Author: "Giuseppe, Remuzzi" - Searchworks@Jio Institute Digital Library Search Results

1,537 results on '"Giuseppe, Remuzzi"'

1. Corrigendum: Bi-specific autoantigen-T cell engagers as targeted immunotherapy for autoreactive B cell depletion in autoimmune diseases

Author: Luca Perico, Federica Casiraghi, Fabiane Sônego, Marta Todeschini, Daniela Corna, Domenico Cerullo, Anna Pezzotta, Patricia Isnard-Petit, Silvia Faravelli, Federico Forneris, Kader Thiam, Ariela Benigni, and Giuseppe Remuzzi
Subjects: autoimmune diseases, membranous nephropathy, anti-PLA2R antibodies, autoreactive B cell, targeted immunotherapies, bi-specific autoantigen-T cell engagers, Immunologic diseases. Allergy, RC581-607
Published: 2025
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2. Tubulointerstitial injury in proteinuric chronic kidney diseases

Author: Monica Cortinovis, Norberto Perico, and Giuseppe Remuzzi
Subjects: proteinuria, tubulointerstitial injury, chronic kidney disease, tubule toxicity, fibrosis, Medicine (General), R5-920
Abstract: Proteinuria is an independent risk factor for chronic kidney disease progression and cardiovascular diseases. Apart from its prognostic role, the load of proteins that pass across the disrupted glomerular capillary wall trigger multiple pathophysiologic processes. These include, among others, intratubular complement activation and excessive proximal tubular reabsorption of filtered proteins, especially albumin and albumin-bound free fatty acids, which can set off several pathways of cellular damage. The activation of these pathways can cause apoptosis of proximal tubular cells and paracrine effects that incite the development of interstitial inflammation and fibrosis, ultimately leading to irreversible kidney injury. In this review, we provide a comprehensive overview of the current understanding on the mechanisms underlying the tubular toxicity of ultrafiltered proteins in the setting of proteinuric chronic kidney diseases. The acquired knowledge is expected to be instrumental for the development of novel therapeutic classes of medications to be tested on top of standard of care with optimized renin-angiotensin-aldosterone blockade and sodium-glucose cotransporter-2 inhibition, in order to further improve the clinical outcomes of patients with proteinuric chronic kidney diseases.
Published: 2024
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3. Proof of concept of a new plasma complement Factor H from waste plasma fraction

Author: Filippo Mori, Giancarlo Pascali, Silvia Berra, Alessandra Lazzarotti, Daniele Panetta, Silvia Rocchiccioli, Elisa Ceccherini, Francesco Norelli, Antonio Morlando, Roberta Donadelli, Alberto Clivio, Claudio Farina, Marina Noris, Piero A. Salvadori, and Giuseppe Remuzzi
Subjects: concentrated complement factor H (FH), plasma purification, high-resolution dynamic PET, C3 glomerulopathy, membrano proliferative glomerulonephritis (MPGN), Immunologic diseases. Allergy, RC581-607
Abstract: IntroductionComplement factor H (FH) is a major regulator of the complement alternative pathway, its mutations predispose to an uncontrolled activation in the kidney and on blood cells and to secondary C3 deficiency. Plasma exchange has been used to correct for FH deficiency and although the therapeutic potential of purified FH has been suggested by in vivo experiments in animal models, a clinical approved FH concentrate is not yet available. We aimed to develop a purification process of FH from a waste fraction rather than whole plasma allowing a more efficient and ethical use of blood and plasma donations.MethodsWaste fractions from industrial plasma fractionation (pooled human plasma) were analyzed for FH content by ELISA. FH was purified from unused fraction III and its decay acceleration, cofactor, and C3 binding capacity were characterized in vitro. Biodistribution was assessed by high-resolution dynamic PET imaging. Finally, the efficacy of the purified FH preparation was tested in the mouse model of C3 glomerulopathy (Cfh−/− mice).ResultsOur purification method resulted in a high yield of highly purified (92,07%), pathogen-safe FH. FH concentrate is intact and fully functional as demonstrated by in vitro functional assays. The biodistribution revealed lower renal and liver clearance of human FH in Cfh-/- mice than in wt mice. Treatment of Cfh-/- mice documented its efficacy in limiting C3 activation and promoting the clearance of C3 glomerular deposits.ConclusionWe developed an efficient and economical system for purifying intact and functional FH, starting from waste material of industrial plasma fractionation. The FH concentrate could therefore constitute possible treatments options of patients with C3 glomerulopathy, particularly for those with FH deficiency, but also for patients with other diseases associated with alternative pathway activation.
Published: 2024
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4. Efficacy and Safety of Iptacopan in Patients With C3 Glomerulopathy

Author: Edwin Wong, Carla Nester, Teresa Cavero, Alexandre Karras, Moglie Le Quintrec, Liz Lightstone, Ute Eisenberger, Maria Jose Soler, David Kavanagh, Erica Daina, Manuel Praga, Nicholas R. Medjeral-Thomas, Anja Gäckler, Clara Garcia-Carro, Andrea Biondani, Frederique Chaperon, Kenneth Kulmatycki, Julie Milojevic, Nicholas J.A. Webb, Prasanna Kumar Nidamarthy, Guido Junge, and Giuseppe Remuzzi
Subjects: complement 3 glomerulopathy, inflammatory kidney disease, iptacopan, kidney transplant, urine protein-to-creatinine ratio, Diseases of the genitourinary system. Urology, RC870-923
Abstract: Introduction: Complement 3 glomerulopathy (C3G) is a rare inflammatory kidney disease mediated by dysregulation of the alternative complement pathway. No targeted therapy exists for this aggressive glomerulonephritis. Efficacy, safety, tolerability, pharmacokinetics (PK), and pharmacodynamics (PD) (measured by complement biomarkers) of iptacopan were assessed in patients with C3G. Methods: In this phase 2, multicenter, open-label, single-arm, nonrandomized study, adults with biopsy-proven, native kidney C3G (native cohort) and kidney transplant recipients with C3G recurrence (recurrent kidney transplant [KT] cohort) received iptacopan twice daily (bid) for 84 days (days 1–21: 10–100 mg; days 22–84: 200 mg). The primary end point was the urine protein-to-creatinine ratio (UPCR; native cohort) and the change in the C3 deposit score of kidney biopsy (recurrent KT cohort). The complement pathway measures included Wieslab assay, soluble C5b9, and serum C3 levels. Results: A total of 27 patients (16 native cohort and 11 recurrent KT cohort) were enrolled and all completed the study. In the native cohort, UPCR levels decreased by 45% from baseline to week 12 (P = 0.0003). In the recurrent KT cohort, the median C3 deposit score decreased by 2.50 (scale: 0–12) on day 84 versus baseline (P = 0.03). Serum C3 levels were normalized in most patients; complement hyperactivity observed pretreatment was reduced. Severe adverse events (AEs) included post-biopsy hematuria and hyperkalemia. No deaths occurred during the study. Conclusion: Iptacopan resulted in statistically significant and clinically important reductions in UPCR and normalization of serum C3 levels in the native cohort and reduced C3 deposit scores in the recurrent KT cohort with favorable safety and tolerability. (ClinicalTrials.gov identifier: NCT03832114).
Published: 2023
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5. Efficacy of erythropoietin as a neuroprotective agent in CKD-associated cognitive dysfunction: A literature systematic review

Author: Michelangela Barbieri, Paolo Chiodini, Piergiacomo Di Gennaro, Gaye Hafez, Sophie Liabeuf, Jolanta Malyszko, Laila-Yasmin Mani, Francesco Mattace-Raso, Marion Pepin, Norberto Perico, Mariadelina Simeoni, Carmine Zoccali, Giovanni Tortorella, Annalisa Capuano, Giuseppe Remuzzi, Giovambattista Capasso, and Giuseppe Paolisso
Subjects: Erythropoietin, rHuEPO, CKD, Cognition, Darbepoetin, Neuroprotection, Therapeutics. Pharmacology, RM1-950
Abstract: Patients with chronic kidney disease (CKD) often experience mild cognitive impairment and other neurocognitive disorders. Studies have shown that erythropoietin (EPO) and its receptor have neuroprotective effects in cell and animal models of nervous system disorders. Recombinant human EPO (rHuEPO), commonly used to treat anemia in CKD patients, could be a neuroprotective agent. In this systematic review, we aimed to assess the published studies investigating the cognitive benefits of rHuEPO treatment in individuals with reduced kidney function. We comprehensively searched Pubmed, Cochrane Library, Scopus, and Web of Science databases from 1990 to 2023. After selection, 24 studies were analyzed, considering study design, sample size, participant characteristics, intervention, and main findings. The collective results of these studies in CKD patients indicated that rHuEPO enhances brain function, improves performance on neuropsychological tests, and positively affects electroencephalography measurements. These findings suggest that rHuEPO could be a promising neuroprotective agent for managing CKD-related cognitive impairment.
Published: 2024
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6. Corrigendum: Time-Trends in Air Pollution Impact on Health in Italy, 1990–2019: An Analysis from the Global Burden of Disease Study 2019

Author: Sara Conti, Carla Fornari, Pietro Ferrara, Ippazio C. Antonazzo, Fabiana Madotto, Eugenio Traini, Miriam Levi, Achille Cernigliaro, Benedetta Armocida, Nicola L. Bragazzi, Ennio Cadum, Michele Carugno, Giacomo Crotti, Silvia Deandrea, Paolo A. Cortesi, Davide Guido, Ivo Iavicoli, Sergio Iavicoli, Carlo La Vecchia, Paolo Lauriola, Paola Michelozzi, Salvatore Scondotto, Massimo Stafoggia, Francesco S. Violante, Cristiana Abbafati, Luciana Albano, Francesco Barone-Adesi, Antonio Biondi, Cristina Bosetti, Danilo Buonsenso, Giulia Carreras, Giulio Castelpietra, Alberico Catapano, Maria S. Cattaruzza, Barbara Corso, Giovanni Damiani, Francesco Esposito, Silvano Gallus, Davide Golinelli, Simon I. Hay, Gaetano Isola, Caterina Ledda, Stefania Mondello, Paolo Pedersini, Umberto Pensato, Norberto Perico, Giuseppe Remuzzi, Francesco Sanmarchi, Rocco Santoro, Biagio Simonetti, Brigid Unim, Marco Vacante, Massimiliano Veroux, Jorge H. Villafañe, Lorenzo Monasta, and Lorenzo G. Mantovani
Subjects: air pollution, particulate matter, ozone, global burden of disease, air quality regulations, Public aspects of medicine, RA1-1270
Published: 2024
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7. COVID-19: the renaissance of science in the face of adversity

Author: Luca Perico and Giuseppe Remuzzi
Subjects: COVID-19, SARS-CoV-2, epidemic models, mRNA vaccines, vaccinology, data science, Science
Published: 2024
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8. SARS-CoV-2 spike protein induces lung endothelial cell dysfunction and thrombo-inflammation depending on the C3a/C3a receptor signalling

Author: Luca Perico, Marina Morigi, Anna Pezzotta, Monica Locatelli, Barbara Imberti, Daniela Corna, Domenico Cerullo, Ariela Benigni, and Giuseppe Remuzzi
Subjects: Medicine, Science
Abstract: Abstract The spike protein of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) can interact with endothelial cells. However, no studies demonstrated the direct effect of the spike protein subunit 1 (S1) in inducing lung vascular damage and the potential mechanisms contributing to lung injury. Here, we found that S1 injection in mice transgenic for human angiotensin converting enzyme 2 (ACE2) induced early loss of lung endothelial thromboresistance at 3 days, as revealed by thrombomodulin loss and von Willebrand factor (vWF) increase. In parallel, vascular and epithelial C3 deposits and enhanced C3a receptor (C3aR) expression were observed. These changes preceded diffuse alveolar damage and lung vascular fibrin(ogen)/platelets aggregates at 7 days, as well as inflammatory cell recruitment and fibrosis. Treatment with C3aR antagonist (C3aRa) inhibited lung C3 accumulation and C3a/C3aR activation, limiting vascular thrombo-inflammation and fibrosis. Our study demonstrates that S1 triggers vascular dysfunction and activates complement system, instrumental to lung thrombo-inflammatory injury. By extension, our data indicate C3aRa as a valuable therapeutic strategy to limit S1-dependent lung pathology.
Published: 2023
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9. Bi-specific autoantigen-T cell engagers as targeted immunotherapy for autoreactive B cell depletion in autoimmune diseases

Author: Luca Perico, Federica Casiraghi, Fabiane Sônego, Marta Todeschini, Daniela Corna, Domenico Cerullo, Anna Pezzotta, Patricia Isnard-Petit, Silvia Faravelli, Federico Forneris, Kader Thiam, Ariela Benigni, and Giuseppe Remuzzi
Subjects: autoimmune diseases, membranous nephropathy, anti-PLA2R antibodies, autoreactive B cell, targeted immunotherapies, bi-specific autoantigen-T cell engagers, Immunologic diseases. Allergy, RC581-607
Abstract: IntroductionIn autoimmune diseases, autoreactive B cells comprise only the 0.1-0.5% of total circulating B cells. However, current first-line treatments rely on non-specific and general suppression of the immune system, exposing patients to severe side effects. For this reason, identification of targeted therapies for autoimmune diseases is an unmet clinical need.MethodsHere, we designed a novel class of immunotherapeutic molecules, Bi-specific AutoAntigen-T cell Engagers (BiAATEs), as a potential approach for targeting the small subset of autoreactive B cells. To test this approach, we focused on a prototype autoimmune disease of the kidney, membranous nephropathy (MN), in which phospholipase A2 receptor (PLA2R) serves as primary nephritogenic antigen. Specifically, we developed a BiAATE consisting of the immunodominant Cysteine-Rich (CysR) domain of PLA2R and the single-chain variable fragment (scFv) of an antibody against the T cell antigen CD3, connected by a small flexible linker.ResultsBiAATE creates an immunological synapse between autoreactive B cells bearing an CysR-specific surface Ig+ and T cells. Ex vivo, the BiAATE successfully induced T cell-dependent depletion of PLA2R-specific B cells isolated form MN patients, sparing normal B cells. Systemic administration of BiAATE to mice transgenic for human CD3 reduced anti-PLA2R antibody levels following active immunization with PLA2R.DiscussionShould this approach be confirmed for other autoimmune diseases, BiAATEs could represent a promising off-the-shelf therapy for precision medicine in virtually all antibody-mediated autoimmune diseases for which the pathogenic autoantigen is known, leading to a paradigm shift in the treatment of these diseases.
Published: 2024
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10. GFR measurement in patients with CKD: Performance and feasibility of simplified iohexol plasma clearance techniques

Author: Fabiola Carrara, Flavio Gaspari, Matias Trillini, Tobia Peracchi, Diego Fidone, Nadia Stucchi, Silvia Ferrari, Daniela Cugini, Norberto Perico, Aneliya Parvanova, Giuseppe Remuzzi, and Piero Ruggenenti
Subjects: Medicine, Science
Published: 2024

11. A GWAS in the pandemic epicenter highlights the severe COVID-19 risk locus introgressed by Neanderthals

Author: Matteo Breno, Marina Noris, Nadia Rubis, Aneliya Ilieva Parvanova, Davide Martinetti, Sara Gamba, Lucia Liguori, Caterina Mele, Rossella Piras, Silvia Orisio, Elisabetta Valoti, Marta Alberti, Olimpia Diadei, Elena Bresin, Miriam Rigoldi, Silvia Prandini, Tiziano Gamba, Nadia Stucchi, Fabiola Carrara, Erica Daina, Ariela Benigni, and Giuseppe Remuzzi
Subjects: Respiratory medicine, Public health, Virology, Genomics, Science
Abstract: Summary: Large GWAS indicated that genetic factors influence the response to SARS-CoV-2. However, sex, age, concomitant diseases, differences in ancestry, and uneven exposure to the virus impacted the interpretation of data. We aimed to perform a GWAS of COVID-19 outcome in a homogeneous population who experienced a high exposure to the virus and with a known infection status. We recruited inhabitants of Bergamo province—that in spring 2020 was the epicenter of the SARS-Cov-2 pandemic in Europe—via an online questionnaire followed by personal interviews. Cases and controls were matched by age, sex and risk factors. We genotyped 1195 individuals and replicated the association at the 3p21.31 locus with severity, but with a stronger effect size that further increased in gravely ill patients. Transcriptome-wide association study highlighted eQTLs for LZTFL1 and CCR9. We also identified 17 loci not previously reported, suggestive for an association with either COVID-19 severity or susceptibility.
Published: 2023
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12. Thyroid hormone treatment counteracts cellular phenotypical remodeling in diabetic organs

Author: Angelo M. Lavecchia, Polyxeni Mantzouratou, Domenico Cerullo, Monica Locatelli, Sara Conti, Matteo Tironi, Fabio Sangalli, Daniela Corna, Carlamaria Zoja, Giuseppe Remuzzi, and Christodoulos Xinaris
Subjects: Biomedical discipline, Cell biology, Human metabolism, Science
Abstract: Summary: Diabetes mellitus and alterations in thyroid hormone (TH) signaling are closely linked. Though the role of TH signaling in cell differentiation and growth is well known, it remains unclear whether its alterations contribute to the pathobiology of diabetic cells. Here, we aim to investigate whether the administration of exogenous T3 can counteract the cellular remodeling that occurs in diabetic cardiomyocytes, podocytes, and pancreatic beta cells.Treating diabetic rats with T3 prevents dedifferentiation, pathological growth, and ultrastructural alterations in podocytes and cardiomyocytes. In vitro, T3 reverses glucose-induced growth in human podocytes and cardiomyocytes, restores cardiomyocyte cytoarchitecture, and reverses pathological alterations in kidney and cardiac organoids. Finally, T3 treatment counteracts glucose-induced transdifferentiation, cell growth, and loss in pancreatic beta cells through TH receptor alpha1 activation.Our studies indicate that TH signaling activation substantially counteracts diabetes-induced pathological remodeling, and provide a potential therapeutic approach for the treatment of diabetes and its complications.
Published: 2023
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13. Current understanding of the molecular mechanisms of circulating permeability factor in focal segmental glomerulosclerosis

Author: Giuseppe Salfi, Federica Casiraghi, and Giuseppe Remuzzi
Subjects: FSGS, immunity, permeability factor, circulating factor, post-transplant recurrence, idiopathic nephrotic syndrome, Immunologic diseases. Allergy, RC581-607
Abstract: The pathogenetic mechanisms underlying the onset and the post-transplant recurrence of primary focal segmental glomerulosclerosis (FSGS) are complex and remain yet to be fully elucidated. However, a growing body of evidence emphasizes the pivotal role of the immune system in both initiating and perpetuating the disease. Extensive investigations, encompassing both experimental models and patient studies, have implicated T cells, B cells, and complement as crucial actors in the pathogenesis of primary FSGS, with various molecules being proposed as potential “circulating factors” contributing to the disease and its recurrence post kidney-transplantation. In this review, we critically assessed the existing literature to identify essential pathways for a comprehensive characterization of the pathogenesis of FSGS. Recent discoveries have shed further light on the intricate interplay between these mechanisms. We present an overview of the current understanding of the engagement of distinct molecules and immune cells in FSGS pathogenesis while highlighting critical knowledge gaps that require attention. A thorough characterization of these intricate immune mechanisms holds the potential to identify noninvasive biomarkers that can accurately identify patients at high risk of post-transplant recurrence. Such knowledge can pave the way for the development of targeted and personalized therapeutic approaches in the management of FSGS.
Published: 2023
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14. A phase I study of autologous mesenchymal stromal cells for severe steroid-dependent nephrotic syndrome

Author: Marina Vivarelli, Manuela Colucci, Mattia Algeri, Federica Zotta, Francesco Emma, Ines L’Erario, Marco Busutti, Stefano Rota, Chiara Capelli, Martino Introna, Marta Todeschini, Federica Casiraghi, Annalisa Perna, Tobia Peracchi, Andrea De Salvo, Nadia Rubis, Franco Locatelli, Giuseppe Remuzzi, and Piero Ruggenenti
Subjects: Clinical trials, Nephrology, Medicine
Abstract: BACKGROUND Severe forms of idiopathic nephrotic syndrome (INS) require prolonged immunosuppressive therapies and repeated courses of high-dose glucocorticoids. Mesenchymal stromal cells (MSCs) have promising immunomodulatory properties that may be employed therapeutically to reduce patient exposure to medications and their side effects.METHODS We performed a phase I open-label trial assessing safety and feasibility of autologous bone marrow–derived MSCs (BM-MSCs) in children and young adults with severe forms of steroid-dependent nephrotic syndrome. Following autologous BM-MSC preparation and infusion, oral immunosuppression was tapered. Safety, efficacy, and immunomodulatory effects in vivo were monitored for 12 months.RESULTS Sixteen patients (10 children, 6 adults) were treated. Adverse events were limited and not related to BM-MSC infusions. All patients relapsed during follow-up, but in the 10 treated children, time to first relapse was delayed (P = 0.02) and number of relapses was reduced (P = 0.002) after BM-MSC infusion, compared with the previous 12 months. Cumulative prednisone dose was also reduced at 12 months compared with baseline (P < 0.05). No treatment benefit was observed in adults.In children, despite tapering of immunosuppression, clinical benefit was mirrored by a significant reduction in total CD19+, mature, and memory B cells and an increase in regulatory T cells in vivo up to 3–6 months following BM-MSC infusionCONCLUSION Treatment with autologous BM-MSCs is feasible and safely reduces relapses and immunosuppression at 12 months in children with severe steroid-dependent INS. Immunomodulatory studies suggest that repeating MSC infusions at 3–6 months may sustain benefit.TRIAL REGISTRATION EudraCT 2016-004804-77.FUNDING AIFA Ricerca Indipendente 2016-02364623.
Published: 2023
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15. La scelta - nuova edizione aggiornata: Perché è importante decidere come vorremmo morire

Author: Giuseppe Remuzzi
Published: 2023

16. Editorial: Global excellence in translational immunology: Europe

Author: Federica Casiraghi, Norberto Perico, and Giuseppe Remuzzi
Subjects: cancer, HLA, B cells, neoantigens, tumor-associated antigens, cancer metabolism, Immunologic diseases. Allergy, RC581-607
Published: 2023
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17. Rationale and design of the CV-PREVITAL study: an Italian multiple cohort randomised controlled trial investigating innovative digital strategies in primary cardiovascular prevention

Author: Roberta Pastorino, Eloisa Arbustini, Andrea Faini, Gianfranco Parati, Grzegorz Bilo, Davide Soranna, Antonella Zambon, Sergio Leonardi, Alessandro Gialluisi, Lorenzo Giovanni Mantovani, Walter Ricciardi, Fabio Blandini, Giovanni Scambia, Catherine Klersy, Marialaura Bonaccio, Augusto Di Castelnuovo, Simona Costanzo, Amalia De Curtis, Mariarosaria Persichillo, Chiara Cerletti, Maria Benedetta Donati, Licia Iacoviello, Giuseppe Remuzzi, Camilla Torlasco, Giuseppe Ambrosio, Gabriele Zoppoli, Maria Chiara Grimaldi, Daniela Pedicino, Giovanna Liuzzo, Serena Pelusi, Daniele Prati, Luca Valenti, Francesca Gorini, Maurizio Sanguinetti, Giuseppe Ferrante, Gianluigi Condorelli, Giulio Pompilio, Stefania Boccia, Luigi Badano, Victor Savevski, Tiziana Bachetti, Gian Franco Gensini, Silvano Bosari, Alice Bonanni, Elena Tremoli, Angelo Santoliquido, Stefano Genovese, Sara Boveri, Gianfranco Gensini, Francesco Gianfagna, Italo Porto, Fabio Tuzzolino, Carolina Lombardi, Egidio Traversi, Fabrizio Veglia, Andrea Urbani, Domenico D’Amario, Gaetano Antonio Lanza, Antonio Uccelli, José Pablo Werba, Livio Luzi, Pietro Ameri, Davide Gentilini, Luisa Gilardini, Cecilia Invitti, Maurizio Volterrani, Maria Teresa La Rovere, Giovanni Gentile, Francesco Clemenza, Mario Urtis, Francesca Ieva, Maria Carla Roncaglioni, Valentina Milani, Paola Baiardi, Debora Rosa, Fabiana Madotto, Emilia Ruggiero, Teresa Panzera, Simona Esposito, Sara Magnacca, Fabrizia Noro, Roberta Parisi, Francesca Bracone, Irene Baroni, Damiano Baldassarre, Roberta Baetta, Luigi Frati, Pier Giulio Conaldi, Massimo Fini, Antonio Di Malta, Mauro Amato, Alice Bonomi, Francesca Colazzo, Martino Pengo, Luciana Auteri, Marta Baviera, Alberico Catapano, Alexis Elias Malavazos, Serenella Castelvecchio, Massimiliano Marco Corsi-Romanelli, Rosanna Cardani, Valentina Agnese, Bianca Pane, Laura Spinardi, Marco Visconti, Anna Di Blasio, Luisa Ojeda-Fernández, Andreana Foresta, Simonetta Scalvini, Antonia Pierobon, Alessandra Gorini, Annarosa Racca, Manuela Bandi, Lorenzo Menicanti, Gualtiero Colombo, Chiara Vavassori, Maria Luisa Biondi, Beatrice Frigerio, Alessio Ravani, Daniela Sansaro, Daniela Coggi, Alessandra Romandini, Monica Giroli, Mattia Giuliani, Maurizio Rondinelli, Catia Trudu, Carmen Cinieri, Massimo Monturano, Elisa Perger, Lucia Zanotti, Lidia Cova, Luca Grappiolo, Laura Papa, Ignazio Romano, Luisa Ojeda, Fiorenza Clerici, Angela Palumbo, Roberto Mattioli, Ermanno Longhi, Anwal Ghulam, Sabatino Orlandi, Sabrina Franciosa, Martina Morelli, Fiorella De Rita, Giovanni de Gaetano, Massimiliano MarcoCorsi Romanelli, Ambra Cerri, Carola Dubini, Manuel Bruno Trevisan, Laura Valentina Renna, Paola Giubbilini, Lucia Ramputi, Giada DeAngeli, Francesca Olmetti, Maurizio Bussotti, Carlo Gaetano, Martina Balbi, Laura Comini, Monica Lorenzoni, Adriana Olivares, Camilla Garrè, Riccardo Sideri, Giuseppe Caruana, Nicola Cuscino, Gabriele Di Gesaro, Alessio Greco, Italia Loddo, Domenico Palombo, Giovanni Spinella, Gaddiel Mozzetta, Alice Finotello, Giovanni Pratesi, Margherita Clerici, Cristiana Bianco, Rossana Carpani, Giulia Periti, Sara Margarita, Anna Severino, Alessia D’Aiello, Ramona Vinci, Mattia Brecciaroli, Simone Filomia, Luca Proto, Dalila Tarquini, Arianna Elia, Alessia Currao, Alessandro Di Toro, Lorenzo Giuliani, Giuseppe Caminiti, Federica Marcolongo, Barbara Sposato, Fiorella Guadagni, Valentina Morsella, Angelica Marziale, and Giulia Protti
Subjects: Medicine
Abstract: Introduction Prevention of cardiovascular disease (CVD) is of key importance in reducing morbidity, disability and mortality worldwide. Observational studies suggest that digital health interventions can be an effective strategy to reduce cardiovascular (CV) risk. However, evidence from large randomised clinical trials is lacking.Methods and analysis The CV-PREVITAL study is a multicentre, prospective, randomised, controlled, open-label interventional trial designed to compare the effectiveness of an educational and motivational mobile health (mHealth) intervention versus usual care in reducing CV risk. The intervention aims at improving diet, physical activity, sleep quality, psycho-behavioural aspects, as well as promoting smoking cessation and adherence to pharmacological treatment for CV risk factors. The trial aims to enrol approximately 80 000 subjects without overt CVDs referring to general practitioners’ offices, community pharmacies or clinics of Scientific Institute for Research, Hospitalization and Health Care (Italian acronym IRCCS) affiliated with the Italian Cardiology Network. All participants are evaluated at baseline and after 12 months to assess the effectiveness of the intervention on short-term endpoints, namely improvement in CV risk score and reduction of major CV risk factors. Beyond the funded life of the study, a long-term (7 years) follow-up is also planned to assess the effectiveness of the intervention on the incidence of major adverse CV events. A series of ancillary studies designed to evaluate the effect of the mHealth intervention on additional risk biomarkers are also performed.Ethics and dissemination This study received ethics approval from the ethics committee of the coordinating centre (Monzino Cardiology Center; R1256/20-CCM 1319) and from all other relevant IRBs and ethics committees. Findings are disseminated through scientific meetings and peer-reviewed journals and via social media. Partners are informed about the study’s course and findings through regular meetings.Trial registration number NCT05339841.
Published: 2023
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18. Time-Trends in Air Pollution Impact on Health in Italy, 1990–2019: An Analysis From the Global Burden of Disease Study 2019

Author: Sara Conti, Carla Fornari, Pietro Ferrara, Ippazio C. Antonazzo, Fabiana Madotto, Eugenio Traini, Miriam Levi, Achille Cernigliaro, Benedetta Armocida, Nicola L. Bragazzi, Ennio Cadum, Michele Carugno, Giacomo Crotti, Silvia Deandrea, Paolo A. Cortesi, Davide Guido, Ivo Iavicoli, Sergio Iavicoli, Carlo La Vecchia, Paolo Lauriola, Paola Michelozzi, Salvatore Scondotto, Massimo Stafoggia, Francesco S. Violante, Cristiana Abbafati, Luciana Albano, Francesco Barone-Adesi, Antonio Biondi, Cristina Bosetti, Danilo Buonsenso, Giulia Carreras, Giulio Castelpietra, Alberico Catapano, Maria S. Cattaruzza, Barbara Corso, Giovanni Damiani, Francesco Esposito, Silvano Gallus, Davide Golinelli, Simon I. Hay, Gaetano Isola, Caterina Ledda, Stefania Mondello, Paolo Pedersini, Umberto Pensato, Norberto Perico, Giuseppe Remuzzi, Francesco Sanmarchi, Rocco Santoro, Biagio Simonetti, Brigid Unim, Marco Vacante, Massimiliano Veroux, Jorge H. Villafañe, Lorenzo Monasta, and Lorenzo G. Mantovani
Subjects: air pollution, particulate matter, ozone, global burden of disease, air quality regulations, Public aspects of medicine, RA1-1270
Abstract: Objectives: We explored temporal variations in disease burden of ambient particulate matter 2.5 μm or less in diameter (PM2.5) and ozone in Italy using estimates from the Global Burden of Disease Study 2019.Methods: We compared temporal changes and percent variations (95% Uncertainty Intervals [95% UI]) in rates of disability adjusted life years (DALYs), years of life lost, years lived with disability and mortality from 1990 to 2019, and variations in pollutant-attributable burden with those in the overall burden of each PM2.5- and ozone-related disease.Results: In 2019, 467,000 DALYs (95% UI: 371,000, 570,000) were attributable to PM2.5 and 39,600 (95% UI: 18,300, 61,500) to ozone. The crude DALY rate attributable to PM2.5 decreased by 47.9% (95% UI: 10.3, 65.4) from 1990 to 2019. For ozone, it declined by 37.0% (95% UI: 28.9, 44.5) during 1990–2010, but it increased by 44.8% (95% UI: 35.5, 56.3) during 2010–2019. Age-standardized rates declined more than crude ones.Conclusion: In Italy, the burden of ambient PM2.5 (but not of ozone) significantly decreased, even in concurrence with population ageing. Results suggest a positive impact of air quality regulations, fostering further regulatory efforts.
Published: 2023
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19. Post-translational modifications by SIRT3 de-2-hydroxyisobutyrylase activity regulate glycolysis and enable nephrogenesis

Author: Luca Perico, Marina Morigi, Anna Pezzotta, Daniela Corna, Valerio Brizi, Sara Conti, Cristina Zanchi, Fabio Sangalli, Piera Trionfini, Sara Buttò, Christodoulos Xinaris, Susanna Tomasoni, Carlamaria Zoja, Giuseppe Remuzzi, Ariela Benigni, and Barbara Imberti
Subjects: Medicine, Science
Abstract: Abstract Abnormal kidney development leads to lower nephron number, predisposing to renal diseases in adulthood. In embryonic kidneys, nephron endowment is dictated by the availability of nephron progenitors, whose self-renewal and differentiation require a relatively repressed chromatin state. More recently, NAD+-dependent deacetylase sirtuins (SIRTs) have emerged as possible regulators that link epigenetic processes to the metabolism. Here, we discovered a novel role for the NAD+-dependent deacylase SIRT3 in kidney development. In the embryonic kidney, SIRT3 was highly expressed only as a short isoform, with nuclear and extra-nuclear localisation. The nuclear SIRT3 did not act as deacetylase but exerted de-2-hydroxyisobutyrylase activity on lysine residues of histone proteins. Extra-nuclear SIRT3 regulated lysine 2-hydroxyisobutyrylation (Khib) levels of phosphofructokinase (PFK) and Sirt3 deficiency increased PFK Khib levels, inducing a glycolysis boost. This altered Khib landscape in Sirt3 −/− metanephroi was associated with decreased nephron progenitors, impaired nephrogenesis and a reduced number of nephrons. These data describe an unprecedented role of SIRT3 in controlling early renal development through the regulation of epigenetics and metabolic processes.
Published: 2021
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20. An ex vivo test to investigate genetic factors conferring susceptibility to atypical haemolytic uremic syndrome

Author: Sara Gastoldi, Sistiana Aiello, Miriam Galbusera, Matteo Breno, Marta Alberti, Elena Bresin, Caterina Mele, Rossella Piras, Lucia Liguori, Donata Santarsiero, Ariela Benigni, Giuseppe Remuzzi, and Marina Noris
Subjects: rare variants, aHUS, complement, endothelial cells, endothelial C5b-9 formation, Immunologic diseases. Allergy, RC581-607
Abstract: IntroductionComprehensive genetic analysis is essential to clinical care of patients with atypical haemolytic uremic syndrome (aHUS) to reinforce diagnosis, and to guide treatment. However, the characterization of complement gene variants remains challenging owing to the complexity of functional studies with mutant proteins. This study was designed: 1) To identify a tool for rapid functional determination of complement gene variants; 2) To uncover inherited complement dysregulation in aHUS patients who do not carry identified gene variants.MethodsTo address the above goals, we employed an ex-vivo assay of serum-induced C5b-9 formation on ADP-activated endothelial cells in 223 subjects from 60 aHUS pedigrees (66 patients and 157 unaffected relatives).ResultsSera taken from all aHUS patients in remission induced more C5b-9 deposition than control sera, independently from the presence of complement gene abnormalities. To avoid the possible confounding effects of chronic complement dysregulation related to aHUS status, and considering the incomplete penetrance for all aHUS-associated genes, we used serum from unaffected relatives. In control studies, 92.7% of unaffected relatives with known pathogenic variants exhibited positive serum-induced C5b-9 formation test, documenting a high sensitivity of the assay to identify functional variants. The test was also specific, indeed it was negative in all non-carrier relatives and in relatives with variants non-segregating with aHUS. All but one variants in aHUS-associated genes predicted in-silico as likely pathogenic or of uncertain significance (VUS) or likely benign resulted as pathogenic in the C5b-9 assay. At variance, variants in putative candidate genes did not exhibit a functional effect, with the exception of a CFHR5 variant. The C5b-9 assay in relatives was helpful in defining the relative functional effect of rare variants in 6 pedigrees in which the proband carried more than one genetic abnormality. Finally, for 12 patients without identified rare variants, the C5b-9 test in parents unmasked a genetic liability inherited from an unaffected parent.DiscussionIn conclusion, the serum-induced C5b-9 formation test in unaffected relatives of aHUS patients may be a tool for rapid functional evaluation of rare complement gene variants. When combined with exome sequencing the assay might be of help in variant selection, to identify new aHUS-associated genetic factors.
Published: 2023
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21. Long-term adaptive response in COVID-19 vaccine recipients and the effect of a booster dose

Author: Luca Perico, Marta Todeschini, Federica Casiraghi, Marilena Mister, Anna Pezzotta, Tobia Peracchi, Susanna Tomasoni, Piera Trionfini, Ariela Benigni, and Giuseppe Remuzzi
Subjects: COVID-19, SARS-CoV-2, Delta, Omicron, mRNA vaccine, neutralizing antibodies, Immunologic diseases. Allergy, RC581-607
Abstract: We examined the immune response in subjects previously infected with SARS-CoV2 and infection-naïve 9 months after primary 2-dose COVID-19 mRNA vaccination and 3 months after the booster dose in a longitudinal cohort of healthcare workers. Nine months after primary vaccination, previously infected subjects exhibited higher residual antibody levels, with significant neutralizing activity against distinct variants compared to infection-naïve subjects. The higher humoral response was associated with higher levels of receptor binding domain (RBD)-specific IgG+ and IgA+ memory B cells. The booster dose increased neither neutralizing activity, nor the B and T cell frequencies. Conversely, infection-naïve subjects needed the booster to achieve comparable levels of neutralizing antibodies as those found in previously infected subjects after primary vaccination. The neutralizing titer correlated with anti-RBD IFNγ producing T cells, in the face of sustained B cell response. Notably, pre-pandemic samples showed high Omicron cross-reactivity. These data show the importance of the booster dose in reinforcing immunological memory and increasing circulating antibodies in infection-naïve subjects.
Published: 2023
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22. CFH and CFHR structural variants in atypical Hemolytic Uremic Syndrome: Prevalence, genomic characterization and impact on outcome

Author: Rossella Piras, Elisabetta Valoti, Marta Alberti, Elena Bresin, Caterina Mele, Matteo Breno, Lucia Liguori, Roberta Donadelli, Miriam Rigoldi, Ariela Benigni, Giuseppe Remuzzi, and Marina Noris
Subjects: atypical hemolytic uremic syndrome (aHUS), eculizumab, factor H (FH), factor H-related proteins (FHRs), complement, copy number variations (CNVs), Immunologic diseases. Allergy, RC581-607
Abstract: IntroductionAtypical hemolytic uremic syndrome (aHUS) is a rare disease that manifests with microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure, and is associated with dysregulation of the alternative complement pathway. The chromosomal region including CFH and CFHR1-5 is rich in repeated sequences, favoring genomic rearrangements that have been reported in several patients with aHUS. However, there are limited data on the prevalence of uncommon CFH-CFHR genomic rearrangements in aHUS and their impact on disease onset and outcomes.MethodsIn this study, we report the results of CFH-CFHR Copy Number Variation (CNV) analysis and the characterization of resulting structural variants (SVs) in a large cohort of patients, including 258 patients with primary aHUS and 92 with secondary forms.ResultsWe found uncommon SVs in 8% of patients with primary aHUS: 70% carried rearrangements involving CFH alone or CFH and CFHR (group A; n=14), while 30% exhibited rearrangements including only CFHRs (group B; n=6). In group A, 6 patients presented CFH::CFHR1 hybrid genes, 7 patients carried duplications in the CFH-CFHR region that resulted either in the substitution of the last CFHR1 exon(s) with those of CFH (CFHR1::CFH reverse hybrid gene) or in an internal CFH duplication. In group A, the large majority of aHUS acute episodes not treated with eculizumab (12/13) resulted in chronic ESRD; in contrast, anti-complement therapy induced remission in 4/4 acute episodes. aHUS relapse occurred in 6/7 grafts without eculizumab prophylaxis and in 0/3 grafts with eculizumab prophylaxis. In group B, 5 subjects had the CFHR31-5::CFHR410 hybrid gene and one had 4 copies of CFHR1 and CFHR4. Compared with group A, patients in group B exhibited a higher prevalence of additional complement abnormalities and earlier disease onset. However, 4/6 patients in this group underwent complete remission without eculizumab treatment. In secondary forms we identified uncommon SVs in 2 out of 92 patients: the CFHR31-5::CFHR410 hybrid and a new internal duplication of CFH.DiscussionIn conclusion, these data highlight that uncommon CFH-CFHR SVs are frequent in primary aHUS and quite rare in secondary forms. Notably, genomic rearrangements involving the CFH are associated with a poor prognosis but carriers respond to anti-complement therapy.
Published: 2023
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23. Sirt3 deficiency promotes endothelial dysfunction and aggravates renal injury

Author: Anna Pezzotta, Luca Perico, Daniela Corna, Marina Morigi, Giuseppe Remuzzi, Ariela Benigni, and Barbara Imberti
Subjects: Medicine, Science
Published: 2023

24. Quando i medici sbagliano: E come discuterne in pubblico

Author: Giuseppe Remuzzi
Published: 2022

25. Low birth weight, nephron number and chronic kidney disease

Author: Dario Manfellotto, Monica Cortinovis, Norberto Perico, and Giuseppe Remuzzi
Subjects: Low birth weight, preterm birth, nephron number, chronic kidney disease., Medicine
Abstract: Chronic kidney diseases have a significant impact on morbidity and mortality worldwide. Low birth weight, fetal growth restriction and prematurity are indicators of fetal growth and development disorders associated with a congenital reduction in nephron number, which predisposes to an increased risk for chronic kidney disease. On an individual basis, a small nephron number at birth is not always enough to determine the onset of chronic kidney disease, but it decreases the ability of the kidneys to resist any insults to renal tissue that may occur later in life, such as exposure to nephrotoxic drugs or episodes of acute kidney injury. The high incidence of low birth weight and preterm birth globally suggests that, at the population level, the impact of alterations in fetal development on the subsequent onset of chronic kidney disease could be significant. The implementation of strategies aimed at reducing the incidence of prematurity, fetal growth restriction, as well as other conditions that lead to low birth weight and a reduced nephron number at birth, provides an opportunity to prevent the development of chronic kidney disease in adulthood. For these purposes the coordinated intervention of several specialists, including obstetricians, gynecologists, neonatologists, nephrologists, and family doctors, is necessary. Such strategies can be particularly useful in resource-poor countries, which are simultaneously burdened by maternal, fetal and child malnutrition; poor health; epidemics caused by communicable diseases; and little access to screening and primary care.
Published: 2022
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26. Drugs for the prevention and treatment of COVID-19 and its complications: An update on what we learned in the past 2 years

Author: Giuseppe Remuzzi, Stefano Schiaffino, Maria Gabriella Santoro, Garret A. FitzGerald, Gennaro Melino, and Carlo Patrono
Subjects: drugs, biologics, COVID-19, treatment, prevention, cell therapy, Therapeutics. Pharmacology, RM1-950
Abstract: The COVID-19 Committee of the Lincei Academy has reviewed the scientific evidence supporting the efficacy and safety of existing and new drugs/biologics for the preventing and treating of COVID-19 and its complications. This position paper reports what we have learned in the field in the past 2 years. The focus was on, but not limited to, drugs and neutralizing monoclonal antibodies, anti-SARS-CoV-2 agents, anti-inflammatory and immunomodulatory drugs, complement inhibitors and anticoagulant agents. We also discuss the risks/benefit of using cell therapies on COVID-19 patients. The report summarizes the available evidence, which supports recommendations from health authorities and panels of experts regarding some drugs and biologics, and highlights drugs that are not recommended, or drugs for which there is insufficient evidence to recommend for or against their use. We also address the issue of the safety of drugs used to treat underlying concomitant conditions in COVID-19 patients. The investigators did an enormous amount of work very quickly to understand better the nature and pathophysiology of COVID-19. This expedited the development and repurposing of safe and effective therapeutic interventions, saving an impressive number of lives in the community as well as in hospitals.
Published: 2022
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27. Sexual dimorphic response to rituximab treatment: A longitudinal observational study in a large cohort of patients with primary membranous nephropathy and persistent nephrotic syndrome

Author: Annalisa Perna, Barbara Ruggiero, Manuel Alfredo Podestà, Luca Perico, Silvia Orisio, Hanna Debiec, Giuseppe Remuzzi, and Piero Ruggenenti
Subjects: sex, membranous nephropathy, rituximab, nephrotic syndrome, remission, anti-PLA2R, Therapeutics. Pharmacology, RM1-950
Abstract: Rituximab is one of the first-line therapies for patients with membranous nephropathy (MN) at high risk of progression towards kidney failure. We investigated whether the response to Rituximab was affected by sex and anti-PLA2R antibody levels in 204 consecutive patients (148 males and 56 females) with biopsy-proven MN who were referred to the Nephrology Unit of the Azienda Socio Sanitaria Territoriale Papa Giovanni XXIII from March 2001 to October 2016 and managed conservatively for at least 6 months. The primary outcome was a combined endpoint of complete (proteinuria 50% reduction vs. baseline) remission. Patients gave written informed consent to Rituximab treatment. The study was internally funded. No pharmaceutical company was involved. Anti-PLA2R antibodies were detectable in 125 patients (61.3%). At multivariable analyses, female gender (p = 0.0198) and lower serum creatinine levels (p = 0.0108) emerged as independent predictors of better outcome (p = 0.0198). The predictive value of proteinuria (p = 0.054) and anti-PLA2R titer (p = 0.0766) was borderline significant. Over a median (IQR) of 24.8 (12.0–36.0) months, 40 females (71.4%) progressed to the combined endpoint compared with 73 males (49.3%). Anti-PLA2R titers at baseline [127.6 (35.7-310.8) vs. 110.1 (39.9–226.7) RU/ml] and after Rituximab treatment were similar between the sexes. However, the event rate was significantly higher in females than in males [HR (95%): 2.12 (1.44–3.12), p = 0.0001]. Forty-five of the 62 patients (72.3%) with anti-PLA2R titer below the median progressed to the combined endpoint versus 35 of the 63 (55.6%) with higher titer [HR (95%): 1.97 (1.26–3.07), p < 0.0029]. The highest probability of progressing to the combined endpoint was observed in females with anti-PLA2R antibody titer below the median (86.7%), followed by females with anti-PLA2R antibody titer above the median (83.3%), males with titer below the median (68.1%), and males with titer above the median (44.4%). This trend was statistically significant (p = 0.0023). Similar findings were observed for complete remission (proteinuria
Published: 2022
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28. Editorial: Insights in renal pharmacology: 2021

Author: Norberto Perico, Matthew D. Griffin, and Giuseppe Remuzzi
Subjects: chronic kidney disease, acute kidney disease, novel drugs, biologic agents, mechanistic targets, Therapeutics. Pharmacology, RM1-950
Published: 2022
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29. Amnion epithelial cells are an effective source of factor H and prevent kidney complement deposition in factor H-deficient mice

Author: Federica Casiraghi, Pamela Yossenaidy Rodriguez Ordonez, Nadia Azzollini, Marta Todeschini, Daniela Rottoli, Roberta Donadelli, Roberto Gramignoli, Ariela Benigni, Marina Noris, and Giuseppe Remuzzi
Subjects: Human amnion epithelial cells, Complement factor H, Complement alternative pathway, Renal glomeruli, Complement deposition, Medicine (General), R5-920, Biochemistry, QD415-436
Abstract: Abstract Complement factor H (FH) is the main plasma regulator of the alternative pathway of complement. Genetic and acquired abnormalities in FH cause uncontrolled complement activation amplifying, with the consequent accumulation of complement components on the renal glomeruli. This leads to conditions such as C3 glomerulopathy (C3G) and atypical hemolytic uremic syndrome (aHUS). There is no effective therapy for these diseases. Half of the patients progress to end-stage renal disease and the condition recurs frequently in transplanted kidneys. Combined liver/kidney transplantation is a valid option for these patients, but the risks of the procedure and donor organ shortages hamper its clinical application. Therefore, there is an urgent need for alternative strategies for providing a normal FH supply. Human amnion epithelial cells (hAEC) have stem cell characteristics, including the capability to differentiate into hepatocyte-like cells in vivo. Here, we administered hAEC into the livers of newborn Cfh −/− mice, which spontaneously developed glomerular complement deposition and renal lesions resembling human C3G. hAEC engrafted at low levels in the livers of Cfh −/− mice and produced sufficient human FH to prevent complement activation and glomerular C3 and C9 deposition. However, long-term engraftment was not achieved, and eventually hAEC elicited a humoral immune response in immunocompetent Cfh −/− mice. hAEC cell therapy could be a valuable therapeutic option for patients undergoing kidney transplantation in whom post-transplant immunosuppression may protect allogeneic hAEC from rejection, while allogeneic cells provide normal FH to prevent disease recurrence.
Published: 2021
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30. The European Rare Kidney Disease Registry (ERKReg): objectives, design and initial results

Author: Giulia Bassanese, Tanja Wlodkowski, Aude Servais, Laurence Heidet, Dario Roccatello, Francesco Emma, Elena Levtchenko, Gema Ariceta, Justine Bacchetta, Giovambattista Capasso, Augustina Jankauskiene, Marius Miglinas, Pietro Manuel Ferraro, Giovanni Montini, Jun Oh, Stephane Decramer, Tanja Kersnik Levart, Jack Wetzels, Elisabeth Cornelissen, Olivier Devuyst, Aleksandra Zurowska, Lars Pape, Anja Buescher, Dieter Haffner, Natasa Marcun Varda, Gian Marco Ghiggeri, Giuseppe Remuzzi, Martin Konrad, Germana Longo, Detlef Bockenhauer, Atif Awan, Ilze Andersone, Jaap W. Groothoff, and Franz Schaefer
Subjects: European Rare Kidney Disease Reference Network (ERKNet), Registry, Epidemiology, Nephrology, Pediatric nephrology, Medicine
Abstract: Abstract Background The European Rare Kidney Disease Reference Network (ERKNet) recently established ERKReg, a Web-based registry for all patients with rare kidney diseases. The main objectives of this core registry are to generate epidemiological information, identify current patient cohort for clinical research, explore diagnostic and therapeutic management practices, and monitor treatment performance and patient’s outcomes. The registry has a modular design that allows to integrate comprehensive disease-specific registries as extensions to the core database. The diagnosis (Orphacode) and diagnostic information (clinical, imaging, histopathological, biochemical, immunological and genetic) are recorded. Anthropometric, kidney function, and disease-specific management and outcome items informing a set of 61 key performance indicators (KPIs) are obtained annually. Data quality is ensured by automated plausibility checks upon data entry and regular offline database checks prompting queries. Centre KPI statistics and benchmarking are calculated automatically. Results Within the first 24 months since its launch, 7607 patients were enrolled to the registry at 45 pediatric and 12 specialized adult nephrology units from 21 countries. A kidney disease diagnosis had been established in 97.1% of these patients at time of enrolment. While 199 individual disease entities were reported by Orphacode, 50% of the cohort could be classified with 11, 80% with 43 and 95% with 92 codes. Two kidney diagnoses were assigned in 6.5% of patients; 5.9% suffered from syndromic disease. Whereas glomerulopathies (54.8%) and ciliopathies including autosomal dominant polycystic kidney disease (ADPKD) (31.5%) were the predominant disease groups among adults, the pediatric disease spectrum encompassed congenital anomalies of the kidney and urinary tract (CAKUT) (33.7%), glomerulopathies (30.7%), ciliopathies (14.0%), tubulopathies (9.2%), thrombotic microangiopathies (5.6%), and metabolic nephropathies (4.1%). Genetically confirmed diagnoses were reported in 24% of all pediatric and 12% adult patients, whereas glomerulopathies had been confirmed by kidney biopsy in 80.4% adult versus 38.5% pediatric glomerulopathy cases. Conclusions ERKReg is a rapidly growing source of epidemiological information and patient cohorts for clinical research, and an innovative tool to monitor management quality and patient outcomes.
Published: 2021
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31. Covid-19 and gender: lower rate but same mortality of severe disease in women—an observational study

Author: Federico Raimondi, Luca Novelli, Arianna Ghirardi, Filippo Maria Russo, Dario Pellegrini, Roberta Biza, Roberta Trapasso, Lisa Giuliani, Marisa Anelli, Mariangela Amoroso, Chiara Allegri, Gianluca Imeri, Claudia Sanfilippo, Sofia Comandini, England Hila, Leonardo Manesso, Lucia Gandini, Pietro Mandelli, Martina Monti, Mauro Gori, Michele Senni, Ferdinando Luca Lorini, Marco Rizzi, Tiziano Barbui, Laura Paris, Alessandro Rambaldi, Roberto Cosentini, Giulio Guagliumi, Simonetta Cesa, Michele Colledan, Maria Sessa, Arianna Masciulli, Antonello Gavazzi, Sabrina Buoro, Giuseppe Remuzzi, Piero Ruggenenti, Annapaola Callegaro, Andrea Gianatti, Claudio Farina, Antonio Bellasi, Sandro Sironi, Stefano Fagiuoli, Fabiano Di Marco, and HPG23 Covid-19 Study Group
Subjects: Covid-19, Gender, Disease severity, Diseases of the respiratory system, RC705-779
Abstract: Abstract Background Gender-related factors might affect vulnerability to Covid-19. The aim of this study was to describe the role of gender on clinical features and 28-day mortality in Covid-19 patients. Methods Observational study of Covid-19 patients hospitalized in Bergamo, Italy, during the first three weeks of the outbreak. Medical records, clinical, radiological and laboratory findings upon admission and treatment have been collected. Primary outcome was 28-day mortality since hospitalization. Results 431 consecutive adult patients were admitted. Female patients were 119 (27.6%) with a mean age of 67.0 ± 14.5 years (vs 67.8 ± 12.5 for males, p = 0.54). Previous history of myocardial infarction, vasculopathy and former smoking habits were more common for males. At the time of admission PaO2/FiO2 was similar between men and women (228 [IQR, 134–273] vs 238 mmHg [150–281], p = 0.28). Continuous Positive Airway Pressure (CPAP) assistance was needed in the first 24 h more frequently in male patients (25.7% vs 13.0%; p = 0.006). Overall 28-day mortality was 26.1% in women and 38.1% in men (p = 0.018). Gender did not result an independent predictor of death once the parameters related to disease severity at presentation were included in the multivariable analysis (p = 0.898). Accordingly, the Kaplan–Meier survival analysis in female and male patients requiring CPAP or non-invasive ventilation in the first 24 h did not find a significant difference (p = 0.687). Conclusion Hospitalized women are less likely to die from Covid-19; however, once severe disease occurs, the risk of dying is similar to men. Further studies are needed to better investigate the role of gender in clinical course and outcome of Covid-19.
Published: 2021
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32. Functional Magnetic Resonance Imaging Versus Kidney Biopsy to Assess Response to Therapy in Nephrotic Syndrome: A Case Report

Author: Anna Caroli, Andrea Remuzzi, Barbara Ruggiero, Camillo Carrara, Paola Rizzo, Paolo Brambilla, Piero Ruggenenti, and Giuseppe Remuzzi
Subjects: Magnetic resonance imaging, DWI, biomarkers, chronic kidney disease, kidney function recovery, case report, Diseases of the genitourinary system. Urology, RC870-923
Abstract: In recent years, kidney functional magnetic resonance imaging (MRI) has seen great advances, with several cross-sectional studies demonstrating correlations between MRI biomarkers and glomerular filtration rate. However, the potential of MRI to monitor response to therapy in kidney disease remains undescribed. In this case report, a man in his 40s with drug-resistant membranous nephropathy was addressed to ofatumumab therapy. He underwent kidney biopsy before and 2 years after treatment and repeat non–contrast-enhanced MRI of the kidney every 6 months. An age- and sex-matched healthy volunteer was included as a normal control. The patient showed a striking positive immunologic response to therapy. Repeat MRI of the kidney documented progressive kidney functional recovery, with a significant widespread increase in kidney diffusivity, assessed using diffusion-weighted imaging, paralleling the increase in glomerular filtration rate and regression of albuminuria. Renal blood flow and ultrafiltration coefficient, assessed using phase-contrast MRI, significantly increased, suggesting an increase in filtration fraction. This case report provides the first clinical evidence in support of MRI of the kidney as a tool to noninvasively monitor pathophysiologic changes occurring in response to treatment. Although kidney biopsy remains critical for diagnosis, functional MRI of the kidney has promise for monitoring disease progression and response to therapy.
Published: 2020
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33. Improving diagnosis for rare diseases: the experience of the Italian undiagnosed Rare diseases network

Author: Marco Salvatore, Agata Polizzi, Maria Chiara De Stefano, Giovanna Floridia, Simone Baldovino, Dario Roccatello, Savino Sciascia, Elisa Menegatti, Giuseppe Remuzzi, Erica Daina, Paraskevas Iatropoulos, Bruno Bembi, Rosalia Maria Da Riol, Alessandra Ferlini, Marcella Neri, Giuseppe Novelli, Federica Sangiuolo, Francesco Brancati, and Domenica Taruscio
Subjects: Undiagnosed, Rare diseases, Omics, Ontology, Diagnosis, Pediatrics, RJ1-570
Abstract: Abstract Background For a number of persons with rare diseases (RDs) a definite diagnosis remains undiscovered with relevant physical, psychological and social consequences. Undiagnosed RDs (URDs) require other than specialised clinical centres, outstanding molecular investigations, common protocols and dedicated actions at national and international levels; thus, many “Undiagnosed RDs programs” have been gradually developed on the grounds of a well-structured multidisciplinary approach. Methods The Italian Undiagnosed Rare Diseases Network (IURDN) was established in 2016 to improve the level of diagnosis of persons with URD living in Italy. Six Italian Centres of Expertise represented the network. The National Centre for Rare Diseases at the Istituto Superiore di Sanità coordinates the whole project. The software PhenoTips was used to collect the information of the clinical cases. Results One hundred and ten cases were analysed between March 2016 and June 2019. The age of onset of the diseases ranged from prenatal age to 51 years. Conditions were predominantly sporadic; almost all patients had multiple organs involvements. A total of 13/71 family cases were characterized by WES; in some families more than one individual was affected, so leading to 20/71 individuals investigated. Disease causing variants were identified in two cases and were associated to previously undescribed phenotypes. In 5 cases, new candidate genes were identified, although confirmatory tests are pending. In three families, investigations were not completed due to the scarce compliance of members and molecular investigations were temporary suspended. Finally, three cases (one familial) remain still unsolved. Twelve undiagnosed clinical cases were then selected to be shared at International level through PhenomeCentral in accordance to the UDNI statement. Conclusions Our results showed a molecular diagnostic yield of 53,8%; this value is comparable to the diagnostic rates reported in other international studies. Cases collected were also pooled with those collected by UDNI International Network. This represents a unique example of global initiative aimed at sharing and validating knowledge and experience in this field. IURDN is a multidisciplinary and useful initiative linking National and International efforts aimed at making timely and appropriate diagnoses in RD patients who still do not have a confirmed diagnosis even after a long time.
Published: 2020
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34. Kidney transplant tolerance associated with remote autologous mesenchymal stromal cell administration

Author: Federica Casiraghi, Norberto Perico, Eliana Gotti, Marta Todeschini, Marilena Mister, Monica Cortinovis, Valentina Portalupi, Anna Rita Plati, Flavio Gaspari, Alessandro Villa, Martino Introna, Elena Longhi, and Giuseppe Remuzzi
Subjects: immunoregulation, immunosuppression withdrawal, kidney transplantation, mesenchymal stromal cells, tolerance, Medicine (General), R5-920, Cytology, QH573-671
Abstract: Abstract Here we report the case of successful immune tolerance induction in a living‐donor kidney transplant recipient remotely treated with autologous bone marrow‐derived mesenchymal stromal cells (MSC). This case report, which to the best of our knowledge is the first in the world in this setting, provides evidence that the modulation of the host immune system with MSC can enable the safe withdrawal of maintenance immunosuppressive drugs while preserving optimal long‐term kidney allograft function.
Published: 2020
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35. A Home-Treatment Algorithm Based on Anti-inflammatory Drugs to Prevent Hospitalization of Patients With Early COVID-19: A Matched-Cohort Study (COVER 2)

Author: Elena Consolaro, Fredy Suter, Nadia Rubis, Stefania Pedroni, Chiara Moroni, Elena Pastò, Maria Vittoria Paganini, Grazia Pravettoni, Umberto Cantarelli, Norberto Perico, Annalisa Perna, Tobia Peracchi, Piero Ruggenenti, and Giuseppe Remuzzi
Subjects: COVID-19, SARS-CoV-2, hospitalization, outpatients, at home management, Medicine (General), R5-920
Abstract: Background and AimWhile considerable success has been achieved in the management of patients hospitalized with severe coronavirus disease 2019 (COVID-19), far less progress has been made with early outpatient treatment. We assessed whether the implementation of a home treatment algorithm—designed based on a pathophysiologic and pharmacologic rationale—and including non-steroidal anti-inflammatory drugs, especially relatively selective cyclooxygenase-2 inhibitors and, when needed, corticosteroids, anticoagulants, oxygen therapy and antibiotics—at the very onset of mild COVID-19 symptoms could effectively reduce hospital admissions.MethodsThis fully academic, matched-cohort study evaluated outcomes in 108 consecutive consenting patients with mild COVID-19, managed at home by their family doctors between January 2021 and May 2021, according to the proposed treatment algorithm and in 108 age-, sex-, and comorbidities-matched patients on other therapeutic schedules (ClinicalTrials.gov: NCT04854824). The primary outcome was COVID-19-related hospitalization. Analyses were by intention-to-treat.ResultsOne (0.9%) patient in the “recommended” cohort and 12 (11.1%) in the “control” cohort were admitted to hospital (P = 0.0136). The proposed algorithm reduced the cumulative length of hospital stays by 85% (from 141 to 19 days) as well as related costs (from €60.316 to €9.058). Only 9.8 patients needed to be treated with the recommended algorithm to prevent one hospitalization event. The rate of resolution of major symptoms was numerically—but not significantly—higher in the “recommended” than in the “control” cohort (97.2 vs. 93.5%, respectively; P = 0.322). Other symptoms lingered in a smaller proportion of patients in the “recommended” than in the “control” cohort (20.4 vs. 63.9%, respectively; P < 0.001), and for a shorter period.ConclusionThe adoption of the proposed outpatient treatment algorithm during the early, mild phase of COVID-19 reduced the incidence of subsequent hospitalization and related costs.
Published: 2022
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36. SARS-CoV-2 Spike Protein 1 Activates Microvascular Endothelial Cells and Complement System Leading to Platelet Aggregation

Author: Luca Perico, Marina Morigi, Miriam Galbusera, Anna Pezzotta, Sara Gastoldi, Barbara Imberti, Annalisa Perna, Piero Ruggenenti, Roberta Donadelli, Ariela Benigni, and Giuseppe Remuzzi
Subjects: COVID-19, SARS-CoV-2 spike protein 1, complement system, endothelial dysfunction, inflammation, thrombosis, Immunologic diseases. Allergy, RC581-607
Abstract: Microvascular thrombosis is associated with multiorgan failure and mortality in coronavirus disease 2019 (COVID-19). Although thrombotic complications may be ascribed to the ability of SARS-CoV-2 to infect and replicate in endothelial cells, it has been poorly investigated whether, in the complexity of viral infection in the human host, specific viral elements alone can induce endothelial damage. Detection of circulating spike protein in the sera of severe COVID-19 patients was evaluated by ELISA. In vitro experiments were performed on human microvascular endothelial cells from the derma and lung exposed to SARS-CoV-2-derived spike protein 1 (S1). The expression of adhesive molecules was studied by immunofluorescence and leukocyte adhesion and platelet aggregation were assessed under flow conditions. Angiotensin converting enzyme 2 (ACE2) and AMPK expression were investigated by Western Blot analysis. In addition, S1-treated endothelial cells were incubated with anti-ACE2 blocking antibody, AMPK agonist, or complement inhibitors. Our results show that significant levels of spike protein were found in the 30.4% of severe COVID-19 patients. In vitro, the activation of endothelial cells with S1 protein, via ACE2, impaired AMPK signalling, leading to robust leukocyte recruitment due to increased adhesive molecule expression and thrombomodulin loss. This S1-induced pro-inflammatory phenotype led to exuberant C3 and C5b-9 deposition on endothelial cells, along with C3a and C5a generation that further amplified S1-induced complement activation. Functional blockade of ACE2 or complement inhibition halted S1-induced platelet aggregates by limiting von Willebrand factor and P-selectin exocytosis and expression on endothelial cells. Overall, we demonstrate that SARS-CoV-2-derived S1 is sufficient in itself to propagate inflammatory and thrombogenic processes in the microvasculature, amplified by the complement system, recapitulating the thromboembolic complications of COVID-19.
Published: 2022
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37. Covid: prevenire, curare, conviverci: Tutte le risposte dell'Istituto Mario Negri

Author: Antonio Clavenna, Giuseppe Remuzzi, Arrigo Schieppati
Published: 2021

38. Global fertility in 204 countries and territories, 1950-2021, with forecasts to 2100: a comprehensive demographic analysis for the Global Burden of Disease Study 2021

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Puvvula, Nameer Hashim Qasim, Ibrahim Qattea, Deepthi R, Mehrdad Rabiee Rad, Amir Radfar, Venkatraman Radhakrishnan, Pourya Raee, Hadi Raeisi Shahraki, Alireza Rafiei, Seyedeh Niloufar Rafiei Alavi, Cat Raggi, Pankaja Raghav Raghav, Fakher Rahim, Md Jillur Rahim, Md Mosfequr Rahman, Mohammad Hifz Ur Rahman, Mosiur Rahman, Muhammad Aziz Rahman, Vahid Rahmanian, Masoud Rahmati, Niloufar Rahnavard, Pramila Rai, Diego Raimondo, Ali Rajabpour-Sanati, Prashant Rajput, Prasanna Ram, Shakthi Kumaran Ramasamy, Juwel Rana, Kritika Rana, Shailendra Singh Rana, Chhabi Lal Ranabhat, Nemanja Rancic, Amey Rane, Shubham Ranjan, Chythra R Rao, Indu Ramachandra Rao, Deepthi Rapaka, Davide Rasella, Sina Rashedi, Vahid Rashedi, Mohammad-Mahdi Rashidi, Azad Rasul, Zubair Ahmed Ratan, Giridhara Rathnaiah Babu, Santosh Kumar Rauniyar, Nakul Ravikumar, David Laith Rawaf, Salman Rawaf, Reza Rawassizadeh, Bharat Rawlley, Murali Mohan Rama Krishna Reddy, Elrashdy Moustafa Mohamed Redwan, Giuseppe Remuzzi, Bhageerathy Reshmi, Nazila Rezaei, Aida Rezaei Nejad, Mohsen Rezaeian, Abanoub Riad, Mavra A Riaz, Jennifer Rickard, Reza Rikhtegar, Hannah Elizabeth Robinson-Oden, Célia Fortuna Rodrigues, Jefferson Antonio Buendia Rodriguez, Ravi Rohilla, Debby Syahru Romadlon, Luca Ronfani, Himanshu Sekhar Rout, Bedanta Roy, Nitai Roy, Priyanka Roy, Enrico Rubagotti, Guilherme de Andrade Ruela, Susan Fred Rumisha, Tilleye Runghien, Manjula S, Chandan S N, Aly M A Saad, Zahra Saadatian, Maha Mohamed Saber-Ayad, Morteza SaberiKamarposhti, Siamak Sabour, Fatos Sada, Basema Saddik, Bashdar Abuzed Sadee, Ehsan Sadeghi, Erfan Sadeghi, Mohammad Reza Saeb, Umar Saeed, Sher Zaman Safi, Dominic Sagoe, Manika Saha, Amirhossein Sahebkar, Soumya Swaroop Sahoo, Monalisha Sahu, Zahra Saif, Joseph W Sakshaug, Payman Salamati, Afeez Abolarinwa Salami, Mohamed A Saleh, Marwa Rashad Salem, Mohammed Z Y Salem, Sohrab Salimi, Sara Samadzadeh, Yoseph Leonardo Samodra, Vijaya Paul Samuel, Abdallah M Samy, Juan Sanabria, Nima Sanadgol, Francesca Sanna, Milena M Santric-Milicevic, Haaris Saqib, Sivan Yegnanarayana Iyer Saraswathy, Aswini Saravanan, Babak Saravi, Yaser Sarikhani, Tanmay Sarkar, Rodrigo Sarmiento-Suárez, Gargi Sachin Sarode, Sachin C Sarode, Arash Sarveazad, Brijesh Sathian, Thirunavukkarasu Sathish, Anudeep Sathyanarayan, Abu Sayeed, Md Abu Sayeed, Nikolaos Scarmeas, Winfried Schlee, Art Schuermans, David C Schwebel, Falk Schwendicke, Siddharthan Selvaraj, Pallav Sengupta, Subramanian Senthilkumaran, Sadaf G Sepanlou, Dragos Serban, Edson Serván-Mori, Yashendra Sethi, SeyedAhmad SeyedAlinaghi, Seyed Arsalan Seyedi, Allen Seylani, Mahan Shafie, Jaffer Shah, Pritik A Shah, Ataollah Shahbandi, Samiah Shahid, Moyad Jamal Shahwan, Ahmed Shaikh, Masood Ali Shaikh, Muhammad Aaqib Shamim, Mehran Shams-Beyranvand, Mohammad Anas Shamsi, Mohd Shanawaz, Abhishek Shankar, Mohammed Shannawaz, Medha Sharath, Sadaf Sharfaei, Amin Sharifan, Javad Sharifi-Rad, Manoj Sharma, Rajesh Sharma, Ujjawal Sharma, Vishal Sharma, Rajesh P Shastry, Amin Shavandi, David H Shaw, Amir Mehdi Shayan, Maryam Shayan, Amr Mohamed Elsayed Shehabeldine, Aziz Sheikh, Rahim Ali Sheikhi, Manjunath Mala Shenoy, Pavanchand H Shetty, Peilin Shi, Desalegn Shiferaw, Mika Shigematsu, Rahman Shiri, Reza Shirkoohi, Aminu Shittu, Velizar Shivarov, Farhad Shokraneh, Sina Shool, Seyed Afshin Shorofi, Kanwar Hamza Shuja, Kerem Shuval, Emmanuel Edwar Siddig, João Pedro Silva, Luís Manuel Lopes Rodrigues Silva, Soraia Silva, Biagio Simonetti, Anjali Singal, Abhinav Singh, Balbir Bagicha Singh, Jasvinder A Singh, Md Shahjahan Siraj, Georgia Smith, Bogdan Socea, Anton Sokhan, Ranjan Solanki, Shipra Solanki, Hamidreza Soleimani, Sameh S M Soliman, Yonatan Solomon, Yimeng Song, Reed J D Sorensen, Michael Spartalis, Chandrashekhar T Sreeramareddy, Vijay Kumar Srivastava, Muhammad Haroon Stanikzai, Vladimir I Starodubov, Antonina V Starodubova, Simona Cătălina Stefan, Paschalis Steiropoulos, Mark A Stokes, Vetriselvan Subramaniyan, Muhammad Suleman, Rizwan Suliankatchi Abdulkader, Abida Sultana, Jing Sun, Chandan Kumar Swain, Bryan L Sykes, Lukasz Szarpak, Mindy D Szeto, Miklós Szócska, Payam Tabaee Damavandi, Rafael Tabarés-Seisdedos, Ozra Tabatabaei Malazy, Seyed-Amir Tabatabaeizadeh, Shima Tabatabai, Karen M Tabb, Mohammad Tabish, Moslem Taheri Soodejani, Jabeen Taiba, Ardeshir Tajbakhsh, Iman M Talaat, Ashis Talukder, Mircea Tampa, Jacques Lukenze Tamuzi, Ker-Kan Tan, Haosu Tang, Derbie Alemu DA Tareke, Mengistie Kassahun Tariku, Vivian Y Tat, Seyed Mohammad Tavangar, Mojtaba Teimoori, Mohamad-Hani Temsah, Reem Mohamad Hani Temsah, Masayuki Teramoto, Dufera Rikitu Terefa, Riki Tesler, Enoch Teye-Kwadjo, Ramna Thakur, Pugazhenthan Thangaraju, Kavumpurathu Raman Thankappan, Rekha Thapar, Samar Tharwat, Rasiah Thayakaran, Nihal Thomas, Ales Tichopad, Jansje Henny Vera Ticoalu, Tenaw Yimer Tiruye, Mariya Vladimirovna Titova, Marcello Tonelli, Marcos Roberto Tovani-Palone, Eugenio Traini, Jasmine T Tran, Nghia Minh Tran, Indang Trihandini, Samuel Joseph Tromans, Thien Tan Tri Tai Truyen, Aristidis Tsatsakis, Evangelia Eirini Tsermpini, Munkhtuya Tumurkhuu, Stefanos Tyrovolas, Sayed Mohammad Nazim Uddin, Aniefiok John Udoakang, Arit Udoh, Atta Ullah, Saeed Ullah, Sana Ullah, Srikanth Umakanthan, Chukwuma David Umeokonkwo, Brigid Unim, Bhaskaran Unnikrishnan, Era Upadhyay, Jibrin Sammani Usman, Marco Vacante, Seyed Mohammad Vahabi, Asokan Govindaraj Vaithinathan, Rohollah Valizadeh, Jef Van den Eynde, Elena Varavikova, Orsolya Varga, Priya Vart, Shoban Babu Varthya, Tommi Juhani Vasankari, Balachandar Vellingiri, Deneshkumar Venugopal, Nicholas Alexander Verghese, Madhur Verma, Massimiliano Veroux, Georgios-Ioannis Verras, Dominique Vervoort, Jorge Hugo Villafañe, Manish Vinayak, Francesco S Violante, Mukesh Vishwakarma, Sergey Konstantinovitch Vladimirov, Vasily Vlassov, Bay Vo, Simona Ruxandra Volovat, Theo Vos, Isidora S Vujcic, Hatem A Wafa, Yasir Waheed, Elias Bekele Wakwoya, Cong Wang, Denny Wang, Fang Wang, Shu Wang, Yanzhong Wang, Yuan-Pang Wang, Paul Ward, Emebet Gashaw Wassie, Stefanie Watson, Marcia R Weaver, Kosala Gayan Weerakoon, Daniel J Weiss, Katherine M Wells, Yi Feng Wen, Ronny Westerman, Taweewat Wiangkham, Dakshitha Praneeth Wickramasinghe, Nuwan Darshana Wickramasinghe, Peter Willeit, Yohannes Addisu Wondimagegene, Felicia Wu, Juan Xia, Hong Xiao, Gelin Xu, Suowen Xu, Xiaoyue Xu, Ali Yadollahpour, Shirin Yaghoobpoor, Tina Yaghoobpour, Sajad Yaghoubi, Zwanden Sule Yahaya, Danting Yang, Lin Yang, Yuichiro Yano, Habib Yaribeygi, Pengpeng Ye, Renjulal Yesodharan, Subah Abderehim Yesuf, Saber Yezli, Amanuel Yigezu, Paul Yip, Dong Keon Yon, Naohiro Yonemoto, Yuyi You, Mustafa Z Younis, Zabihollah Yousefi, Chuanhua Yu, Yong Yu, Chun-Wei Yuan, Nima Zafari, Fathiah Zakham, Nazar Zaki, Giulia Zamagni, Milad Zandi, Ghazal G Z Zandieh, Moein Zangiabadian, Mikhail Sergeevich Zastrozhin, Haijun Zhang, Meixin Zhang, Yunquan Zhang, Chenwen Zhong, Juexiao Zhou, Bin Zhu, Lei Zhu, Magdalena Zielińska, Zhiyong Zou, Samer H Zyoud, Christopher J L Murray, Amanda E Smith, and Stein Emil Vollset
Abstract: Background: Accurate assessments of current and future fertility-including overall trends and changing population age structures across countries and regions-are essential to help plan for the profound social, economic, environmental, and geopolitical challenges that these changes will bring. Estimates and projections of fertility are necessary to inform policies involving resource and health-care needs, labour supply, education, gender equality, and family planning and support. The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2021 produced up-to-date and comprehensive demographic assessments of key fertility indicators at global, regional, and national levels from 1950 to 2021 and forecast fertility metrics to 2100 based on a reference scenario and key policy-dependent alternative scenarios. Methods: To estimate fertility indicators from 1950 to 2021, mixed-effects regression models and spatiotemporal Gaussian process regression were used to synthesise data from 8709 country-years of vital and sample registrations, 1455 surveys and censuses, and 150 other sources, and to generate age-specific fertility rates (ASFRs) for 5-year age groups from age 10 years to 54 years. ASFRs were summed across age groups to produce estimates of total fertility rate (TFR). Livebirths were calculated by multiplying ASFR and age-specific female population, then summing across ages 10-54 years. To forecast future fertility up to 2100, our Institute for Health Metrics and Evaluation (IHME) forecasting model was based on projections of completed cohort fertility at age 50 years (CCF50; the average number of children born over time to females from a specified birth cohort), which yields more stable and accurate measures of fertility than directly modelling TFR. CCF50 was modelled using an ensemble approach in which three sub-models (with two, three, and four covariates variously consisting of female educational attainment, contraceptive met need, population density in
Published: 2024

39. Case Report: Tackling Complement Hyperactivation With Eculizumab in Atypical Hemolytic Uremic Syndrome Triggered by COVID-19

Author: Valentina Fanny Leone, Amantia Imeraj, Sara Gastoldi, Caterina Mele, Lucia Liguori, Carmelita Condemi, Piero Ruggenenti, Giuseppe Remuzzi, and Camillo Carrara
Subjects: eculizumab, coronavirus disease 2019 (COVID-19), severe acute respiratory syndrome coronavirus-2 (SARS-Cov-2), thrombotic microangiopathy, hemolytic uremic syndrome, Therapeutics. Pharmacology, RM1-950
Abstract: Hemolytic uremic syndrome (HUS) is a rare life-threatening disease of unrestrained complement system dysregulation, microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure in genetically predisposed individuals. In this report, we describe two cases of SARS-CoV-2–associated HUS treated with eculizumab, a C5-blocking monoclonal antibody reported to be remarkably effective in the treatment of HUS. Detailed biochemical and genetic complement system analysis is reported, and the prompt clinical response after C5 pharmacological blockade is documented. Our report provides the rationale and supports the use of terminal complement pathway inhibition for the treatment of SARS-CoV-2–associated HUS.
Published: 2022
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40. Nephrotic-range proteinuria in type 2 diabetes: Effects of empagliflozin on kidney disease progression and clinical outcomes

Author: Piero Ruggenenti, Bettina J. Kraus, Silvio E. Inzucchi, Bernard Zinman, Stefan Hantel, Michaela Mattheus, Maximilian von Eynatten, Giuseppe Remuzzi, Audrey Koitka-Weber, and Christoph Wanner
Subjects: Type 2 diabetes, Empagliflozin, SGLT2 inhibitor, Kidney disease, Nephrotic, Proteinuria, Medicine (General), R5-920
Abstract: Summary: Background: Diabetic kidney disease with nephrotic-range proteinuria (NRP) is commonly associated with rapid kidney function loss, increased cardiovascular risk, and premature mortality. We explored the effect of empagliflozin in patients with type 2 diabetes and cardiovascular disease, complicated by presence of this major risk factor for progressive kidney disease, in a post-hoc analysis of data from the EMPA-REG OUTCOME trial (NCT01131676). Methods: Cox proportional hazards models were used to investigate the risk of cardiovascular and kidney outcomes in participants with and without NRP, defined by urine albumin-to-creatinine ratio (UACR) ≥2200 mg/g at baseline. Annual loss of eGFR during chronic treatment (eGFR slopes) and hypothetical time to projected end-stage kidney disease (ESKD), conditioning upon linearity of eGFR change over time if a patient did not decease before projected ESKD, were calculated using a random-intercept random-coefficient model. Safety was described based on investigator-reported adverse events. Findings: 112 participants (pooled empagliflozin, n = 70; placebo, n = 42; median on-treatment follow-up of 1·9 years on placebo compared with 2·3 years on empagliflozin) presented with NRP at baseline; eGFR and UACR were balanced between treatments. Empagliflozin benefits on cardiovascular death, hospitalisation for heart failure, or kidney outcomes, were consistent in participants with and without NRP (pinteraction >0·1). Treatment effects of empagliflozin on adjusted annual mean eGFR slope were more pronounced in participants with NRP versus those without (pinteraction 0·005). Empagliflozin was estimated to double the median hypothetical time to projected ESKD in participants with NRP. The overall safety profile of empagliflozin was comparable between participants with and without NRP at baseline. Interpretation: Our data suggests that empagliflozin might slow kidney function loss and delay the estimated onset of projected ESKD in patients with type 2 diabetes and cardiovascular disease complicated by NRP.
Published: 2022
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41. Fresh lemon juice supplementation for the prevention of recurrent stones in calcium oxalate nephrolithiasis: A pragmatic, prospective, randomised, open, blinded endpoint (PROBE) trial

Author: Piero Ruggenenti, Maria Rosa Caruso, Monica Cortinovis, Annalisa Perna, Tobia Peracchi, Giovanni Antonio Giuliano, Stefano Rota, Paolo Brambilla, Giuliana Invernici, Davide Villa, Olimpia Diadei, Matias Trillini, Grazia Natali, and Giuseppe Remuzzi
Subjects: Nephrolithiasis, Kidney stones, Calcium oxalate, Juice supplementation, Medicine (General), R5-920
Abstract: Summary: Background: Standard diet with normal calcium and reduced animal proteins and salt content reduces stone recurrence in calcium oxalate nephrolithiasis. Whether lemon juice supplementation further reduces recurrence rate is unknown. Methods: In this single-centre, prospective, randomised, open, blinded endpoint trial (Clinical Trials gov NCT01217372) we evaluated the effects of fresh lemon juice supplementation (60 mL twice daily) versus no supplementation, on time to stone recurrence in 203 patients with recurrent idiopathic calcium oxalate nephrolithiasis who were all prescribed a standard diet. Patients were included between July 2009 and March 2017 at the Nephrology Unit of the Papa Giovanni XXIII hospital in Bergamo, Italy. Time to stone recurrence at 2 years of follow-up was the primary outcome. Analyses were by intention-to-treat. Findings: During two years of follow-up 21 of 100 patients randomised to lemon juice supplementation and 32 of 103 controls randomised to no supplementation had stone recurrence [HR (95% CI): 0·62 (0·35–1·07), p = 0·089]. Patient adherence to lemon juice supplementation, however, progressively decreased from 68% at one-year to 48% at two-year follow-up. At explorative analyses restricted at one-year follow-up, ten patients with supplementation versus 22 controls had stone recurrence [0·43 (0·20–0·89), p = 0·028]. After adjustment by age, sex and normo or hypocitraturia, the HR (95%) was still significant [0·45 (0·20–0·93), p = 0·036]. At six months, 24 hour urinary sodium excretion decreased by 8·60±65·68 mEq/24 h in patients receiving lemon juice supplementation and increased by 3·88±64·78 mEq/24 h in controls. Changes significantly differed between groups (p = 0·031). This difference was subsequently lost. Treatment was safe. In patients with lemon juice supplementation gastrointestinal disorders were more frequent (p
Published: 2022
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42. Low Nephron Number Induced by Maternal Protein Restriction Is Prevented by Nicotinamide Riboside Supplementation Depending on Sirtuin 3 Activation

Author: Anna Pezzotta, Luca Perico, Marina Morigi, Daniela Corna, Monica Locatelli, Carlamaria Zoja, Ariela Benigni, Giuseppe Remuzzi, and Barbara Imberti
Subjects: renal development, fetal programming, glomerular number, low protein diet, sirtuin 3, mitochondria, Cytology, QH573-671
Abstract: A reduced nephron number at birth, due to critical gestational conditions, including maternal malnutrition, is associated with the risk of developing hypertension and chronic kidney disease in adulthood. No interventions are currently available to augment nephron number. We have recently shown that sirtuin 3 (SIRT3) has an important role in dictating proper nephron endowment. The present study explored whether SIRT3 stimulation, by means of supplementation with nicotinamide riboside (NR), a precursor of the SIRT3 co-substrate nicotinamide adenine dinucleotide (NAD+), was able to improve nephron number in a murine model of a low protein (LP) diet. Our findings show that reduced nephron number in newborn mice (day 1) born to mothers fed a LP diet was associated with impaired renal SIRT3 expression, which was restored through supplementation with NR. Glomerular podocyte density, as well as the rarefaction of renal capillaries, also improved through NR administration. In mechanistic terms, the restoration of SIRT3 expression through NR was mediated by the induction of proliferator-activated receptor γ (PPARγ) coactivator-1α (PGC-1α). Moreover, NR restored SIRT3 activity, as shown by the reduction of the acetylation of optic atrophy 1 (OPA1) and superoxide dismutase 2 (SOD2), which resulted in improved mitochondrial morphology and protection against oxidative damage in mice born to mothers fed the LP diet. Our results provide evidence that it is feasible to prevent nephron mass shortage at birth through SIRT3 boosting during nephrogenesis, thus providing a therapeutic option to possibly limit the long-term sequelae of reduced nephron number in adulthood.
Published: 2022
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43. Human iPSC-derived neural crest stem cells can produce EPO and induce erythropoiesis in anemic mice

Author: Valerio Brizi, Sara Buttò, Domenico Cerullo, Angelo Michele Lavecchia, Raquel Rodrigues-Diez, Rubina Novelli, Daniela Corna, Ariela Benigni, Giuseppe Remuzzi, and Christodoulos Xinaris
Subjects: Pluripotent stem cells, Neural crest cells, Erythropoietin, Anemia, Erythropoiesis, Biology (General), QH301-705.5
Abstract: Inadequate production of erythropoietin (EPO) leads to anemia. Although erythropoiesis-stimulating agents can be used to treat anemia, these approaches are limited by high costs, adverse effects, and the need for frequent injections. Developing methods for the generation and transplantation of EPO-producing cells would allow for the design of personalized and complication-free therapeutic solutions. In mice, the first EPO source are neural crest cells (NCCs), which ultimately migrate to the fetal kidney to differentiate into EPO-producing fibroblasts. In humans however, it remains unknown whether NCCs can produce EPO in response to hypoxia. Here, we developed a new protocol to differentiate human induced pluripotent stem cells (hiPSCs) into NCCs and showed that cthese cells can produce functional EPO that can induce human CD34+ hematopoietic progenitor differentiation into erythroblasts in vitro. Moreover, we showed that hiPSC-derived NCCs can be embedded in clinical-grade atelocollagen scaffolds and subcutaneously transplanted into anemic mice to produce human EPO, accelerate hematocrit recovery, and induce erythropoiesis in the spleen. Our findings provide unprecedented evidence of the ability of human NCCs to produce functional EPO in response to hypoxia, and proof-of-concept for the potential clinical use of NCC-containing scaffolds as cell therapy for renal and non-renal anemia.
Published: 2021
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44. Preventing microalbuminuria with benazepril, valsartan, and benazepril-valsartan combination therapy in diabetic patients with high-normal albuminuria: A prospective, randomized, open-label, blinded endpoint (PROBE) study.

Author: Piero Ruggenenti, Monica Cortinovis, Aneliya Parvanova, Matias Trillini, Ilian P Iliev, Antonio C Bossi, Antonio Belviso, Maria C Aparicio, Roberto Trevisan, Stefano Rota, Annalisa Perna, Tobia Peracchi, Nadia Rubis, Davide Martinetti, Silvia Prandini, Flavio Gaspari, Fabiola Carrara, Salvatore De Cosmo, Giancarlo Tonolo, Ruggero Mangili, Giuseppe Remuzzi, and VARIETY Study Organization
Subjects: Medicine
Abstract: BackgroundAngiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) prevent microalbuminuria in normoalbuminuric type 2 diabetic patients. We assessed whether combined therapy with the 2 medications may prevent microalbuminuria better than ACE inhibitor or ARB monotherapy.Methods and findingsVARIETY was a prospective, randomized, open-label, blinded endpoint (PROBE) trial evaluating whether, at similar blood pressure (BP) control, combined therapy with benazepril (10 mg/day) and valsartan (160 mg/day) would prevent microalbuminuria more effectively than benazepril (20 mg/day) or valsartan (320 mg/day) monotherapy in 612 type 2 diabetic patients with high-normal albuminuria included between July 2007 and April 2013 by the Istituto di Ricerche Farmacologiche Mario Negri IRCCS and 8 diabetology or nephrology units in Italy. Time to progression to microalbuminuria was the primary outcome. Analyses were intention to treat. Baseline characteristics were similar among groups. During a median [interquartile range, IQR] follow-up of 66 [42 to 83] months, 53 patients (27.0%) on combination therapy, 57 (28.1%) on benazepril, and 64 (31.8%) on valsartan reached microalbuminuria. Using an accelerated failure time model, the estimated acceleration factors were 1.410 (95% CI: 0.806 to 2.467, P = 0.229) for benazepril compared to combination therapy, 0.799 (95% CI: 0.422 to 1.514, P = 0.492) for benazepril compared to valsartan, and 1.665 (95% CI: 1.007 to 2.746, P = 0.047) for valsartan compared to combination therapy. Between-group differences in estimated acceleration factors were nonsignificant after adjustment for predefined confounders. BP control was similar across groups. All treatments were safe and tolerated well, with a slight excess of hyperkalemia and hypotension in the combination therapy group. The main study limitation was the lower than expected albuminuria at inclusion.ConclusionsRisk/benefit profile of study treatments was similar. Dual renin-angiotensin system (RAS) blockade is not recommended as compared to benazepril or valsartan monotherapy for prevention of microalbuminuria in normoalbuminuric type 2 diabetic patients.Trial registrationEudraCT 2006-005954-62; ClinicalTrials.gov NCT00503152.
Published: 2021
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45. A simple, home-therapy algorithm to prevent hospitalisation for COVID-19 patients: A retrospective observational matched-cohort study

Author: Fredy Suter, Elena Consolaro, Stefania Pedroni, Chiara Moroni, Elena Pastò, Maria Vittoria Paganini, Grazia Pravettoni, Umberto Cantarelli, Nadia Rubis, Norberto Perico, Annalisa Perna, Tobia Peracchi, Piero Ruggenenti, and Giuseppe Remuzzi
Subjects: COVID-19, SARS-CoV-2, Simple home-therapy algorithm, Matched-cohort observational study, Family physicians, Early symptoms at home, Medicine (General), R5-920
Abstract: Background: Effective home treatment algorithms implemented based on a pathophysiologic and pharmacologic rationale to accelerate recovery and prevent hospitalisation of patients with early coronavirus disease 2019 (COVID-19) would have major implications for patients and health system. Methods: This academic, matched-cohort study compared outcomes of 90 consecutive consenting patients with mild COVID-19 treated at home by their family physicians between October 2020 and January 2021 in Northern and Central Italy, according to the proposed recommendation algorithm, with outcomes for 90 age-, sex-, and comorbidities-matched patients who received other therapeutic regimens. Primary outcome was time to resolution of major symptoms. Secondary outcomes included prevention of hospitalisation. Analyses were by intention-to-treat. Findings: All patients achieved complete remission. The median [IQR] time to resolution of major symptoms was 18 [14–23] days in the ‘recommended schedule' cohort and 14 [7–30] days in the matched ‘control’ cohort (p = 0·033). Other symptoms persisted in a lower percentage of patients in the ‘recommended’ than in the ‘control’ cohort (23·3% versus 73·3%, respectively, p90%. Interpretation: Implementation of an early home treatment algorithm failed to accelerate recovery from major symptoms of COVID-19, but reduced the risk of hospitalisation and related treatment costs. Given the study design, additional research would be required to consolidate the proposed treatment recommendations. Funding: Fondazione Cav.Lav. Carlo Pesenti
Published: 2021
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46. Case Report: Effects of Anti-SARS-CoV-2 Convalescent Antibodies Obtained With Double Filtration Plasmapheresis

Author: Diego Curtò, Federica Tomatis, Sara Gastoldi, Miriam Galbusera, Marina Noris, Federico Raimondi, Ferdinando Luca Lorini, Anna Falanga, Marina Marchetti, Giuseppe Remuzzi, and Piero Ruggenenti
Subjects: convalescent antibodies, COVID-19, double filtration plasmapheresis, rituximab, immunosuppression, coagulation biomarkers, Immunologic diseases. Allergy, RC581-607
Abstract: Passive antibody therapy has been used to treat outbreaks of viral disease, including the ongoing pandemic of severe respiratory acute respiratory syndrome (SARS) coronavirus 2 (SARS-CoV-2) or COVID-19. However, the real benefits of the procedure are unclear. We infused a concentrated solution of neutralizing anti-SARS-CoV-2 antibodies obtained from a convalescent donor with a single session of double filtration plasmapheresis (DFPP) into a 56-year-old woman with long history of unremitting, severe COVID-19. She was unable to establish an adequate antiviral immune response because of previous chemotherapy, including the infusion of the anti-CD20 monoclonal antibody rituximab, administered to treat a diffuse large B-cell lymphoma. The disease promptly recovered despite evidence of no endogenous anti-SARS-CoV-2 antibody production. The observation that passive antibody therapy might prove particularly effective in immunodepressed COVID-19 patients requires evaluation in prospective randomized controlled trial.
Published: 2021
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47. Mycophenolate mofetil versus azathioprine in kidney transplant recipients on steroid-free, low-dose cyclosporine immunosuppression (ATHENA): A pragmatic randomized trial.

Author: Piero Ruggenenti, Paolo Cravedi, Eliana Gotti, Annarita Plati, Maddalena Marasà, Silvio Sandrini, Nicola Bossini, Franco Citterio, Enrico Minetti, Domenico Montanaro, Ettore Sabadini, Regina Tardanico, Davide Martinetti, Flavio Gaspari, Alessandro Villa, Annalisa Perna, Francesco Peraro, and Giuseppe Remuzzi
Subjects: Medicine
Abstract: BackgroundWe compared protection of mycophenolate mofetil (MMF) and azathioprine (AZA) against acute cellular rejection (ACR) and chronic allograft nephropathy (CAN) in kidney transplant recipients on steroid-free, low-dose cyclosporine (CsA) microemulsion maintenance immunosuppression.Methods and findingsATHENA, a pragmatic, prospective, multicenter trial conducted by 6 Italian transplant centers, compared the outcomes of 233 consenting recipients of a first deceased donor kidney transplant induced with low-dose thymoglobulin and basiliximab and randomized to MMF (750 mg twice/day, n = 119) or AZA (75 to 125 mg/day, n = 114) added-on maintenance low-dose CsA microemulsion and 1-week steroid. In patients without acute clinical or subclinical rejections, CsA dose was progressively halved. Primary endpoint was biopsy-proven CAN. Analysis was by intention to treat. Participants were included between June 2007 and July 2012 and followed up to August 2016. Between-group donor and recipient characteristics, donor/recipient mismatches, and follow-up CsA blood levels were similar. During a median (interquartile range (IQR)) follow-up of 47.7 (44.2 to 48.9) months, 29 of 87 biopsied patients on MMF (33.3%) versus 31 of 88 on AZA (35.2%) developed CAN (hazard ratio (HR) [95% confidence interval (CI)]: 1.147 (0.691 to 1.904, p = 0.595). Twenty and 21 patients on MMF versus 34 and 14 on AZA had clinical [HR (95% CI): 0.58 (0.34 to 1.02); p = 0.057) or biopsy-proven subclinical [HR (95% CI): 1.49 (0.76 to 2.92); p = 0.249] ACR, respectively. Combined events [HR (95% CI): 0.85 (0.56 to 1.29); p = 0.438], patient and graft survival, delayed graft function (DGF), 3-year glomerular filtration rate (GFR) [53.8 (40.6;65.7) versus 49.8 (36.8;62.5) mL/min/1.73 m2, p = 0.50], and adverse events (AEs) were not significantly different between groups. Chronicity scores other than CAN predict long-term graft outcome. Study limitations include small sample size and unblinded design.ConclusionsIn this study, we found that in deceased donor kidney transplant recipients on low-dose CsA and no steroids, MMF had no significant benefits over AZA. This finding suggests that AZA, due to its lower costs, could safely replace MMF in combination with minimized immunosuppression.Trial registrationClinicalTrials.gov NCT00494741; EUDRACT 2006-005604-14.
Published: 2021
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48. CFH and CFHR Copy Number Variations in C3 Glomerulopathy and Immune Complex-Mediated Membranoproliferative Glomerulonephritis

Author: Rossella Piras, Matteo Breno, Elisabetta Valoti, Marta Alberti, Paraskevas Iatropoulos, Caterina Mele, Elena Bresin, Roberta Donadelli, Paola Cuccarolo, Richard J. H. Smith, Ariela Benigni, Giuseppe Remuzzi, and Marina Noris
Subjects: C3 glomerulopathy (C3G), immune complex-mediated membranoproliferative glomerulonephritis (IC-MPGN), factor H (FH), factor H-related proteins (FHRs), complement, copy number variations (CNVs), Genetics, QH426-470
Abstract: C3 Glomerulopathy (C3G) and Immune Complex-Mediated Membranoproliferative glomerulonephritis (IC-MPGN) are rare diseases characterized by glomerular deposition of C3 caused by dysregulation of the alternative pathway (AP) of complement. In approximately 20% of affected patients, dysregulation is driven by pathogenic variants in the two components of the AP C3 convertase, complement C3 (C3) and Factor B (CFB), or in complement Factor H (CFH) and Factor I (CFI), two genes that encode complement regulators. Copy number variations (CNVs) involving the CFH-related genes (CFHRs) that give rise to hybrid FHR proteins also have been described in a few C3G patients but not in IC-MPGN patients. In this study, we used multiplex ligation-dependent probe amplification (MLPA) to study the genomic architecture of the CFH-CFHR region and characterize CNVs in a large cohort of patients with C3G (n = 103) and IC-MPGN (n = 96) compared to healthy controls (n = 100). We identified new/rare CNVs resulting in structural variants (SVs) in 5 C3G and 2 IC-MPGN patients. Using long-read single molecule real-time sequencing (SMRT), we detected the breakpoints of three SVs. The identified SVs included: 1) a deletion of the entire CFH in one patient with IC-MPGN; 2) an increased number of CFHR4 copies in one IC-MPGN and three C3G patients; 3) a deletion from CFHR3-intron 3 to CFHR3-3′UTR (CFHR34–6Δ) that results in a FHR3-FHR1 hybrid protein in a C3G patient; and 4) a CFHR31–5-CFHR410 hybrid gene in a C3G patient. This work highlights the contribution of CFH-CFHR CNVs to the pathogenesis of both C3G and IC-MPGN.
Published: 2021
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49. Add-On Cyclic Angiotensin-(1-7) with Cyclophosphamide Arrests Progressive Kidney Disease in Rats with ANCA Associated Glomerulonephritis

Author: Domenico Cerullo, Daniela Rottoli, Daniela Corna, Mauro Abbate, Ariela Benigni, Giuseppe Remuzzi, and Carlamaria Zoja
Subjects: crescentic glomerulonephritis, myeloperoxidase, anti-neutrophil cytoplasmic antibodies, cyclophosphamide, angiotensin-(1-7), glomerular crescents, Cytology, QH573-671
Abstract: Rapidly progressive crescentic glomerulonephritis associated with anti-neutrophil cytoplasmic antibodies (ANCA-GN) is a major cause of renal failure. Current immunosuppressive therapies are associated with severe side effects, intensifying the need for new therapeutic strategies. The activation of Mas receptor/Angiotensin-(1-7) axis exerted renoprotection in chronic kidney disease. Here, we investigated the effect of adding the lanthionine-stabilized cyclic form of angiotensin-1-7 [cAng-(1-7)] to cyclophosphamide in a rat model of ANCA-GN. At the onset of proteinuria, Wistar Kyoto rats with ANCA-GN received vehicle or a single bolus of cyclophosphamide, with or without daily cAng-(1-7). Treatment with cAng-(1-7) plus cyclophosphamide reduced proteinuria by 85% vs. vehicle, and by 60% vs. cyclophosphamide, and dramatically limited glomerular crescents to less than 10%. The addition of cAng-(1-7) to cyclophosphamide protected against glomerular inflammation and endothelial rarefaction and restored the normal distribution of parietal epithelial cells. Ultrastructural analysis revealed a preserved GBM, glomerular endothelium and podocyte structure, demonstrating that combination therapy provided an additional layer of renoprotection. This study demonstrates that adding cAng-(1-7) to a partially effective dose of cyclophosphamide arrests the progression of renal disease in rats with ANCA-GN, suggesting that cAng-(1-7) could be a novel clinical approach for sparing immunosuppressants.
Published: 2022
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50. Post-COVID condition: dispensation of drugs and diagnostic tests as proxies of healthcare impact

Author: Alessandro Nobili, Barbara D’Avanzo, Mauro Tettamanti, Alessia Antonella Galbussera, Giuseppe Remuzzi, Ida Fortino, Olivia Leoni, Sergio Harari, and Pier Mannuccio Mannucci
Subjects: Emergency Medicine, Internal Medicine
Published: 2023
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