide-based regimen (either alone or combined with rituximab) is considered preferable as induction therapy. Case report: Here we describe the case of a 62-year-old Caucasian male with a prior history of gout who presented with severe acute kidney injury. One month before diagnosis, he developed severe asthenia, weight loss (15 kg in one year), and severe acute kidney injury. Laboratory tests showed high anti- myeloperoxidase (MPO) titers. Renal biopsy revealed pauci-immune necrotizing glomerulonephritis, focal class, with severe chronic lesions suggesting poor renal prognosis. The 3-year renal survival was estimated to be 54%, according to the improved Antineutrophil cytoplasmic antibody (ANCA) Kidney Risk Score. Induction therapy consisted of intravenous corticosteroids followed by rituximab, and was associated with a mild renal response at six months (serum creatinine 5.29 mg/dL to 2.38 mg/dL). The patient did not need dialysis. The maintenance therapy included prolonged rituximab infusions and low-dose oral corticosteroids for 54 months. The patient experienced slow and sustained improvement of proteinuria and renal function (serum creatinine 1.5 mg/dL at 24 months; 1.6 mg/dL at 54 months). Conclusions: This case demonstrates the possibility of sustained renal recovery, despite unfavorable initial prognostic features, and the use of Rituximab in a patient with severely reduced estimated GFR (i.e., serum creatinine > 4 mg/dL).

Pulmonary congestion (PC) is common in hemodialysis (HD) patients. We explored the association of anemia and pulmonary congestion in HD patients. A prospective pilot observational study included 18 patients on maintenance HD. Individual B-lines scores (BLS; 8-sites method) were obtained by lung ultrasound, before and after the first two consecutive HD sessions of the week (HD1-HD2), with different inter-dialytic intervals (68 vs. 44 h). Bioimpedance spectroscopy body composition (BIS) was performed before each HD session. Hemoglobin (Hb) levels, in addition to circulating markers of chronic inflammation (soluble urokinase Plasminogen Activator Receptor [suPAR], soluble Suppression of Tumorigenicity 2 [sST2]) were obtained. Mean (±SD) BLS values were quite elevated at all time points: Pre-HD1 (16 ± 5.53), post-HD1 (15.3 ± 6.63), pre-HD2 (16.3 ± 5.26) and post-HD2 (13.6 ± 5.83), respectively. No direct significant correlation was found between inflammation markers levels and BLS. However, mean levels (±SD, ng/mL) of suPAR pre-HD1 (7.88 ± 3.07) and pre-HD2 (7.78 ± 3.02) remained significantly above the normal range (<4 ng/mL), and sST2 levels reached 2-fold the upper normal value in most patients (27.4 ± 17.8). Pulmonary congestion reflected by BLS was negatively correlated to Hb levels pre-HD1 (R² = 0.439, p = 0.003), and pre-HD2 (R² = 0.301, p = 0.018). In addition, Hb levels were negatively correlated to global volume status estimated by BIS (R² = 0.351, p = 0.009). Hemoglobin levels were negatively correlated to pulmonary congestion and to the global volume status evaluated by BIS. Chronic inflammation markers were increased in HD patients, suggesting a complex volume- and non-volume-dependent pathophysiology of pulmonary congestion in HD patients.

Introduction: Endothelial dysfunction is a common feature of end-stage kidney disease, requiring hemodialysis (HD) and antiphospholipid antibody (aPL) persistent positivity. Endothelial dysfunction can be assessed with noninvasive tests such as flow-mediated dilation (FMD). In the HD population, it is not known whether aPL persistent positivity is associated with a more severe endothelial dysfunction. Methods: We performed a cross-sectional study in our HD patients. The FMD of the brachial artery was measured in 17 aPL-positive patients who fulfilled the inclusion criteria and were matched to 17 controls according to age, gender, diabetes mellitus, smoking status and markers of dialysis adequacy (Kt/V). Results: FMD was significantly lower in the aPL group with a mean of 6.9% and 11.8% in the aPL-positive and the control groups, respectively (mean difference (IC 95%): −4.9 (−8.3; −1.6), p = 0.006). aPL was associated with a higher c-reactive protein level, and longer HD vintage. There was no statistical difference between groups in terms of pre-dialysis urea and urinary output, dialysis adequacy (Kt/V), and history of cardiovascular disease or treatments. Conclusions: aPL persistent positivity in HD patients was associated with worse endothelial dysfunction, reflected by FMD measurements. These findings have to be confirmed in larger studies.