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Aims: Cardiac conduction disorders are common in haemodialysis patients, with a relatively high rate of pacemaker implantations. Pacemaker-related complications, especially lead infections and central venous stenosis, pose significant challenges in this population. This study aims to compare single-chamber leadless pacemaker to single-chamber transvenous pacemakers in terms of survival and related complications in haemodialysis patients., Methods and Results: This retrospective study included adult haemodialysis patients who received a first single-chamber transvenous or leadless pacemaker between January 2017 and December 2020. Data were obtained from the French national REIN registry matched to the national health databases (Système National des Données de Santé). Propensity score matching was used to balance baseline characteristics. Survival and complications were compared between groups by Cox regression and by competitive risk models, respectively. One hundred and seventy-eight patients were included after propensity score matching, with 89 patients in each group. The median follow-up time was 24 (range 7-37) months. Leadless pacemakers were associated with significantly lower all-cause mortality rates compared to transvenous pacemakers [hazard ratio (HR) = 0.68, 95% confidence interval (CI) (0.47-0.99)]. Device-related infections are significantly lower with leadless pacemakers throughout the follow-up period (HR 0.43, 95% CI 0.21-0.86). Leadless pacemaker recipients also required fewer vascular access interventions [odds ratio 0.53, 95% CI (0.33-0.68)] on arteriovenous fistula., Conclusion: With the limitations of its observational design, this study suggests that leadless pacemakers are associated with a lower rate of complications and better survival as compared with transvenous VVI pacemakers in haemodialysis patients, supporting to consider their preferential use in this population., Competing Interests: Conflict of interest: E.M. is a consultant and received research grants from Medtronic. All remaining authors have declared no conflicts of interest., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Competing Interests: Potential conflicts of interest. E. L. reports support for attending meetings and/or travel from Gilead, ViiV Healthcare, Shionogi, Correvio, Exafield, and Menarini. D. B. reports honoraria paid to author for presentations unrelated to this work from Gilead Sciences. G. P. reports consulting fees from Gilead Sciences, Merck, ViiV Healthcare, and Takeda; payment to author for lectures, presentations, speaker’s bureaus, manuscript writing, or educational events from Gilead Sciences, Merck, ViiV Healthcare, and Takeda; and support for attending meetings and/or travel from Gilead Sciences. All other authors report no potential conflicts. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed.

Background: Epstein-Barr virus (EBV) is a herpesvirus linked to nine different human tumors and lymphoproliferative disorders. Immunosuppression promotes EBV-driven malignancies. The most frequent EBV-induced malignancies are lymphomas and nasopharyngeal carcinoma. By promoting smooth muscle proliferation, EBV can induce EBV-associated smooth muscle tumors (EBV-SMT). EBV-SMT is a rare oncological entity for which no current guideline for diagnosis or management exists. Data on posttransplant EBV-SMT (PT-SMT) are scarce in kidney transplant recipients., Methods: We conducted a national multicentric retrospective study and collected cases among transplantation centers in France. Kidney transplant recipients experiencing histologically proven PT-SMT were included. We collected data on demographic characteristics of patient, history of kidney transplantation, history of PT-SMT, evolution of graft function, and patient survival., Results: Eight patients were included. The median age at PT-SMT diagnosis was 31 years (range 6.5-40). PT-SMT occurred after a median delay of 37.8 months after transplantation (range 6-175). PT-SMT management consisted in immunosuppressive regimen minimization in all patients. Introduction of mTOR inhibitors was performed in two patients. Four patients (50%) needed chemotherapy. Surgical resection was performed in four patients. At last follow-up after PT-SMT diagnosis (median 33 months (range 17-132)), five patients were considered in complete remission, and two patients had died. Two patients experienced graft rejection; two resumed dialysis (25%). All patients with available data presented with impaired graft function at last follow-up., Conclusion: PT-SMT is a subacute and progressive disease during kidney transplantation. Even if the risk of developing PT-SMT is low in kidney transplant recipients (0.07% in our cohort), PT-SMT is associated with significant graft loss, possibly due to reduced immunosuppression. Developing guidelines could help transplantation teams better manage these patients., (© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Background: Health policy-making require careful assessment of chronic kidney disease (CKD) epidemiology to develop efficient and cost-effective care strategies. The aim of the present study was to use the RENALGO-EXPERT algorithm to estimate the global prevalence of CKD in France., Methods: An expert group developed the RENALGO-EXPERT algorithm based on healthcare consumption. This algorithm has been applied to the French National Health claims database (SNDS), where no biological test findings are available to estimate a national CKD prevalence for the years 2018-2021. The CONSTANCES cohort (+219 000 adults aged 18-69 with one CKD-EPI eGFR) was used to discuss the limit of using health claims data., Results: Between 2018 and 2021, the estimated prevalence in the SNDS increased from 8.1% to 10.5%. The RENALGO-EXPERT algorithm identified 4.5% of the volunteers in the CONSTANCES as CKD. The RENALGO-EXPERT algorithm had a positive predictive value of 6.2% and negative predictive value of 99.1% to detect an eGFR<60 ml/min/1.73 m². Half of 252 false positive cases (ALGO+, eGFR > 90) had been diagnosed with kidney disease during hospitalization, and the other half based on healthcare consumption suggestive of a 'high-risk' profile; 95% of the 1661 false negatives (ALGO-, eGFR < 60) had an eGFR between 45 and 60 ml/min, half had medication and two-thirds had biological exams possibly linked to CKD. Half of them had a hospital stay during the period but none had a diagnosis of kidney disease., Conclusions: Our result is in accordance with other estimations of CKD prevalence in the general population. Analysis of diverging cases (FP and FN) suggests using health claims data have inherent limitations. Such an algorithm can identify patients whose care pathway is close to the usual and specific CKD pathways. It does not identify patients who have not been diagnosed or whose care is inappropriate or at early stage with stable GFR., Competing Interests: The authors declare that they have no conflict of interest., (© The Author(s) 2024. Published by Oxford University Press on behalf of the ERA.)

Long-chain acyl-CoA synthetase family 4 (ACSL4) metabolizes long-chain polyunsaturated fatty acids (PUFAs), enriching cell membranes with phospholipids susceptible to peroxidation and drive ferroptosis. The role of ACSL4 and ferroptosis upon endoplasmic-reticulum (ER)-stress-induced acute kidney injury (AKI) is unknown. We used lipidomic, molecular, and cellular biology approaches along with a mouse model of AKI induced by ER stress to investigate the role of ACSL4 regulation in membrane lipidome remodeling in the injured tubular epithelium. Tubular epithelial cells (TECs) activate ACSL4 in response to STAT3 signaling. In this context, TEC membrane lipidome is remodeled toward PUFA-enriched triglycerides instead of PUFA-bearing phospholipids. TECs expressing ACSL4 in this setting are not vulnerable to ferroptosis. Thus, ACSL4 activity in TECs is driven by STAT3 signaling, but ACSL4 alone is not enough to sensitize ferroptosis, highlighting the significance of the biological context associated with the study model., Competing Interests: The authors declare no competing interests., (© 2024 The Author(s).)