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1. Glucocorticoid Minimization in Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis: An International Survey of Clinicians

Author

David Massicotte-Azarniouch, Mark Canney, Priscilla Karnabi, Peter A. Merkel, Rachel B. Jones, Ruth J. Pepper, Alan D. Salama, Vimal K. Derebail, Nataliya Milman, Mats Junek, Christian Pagnoux, David R.W. Jayne, and Michael Walsh

Subjects
Anti-neutrophil cytoplasmic antibody-associated vasculitis, cyclophosphamide, glucocorticoid, rituximab, survey, Diseases of the genitourinary system. Urology, RC870-923
Abstract

Rationale & Objective: Research in anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV) has focused on reducing treatment toxicities, notably through reduction of exposure to glucocorticoids. Glucocorticoid-sparing therapies such as avacopan are not widely available in many countries, and patients are exposed to high glucocorticoid doses. There is little data concerning what clinicians should accept as the lowest glucocorticoid dosing that can be used in induction therapy for AAV. Study Design: International, online survey. Setting & Participants: Clinicians in various countries with experience in managing vasculitis. Exposure and Outcomes: Survey questions to gauge interest and preferences in studying an induction of remission regimen for severe AAV using only 2 or 4 weeks of glucocorticoids without avacopan. Data collected included general opinions about standard of care for induction agents, glucocorticoids, and avacopan. Respondents were presented with 3 candidate trial designs, 2 of which proposed a combination of cyclophosphamide and rituximab induction. Analytical Approach: Using a 10-point Likert scale, respondents ranked each candidate trial on its usefulness in demonstrating whether a minimal glucocorticoid regimen would be safe and effective and their willingness to randomize into the trial. Results: There were 210 respondents to the survey. The candidate trials were rated moderate-to-high for usefulness to demonstrate safety and efficacy (scores 6-7/10), and moderate (scores 5-6/10) for willingness to randomize. Four-week glucocorticoid duration was preferred to 2 weeks, and combination cyclophosphamide-rituximab with 4-week glucocorticoids was the most preferred design. Forty-two percent of respondents felt avacopan had to be incorporated into a minimal GC trial design to want to recruit patients. Limitations: Representativeness of survey sample and generalizability of findings. Conclusions: Combination cyclophosphamide-rituximab may be the ideal way of studying minimal glucocorticoid use in severe AAV. Given its increasing uptake, incorporating avacopan into a potential trial design is important. Plain Language Summary: Research in anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV) has focused on using less glucocorticoids to limit side effects. New drugs that drastically limit glucocorticoid use are not available in many countries. Studies are needed to find other ways of reducing glucocorticoid exposure to treat AAV, but it is unclear how best to achieve this. We administered a survey to doctors with experience in treating AAV and had them grade different combinations of widely available treatments with 2 or 4 weeks of glucocorticoids. We found that a combination of 2 doses cyclophosphamide with 2 doses rituximab and 4 weeks of glucocorticoids was the preferred treatment. The results will guide the development of a trial studying minimal use of glucocorticoids for the treatment of AAV.

Published
2024
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3. Rituximab in Membranous Nephropathy

Author

Philipp Gauckler, Jae Il Shin, Federico Alberici, Vincent Audard, Annette Bruchfeld, Martin Busch, Chee Kay Cheung, Matija Crnogorac, Elisa Delbarba, Kathrin Eller, Stanislas Faguer, Kresimir Galesic, Siân Griffin, Martijn W.F. van den Hoogen, Zdenka Hrušková, Anushya Jeyabalan, Alexandre Karras, Catherine King, Harbir Singh Kohli, Gert Mayer, Rutger Maas, Masahiro Muto, Sergey Moiseev, Balazs Odler, Ruth J. Pepper, Luis F. Quintana, Jai Radhakrishnan, Raja Ramachandran, Alan D. Salama, Ulf Schönermarck, Mårten Segelmark, Lee Smith, Vladimír Tesař, Jack Wetzels, Lisa Willcocks, Martin Windpessl, Ladan Zand, Reza Zonozi, and Andreas Kronbichler

Subjects
B cells, membranous nephropathy, nephrotic syndrome, rituximab, Diseases of the genitourinary system. Urology, RC870-923
Abstract

Membranous nephropathy (MN) is the most common cause of primary nephrotic syndrome among adults. The identification of phospholipase A2 receptor (PLA2R) as target antigen in most patients changed the management of MN dramatically, and provided a rationale for B-cell depleting agents such as rituximab. The efficacy of rituximab in inducing remission has been investigated in several studies, including 3 randomized controlled trials, in which complete and partial remission of proteinuria was achieved in approximately two-thirds of treated patients. Due to its favorable safety profile, rituximab is now considered a first-line treatment option for MN, especially in patients at moderate and high risk of deterioration in kidney function. However, questions remain about how to best use rituximab, including the optimal dosing regimen, a potential need for maintenance therapy, and assessment of long-term safety and efficacy outcomes. In this review, we provide an overview of the current literature and discuss both strengths and limitations of “the new standard.”

Published
2021
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4. Relapse in Anti-Neutrophil Cytoplasm Antibody (ANCA)–Associated Vasculitis

Author

Alan D. Salama

Subjects
Diseases of the genitourinary system. Urology, RC870-923
Abstract

Clinical relapses are common in anti-neutrophil cytoplasm antibody (ANCA)–associated vasculitis, necessitating repeated treatment with immunosuppressive therapy, and increasing the risks of severe adverse events. Better understanding the basis of relapse would help stratify patients, testing the notion that more treatment may prevent development of relapse, whereas in those at low risk of disease flares, treatment minimization may be appropriate, reducing risks of adverse events, most notably infectious complications and drug toxicity. However, relapse can only occur following remission, and although defining clinical remission may seem straightforward, there is evidence in many remission patients of persistent inflammatory and immunological activity, at levels above those found in healthy individuals. This suggests that we may not truly be achieving disease remission in many patients and these persistent responses may set the patient up for subsequent disease flares. Understanding the underlying pathophysiological basis of disease activity and remission is paramount to help define better biomarkers of relapse, which should positively affect adverse events and patient outcomes. Keywords: ANCA, relapse, vasculitis

Published
2020
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5. Patient Outcomes in Renal-Limited Antineutrophil Cytoplasmic Antibody Vasculitis With Inactive Histology

Author

Tessa K. Novick, Min Chen, Jennifer Scott, Frank B. Cortazar, Isabelle Ayoub, Mark A. Little, Zdenka Hruskova, Alan D. Salama, Christian Pagnoux, and Duvuru Geetha

Subjects
Diseases of the genitourinary system. Urology, RC870-923
Abstract

Introduction: Little is known about the anticipated disease course for individuals who present with renal-limited antineutrophil cytoplasmic antibody (ANCA)−associated vasculitis but who lack inflammation on a kidney biopsy. The impact of immunosuppression on renal and overall survival is unknown. Methods: Patients were recruited from 2005 to 2016 from 8 centers worldwide (N = 16) for this descriptive study. All had positive ANCA, elevated serum creatinine with active urine sediment, histologic evidence of pauci-immune glomerulonephritis without active lesions, and had no evidence of extrarenal vasculitis. We describe the characteristics of this cohort and the differences in the clinical, histologic, and therapeutic parameters of those who developed primary outcomes of end-stage renal disease (ESRD) and vasculitis relapse. Results: The cohort was 63% Caucasian, and 75% were men, with a median age of 62 years. At entry, the mean ± SD estimated glomerular filtration rate (eGFR) was 24 ± 20 ml/min per 1.73 m2, and 5 patients required dialysis. Twelve patients received immunosuppressive therapy, 25% experienced disease relapse, and 38% developed ESRD. Patients who developed ESRD had lower baseline eGFRs (8 ± 5 ml/min per 1.73 m2 vs. 35 ± 18 ml/min per 1.73 m2; P = 0.001) and more often required dialysis at presentation (83% vs. 0%; P = 0.001). Patients who relapsed were less likely to receive immunosuppression (25% for the relapsed group vs. 92% for the nonrelapsed group; relative risk: 0.27, risk difference: 67%; P = 0.03). Conclusion: Among these patients, lower initial eGFR and dialysis dependence at presentation might increase the risk for ESRD. Immunosuppression did not affect renal outcomes in this sample of patients but was associated with a reduced risk for vasculitis relapse. More information is needed on factors that predict treatment response in this high-risk group. Keywords: ANCA-associated vasculitis, glomerulonephritis, renal limited vasculitis

Published
2018
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6. Treatment with Quinoline-3-carboxamide does not successfully prevent immune-mediated glomerulonephritis in mice

Author

Juliana Draibe, Ruth J. Pepper, and Alan D. Salama

Subjects
Glomerulonephritis, Animal model, Calprotectin, Paquinimod, Diseases of the genitourinary system. Urology, RC870-923
Abstract

Introduction: Quinoline-3-carboximide compounds, such as paquinimod, which targets the protein S100A9, have demonstrated efficacy in treating autoimmune diseases. S100A9, in association with S100A8, forms the heterodimer S100A8/S100A9, known as calprotectin; that has been shown to be upregulated in numerous inflammatory disorders. We had previously demonstrated protection from glomerular disease in S100A9-deficient mice. The aim of this study was to assess the efficacy of paquinimod in the prevention and treatment of experimental glomerulonephritis. Methods: Nephrotoxic nephritis (NTN) was induced in C57BL/6 mice according to our standard protocol. Mice were treated with different doses of paquinimod either at disease induction (prevention group) or two days following induction (therapeutic group) and sacrificed 8 days following induction. Disease was assessed histologically (number of glomerular crescents, degree of glomerular thrombosis, number of infiltrating leucocytes and calprotectin expression) and biochemically (serum creatinine and urea levels, and urinary levels of protein). Results: Neither treatment with low (0.5 mg/kg) or high (25 mg/kg) doses of paquinimod, given preventatively or therapeutically, led to disease attenuation, as assessed by biochemical or histological parameters. Additionally, we found trends for an increase in renal glomerular calprotectin expression in the high dose groups, suggesting a possible feedback regulation of calprotectin expression. Conclusions: Our results show that paquinimod does not successfully prevent or treat mice with NTN. Other models of immune-mediated glomerulonephritis need to be tested to investigate the therapeutic potential of this compound in renal disease.

Published
2016
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7. Urinary T Cells Identify Renal Antineutrophil Cytoplasmic Antibody-Associated Vasculitis and Predict Prognosis: A Proof of Concept Study

Author

Janis Sonnemann, Jan Klocke, Markus Bieringer, Anthony Rousselle, Kai-Uwe Eckardt, Saban Elitok, Suncica Popovic, Sebastian Bachmann, Ralph Kettritz, Alan D. Salama, Philipp Enghard, and Adrian Schreiber

Subjects
Nephrology, Cardiovascular and Metabolic Diseases, Translational Research
Abstract

INTRODUCTION: Necrotizing crescentic glomerulonephritis is a major contributor to morbidity and mortality in Antineutrophil cytoplasmic antibodies (ANCA)-associated vasculitis (AAV). Because therapy relies on immunosuppressive agents with potentially severe adverse effects, a reliable noninvasive biomarker of disease activity is needed to guide treatment. METHODS: We used flow cytometry to quantify T cell subsets in blood and urine samples from 95 patients with AAV and 8 controls to evaluate their biomarker characteristics. These were compared to soluble markers, monocyte chemoattractant protein-1 (MCP-1), soluble CD163 (sCD163), soluble CD25 (sCD25), and complement C5a (C5a), measured using multiplex analysis. Available kidney biopsies (n = 21) were classified according to Berden. RESULTS: Patients with active renal AAV (rAAV) showed significantly higher urinary cell counts than those in remission, or those with extrarenal manifestation, or healthy controls. Urinary T cells showed robust discrimination of disease activity with superior performance compared to MCP-1 and sCD163. Patients whose kidney biopsies had been classified as "crescentic" according to Berden classification showed higher urinary T cell counts. Discordant regulatory T cells (T(reg)) proportions and CD4(+)/CD8(+) ratio in blood and urine suggested that urinary cells reflect tissue migration rather than mere micro-bleeding. Furthermore, urinary T(reg) and T helper cells (T(H)17) patterns were associated with clinical response and risk of renal relapse. CONCLUSION: Urinary T cells reflect the renal inflammatory milieu in AAV and provide further insights into the pathogenesis of this chronic condition. Their promising potential as noninvasive diagnostic and prognostic biomarkers deserves further exploitation.

Published
2023

9. Contributors

Author

Andrew Advani, Michael Allon, Amanda Hyre Anderson, Gerald B. Appel, Suheir Assady, Anthony Atala, Colin Baigent, Sevcan A. Bakkaloglu, Gina-Marie Barletta, Gavin J. Becker, Rinaldo Bellomo, Jeffrey S. Berns, Vivek Bhalla, Jürg Biber, Daniel G. Bichet, René J.M. Bindels, Melissa B. Bleicher, Jon D. Blumenfeld, Alain Bonnardeaux, Joseph V. Bonventre, William D. Boswell, Donald W. Bowden, Barry M. Brenner, Matthew D. Breyer, Richard M. Breyer, Dennis Brown, Carlo Brugnara, Timothy E. Bunchman, David A. Bushinsky, Stéphan Busque, Juan Jesús Carrero, Daniel Cattran, James C. Chan, Anil Chandraker, Ingrid J. Chang, Devasmita Choudhury, Fredric L. Coe, John F. Collins, H. Terence Cook, Ricardo Correa-Rotter, Shawn E. Cowper, Paolo Cravedi, Alfonso M. Cueto-Manzano, Vivette D. D’Agati, Mogomat Razeen Davids, Scott E. Delacroix, Bradley M. Denker, Thomas A. Depner, Thomas D. DuBose, Kai-Uwe Eckardt, Mohamed T. Eldehni, David H. Ellison, Michael Emmett, Ronald J. Falk, Harold I. Feldman, Robert A. Fenton, Andrew Z. Fenves, Kevin W. Finkel, Paola Fioretto, Damian G. Fogarty, John R. Foringer, Denis Fouque, Barry I. Freedman, Jørgen Frøkiaer, John W. Funder, David S. Game, Richard E. Gilbert, Jared J. Grantham, Mitchell L. Halperin, Matthew Hand, Donna S. Hanes, David C.H. Harris, Raymond C. Harris, Richard Haynes, Joost G.J. Hoenderop, Ewout J. Hoorn, Thomas H. Hostetter, Chi-yuan Hsu, Shih Hua-Lin, Hassan N. Ibrahim, Ajay K. Israni, Jossein Jadvar, J. Charles Jennette, Eric Jonasch, Kamel S. Kamel, S. Ananth Karumanchi, Bertram L. Kasiske, John A. Kellum, Carolyn J. Kelly, Ramesh Khanna, David K. Klassen, Christine J. Ko, Harbir Singh Kohli, Curtis K. Kost, L. Spencer Krane, Jordan Kreidberg, Tae-Hwan Kwon, Amit Lahoti, Martin J. Landray, John H. Laragh, Harold E. Layton, Moshe Levi, Bengt Lindholm, Frank Liu, Valerie A. Luyckx, David A. Maddox, Yoshiro Maezawa, Arthur J. Matas, Michael Mauer, Ivan D. Maya, Sharon E. Maynard, Alicia A. McDonough, Christopher W. McIntyre, Timothy W. Meyer, William E. Mitch, Orson W. Moe, Sharon M. Moe, Bruce A. Molitoris, Alvin H. Moss, David B. Mount, Karen A. Munger, Patrick H. Nachman, Saraladevi Naicker, Søren Nielsen, Eric G. Neilson, Lindsay E. Nicolle, Daniel B. Ornt, Manuel Palacín, Paul M. Palevsky, Suzanne L. Palmer, Hans-Henrik Parving, Jaakko Patrakka, David Pearce, Roberto Pecoits-Filho, Carmen A. Peralta, Norberto Perico, Neil R. Powe, Kearkiat Praditpornsilpa, Jeppe Prætorius, Susan E. Quaggin, L. Darryl Quarles, Jai Radhakrishnan, Rawi Ramadan, Piero Reggenenti, Heather N. Reich, Andrea Remuzzi, Giuseppe Remuzzi, Stephen S. Rich, Miguel C. Riella, Eberhard Ritz, Claudio Ronco, Norman D. Rosenblum, Peter Rossing, Dvora Rubinger, Robert K. Rude, Ernesto Sabath, Venkata Sabbisetti, Vinay Sakhuja, Alan D. Salama, Jeff M. Sands, Fernando Santos, Mohamed H. Sayegh, John D. Scandling, Franz Schaefer, Jon I. Scheinman, John C. Schwartz, Asif A. Sharfuddin, Susan Shaw, Visith Sitprija, Karl L. Skorecki, Itzchak N. Slotki, James P. Smith, Miroslaw J. Smogorzewski, Stuart M. Sprague, Peter Stenvinkel, John B. Stokes, Maarten W. Taal, Manjula Kurella Tamura, Jane C. Tan, Stephen C. Textor, Ravi Thadhani, Scott C. Thomson, Vincente E. Torres, Karl Tryggvason, Meryem Tuncel, Kriang Tungsanga, Joseph G. Verbalis, Jill W. Verlander, Shoyab Wadee, I. David Weiner, Matthew R. Weir, Steven D. Weisbord, David C. Wheeler, Christopher S. Wilcox, Christopher G. Wood, Stephen H. Wright, Jane Y. Yeun, Alan S.L. Yu, Kambiz Zandi-Nejad, and Mark L. Zeidel

Published
2012

10. The Renal Biopsy

Author

H. Terence Cook and Alan D. Salama

Subjects
medicine.medical_specialty, medicine.diagnostic_test, Renal pathology, business.industry, medicine, Urology, Renal biopsy, business
Published
2012

13. Contributors

Author

Sharon Adler, Horacio J. Adrogué, Nidhi Aggarwal, Michael Allon, Sharon Anderson, Sharon Phillips Andreoli, Gerald B. Appel, Vicente Arroyo, Phyllis August, George L. Bakris, James E. Balow, Srinivasan Beddhu, Jeffrey S. Berns, Joseph V. Bonventre, Larissa Braga, Josephine P. Briggs, Maria Luiza Caramori, Daniel C. Cattran, Arlene B. Chapman, Glenn M. Chertow, Alfred K. Cheung, Kerry C. Cho, Thomas M. Coffman, Peter J. Conlon, Jeffrey J. Connaire, Gary Curhan, Paula Dennen, Thomas D. DuBose, David H. Ellison, Michael Emmett, Ronald J. Falk, Javier Fernández, Catherine M. Goeddeke-Merickel, D. Jordi Goldstein-Fuchs, Arthur Greenberg, Martin C. Gregory, Antonio Guasch, Lakshman Gunaratnam, William L. Henrich, Friedhelm Hildebrandt, Ronald J. Hogg, Jean L. Holley, Chi-yuan Hsu, Alastair J. Hutchison, A. David Jayne, J. Charles Jennette, Wladimiro Jiménez, Bertram L. Kasiske, Nitin Khosla, Paul E. Klotman, Eugene C. Kovalik, Jean-Paul Kovalik, Michelle Whittier Krause, Wilhelm Kriz, Andrew S. Levey, Fang-Ying Lin, Stuart Linas, Nicolaos E. Madias, Roslyn B. Mannon, Diego R. Martin, Gary R. MatzkePharmD, Michael Maver, Rory McQuillan, Ankit N. Mehta, Catherine M. Meyers, Alain Meyrier, Sharon M. Moe, Marianne Monahan, Narayana S. Murali, Cynthia C. Nast, Karl A. Nath, Lindsay E. Nicolle, John F. O'Toole, Biff F. Palmer, Roberto Pisoni, Tiina Podymow, Charles D. Pusey, L. Darryl Quarles, Maya K. Rao, Giuseppe Remuzzi, Eberhard Ritz, Akber Saifullah, Alan D. Salama, Paul W. Sanders, Mark J. Sarnak, Steven J. Scheinman, Arrigo Schieppati, Jürgen B. Schnermann, Richard C. Semelka, Lesley A. Stevens, Nicholas Stoycheff, Harold M. Szerlip, Nadine D. Tanenbaum, Howard Trachtman, Joseph G. Verbalis, Anand Vardhan, Daniel E. Weiner, Christopher S. Wilcox, Jay B. Wish, Christina M. Wyatt, and Fuad N. Ziyadeh

Published
2009

14. Contributors

Author

Cataldo Abaterusso, Stéphane P. Ahern, Maria Cristina Aisa, Robert C. Albright, Vicente Alfaro, Ali Al-Khafaji, Jean-Christophe Allo, Richard Amerling, Alessandro Amore, Robert J. Anderson, Michele Andreucci, Vittorio E. Andreucci, Emilios Andrikos, Vicente Arroyo, John M. Arthur, Stephen R. Ash, Emilio Assanelli, Filippo Aucella, Sean M. Bagshaw, Olga Balafa, André Luís Balbi, Ian Baldwin, Marco Ballestri, Joanne M. Bargman, Gina-Marie Barletta, Jeffrey F. Barletta, Libero Barozzi, Rashad S. Barsoum, Monica Beaulieu, Donna Beer-Stolz, Rinaldo Bellomo, Jose Bernardo, Michele Bertolotto, John T. Bestoso, Gerard A. Betro, Mallar Bhattacharya, Geoffrey R. Bihl, Stijn I. Blot, Willem Boer, Mirian A. Boim, Monica Bonello, Joseph V. Bonventre, A.D. Booth, Edmund Bourke, George Braitberg, Diego Brancaccio, Alessandra Brendolan, Brigida Brezzi, James C. Brodie, Patrick D. Brophy, Ryan Brown, Richard Bucala, Jonathan Buckmaster, Milos N. Budisavljevic, Timothy E. Bunchman, Emmanuel A. Burdmann, Benedetta Bussolati, Matthew A. Butkus, Daniela Buzzelli, Paolo Calzavacca, Giovanni Camussi, Bernard Canaud, Noël J.M. Cano, Vincenzo Cantaluppi, Giovambattista Capasso, Gianni Cappelli, Eleonora Carlesso, Francesco G. Casino, Leticia Castillo, Roberta Cerutti, Lakhmir S. Chawla, Chang Yin Chionh, Alexander Chiu, May T. Chow, Kirpal S. Chugh, Bruno Cianciaruso, Mauro Cignarelli, Yann-Erick Claessens, John A. Clark, William R. Clark, David J. Cohen, Scott D. Cohen, Peter Constable, Rosanna Coppo, Howard E. Corey, Mario Cozzolino, Maureen Craig, Carl H. Cramer, Mark Crandall, Paolo Cravedi, Carlo Crepaldi, R. John Crew, Donald F. Cronin, Dinna N. Cruz, Antonio Dal Canton, Maurizio Dan, Angela D'Angelo, Andrew Davenport, Andrew R. Davies, James W. Dear, Andrea De Gasperi, Roberto Dell'Aquila, Giorgio Della Rocca, Dorella Del Prete, Russell L. Delude, Thomas Depner, Lorenzo E. Derchi, Prasad Devarajan, Jan J. De Waele, Jean-François Dhainaut, José A. Diaz-Buxo, Lucia Di Micco, José Carolina Divino-Filho, Sarah Doernberg, Gordon S. Doig, David J. Dries, Francesco Maria Drudi, Wilfred Druml, Graeme Duke, Andrew Durward, Moritoki Egi, Ciro Esposito, Pieter Evenepoel, Teresa Faga, Sheung Tat Fan, Donald A. Feinfeld, Eric Féraille, Javier Fernández, Simon Finfer, Mitchell P. Fink, Kevin W. Finkel, Michael F. Flessner, Marco Formica, Lui G. Forni, James D. Fortenberry, Craig French, Roberto Fumagalli, Mario Furlanut, Micheline Djouguela Fute, Daniela Ponce Gabriel, Andrea Galassi, Miriam Galbusera, Francesco Galli, Giovanni Galli, Maurizio Gallieni, Giampiero Gallo, Giovanni Gambaro, Hilary S. Gammill, Ezio Nicola Gangemi, Dayong Gao, Susan Garwood, Francesco Garzotto, Antonietta M. Gatti, Luciano Gattinoni, John P. Geibel, Stephen George, Loreto Gesualdo, R.T. Noel Gibney, Debbie S. Gipson, Ilya G. Glezerman, Griet Glorieux, Stuart L. Goldstein, Thomas A. Golper, Manjula Gowrishankar, Fabio Grandi, Cesare Gregoretti, Brian W. Grinnell, A.B. Johan Groeneveld, Steven J. Gruber, Gualtiero Guadagni, Kyle J. Gunnerson, Akanksha Gupta, Victor Gura, Isabella Guzzo, Richard Hackbarth, Mitchell L. Halperin, Nikolas Harbord, Jean-Philippe Haymann, Alan C. Heffner, Anthony J. Hennessy, Samuel N. Heyman, Graham L. Hill, Philip J. Hilton, Jonathan Himmelfarb, Hiroyuki Hirasawa, Nicholas A. Hoenich, Stephen R. Holdsworth, Anthony Holley, Patrick M. Honoré, Eric A.J. Hoste, Andrew A. House, David T. Huang, Zhongping Huang, Rolf D. Hubmayr, Alun D. Hughes, H. David Humes, T. Alp Ikizler, Barbara Imberti, Todd S. Ing, Bertrand L. Jaber, Gérard Janvier, Arundhathi Jeyabalan, Vivekanand Jha, Olivier Joannes-Boyau, Michael Joannidis, Daryl A. Jones, Achim Jörres, Kamel S. Kamel, Ryan C. Kamp, Neeta Kannan, Lewis J. Kaplan, Özgür Karacan, Vijay Karajala-Subramanyam, Gur P. Kaushal, John A. Kellum, Markus J. Kemper, Asjad Khan, Ramesh Khanna, Vijay Kher, Paul L. Kimmel, Detlef Kindgen-Milles, A. Richard Kitching, Carl M. Kjellstrand, Orly F. Kohn, Laura A. Kooienga, Jeroen P. Kooman, Peter Kotanko, Raymond T. Krediet, A.A. Kroon, Dingwei Kuang, Martin K. Kuhlmann, Jan Willem Kuiper, Man-Fai Lam, Olga Lamacchia, Norbert Lameire, Christoph Langenberg, Gianfranco Lauri, Martine Leblanc, Ingrid Ledebo, Paolo Lentini, Edward F. Leonard, Jeffrey J. Letteri, Karel M. Leunissen, Xavier M. Leverve, Adeera Levin, John K. Leypoldt, Orfeas Liangos, Elisa Licari, Wilfred Lieberthal, Peter K. Linden, Jeffrey Lipman, Kathleen D. Liu, Shiguang Liu, Sergio Livigni, Wai-Kei Lo, Manuela Lugano, Sing-Leung Lui, Antonio Lupo, Valerie A. Luyckx, William L. Macias, Nicholas Madden, François Madore, Daniel S. Majors, Elena Mancini, Filippo Mangione, Sunil Mankad, Pier Paolo Manzini, Martino Marangella, Giancarlo Marenzi, Filippo Mariano, Paul E. Marik, John J. Marini, François Marquis, John C. Marshall, Mark R. Marshall, Roy Mathew, Kenichi Matsuda, Michael A. Matthay, Norma J. Maxvold, Clive N. May, Jerry McCauley, Maureen McCunn, Joseph McKenna, Ravindra L. Mehta, Caterina Mele, Aicha Merouani, Laurent Mesnard, Piergiorgio Messa, Philipp G.H. Metnitz, Madhukar Misra, Steffen R. Mitzner, Barry A. Mizock, Babak Mokhlesi, Bruce A. Molitoris, Andrea Morelli, Thomas John Morgan, Marina Morigi, Peter Mount, Roberto Pozzi Mucelli, Bruce A. Mueller, Patrick Murray, Raghavan Murugan, Masataka Nakamura, Federico Nalesso, Carla M. Nester, Allen Nissenson, Karl Nolph, Catalina Ocampo, Shigeto Oda, Mark D. Okusa, Steven M. Opal, Helen Opdam, Hartmut Osswald, Heleen M. Oudemans–van Straaten, Massimo A. Padalino, Matthew L. Paden, Emil P. Paganini, Paul M. Palevsky, Mani John Panat, Francesco Paolini, Dipen Parikh, Nicolò Patroniti, Pietro Pavlica, Didier Payen de La Garanderie, Federico Pea, Zhiyong Peng, Mark A. Perazella, Angelo F. Perego, Estela Regina Pereira, Evans R. Fernández Pérez, Norberto Perico, Nicoletta Pertica, Giovanni Pertosa, Licia Peruzzi, Dimitris Petras, Phuong-Chi Pham, Phuong-Thu Pham, Richard K.S. Phoon, Stefano Picca, Pasquale Piccinni, Maury N. Pinsk, Michael R. Pinsky, Marta Piroddi, Isabelle Plamondon, Lindsay D. Plank, Frans B. Plötz, Lusine Poghosyan, Natalia Polanco, Patricio M. Polanco, Hans Dietrich Polaschegg, Rafael Ponikvar, Silvia Porecca, Didier Portilla, T. Brian Powell, Raymond Quigley, Hamid Rabb, Maximilian Ragaller, Teresa Rampino, Reena Ranpuria, Anjay Rastogi, Ranistha Ratanarat, Naem Raza, Michael C. Reade, John H. Reeves, Karl Reiter, Giuseppe Remuzzi, Zaccaria Ricci, Sven-Erik Ricksten, Christophe Ridel, Kinan Rifai, Troels Ring, Julie Riopel, Eduardo Rocha, Eric Roessler, Roberto Rona, Claudio Ronco, Eric Rondeau, Seymour Rosen, Christian Rosenberger, Shane Rowan, Thomas Roy, Georges Saab, Tomohito Sadahiro, Carla Sala, Chiara Sala, Alan D. Salama, Adrian Salmon, Gabriela Salvatori, Ramin Sam, Ruben M. Sandoval, Antonio Santoro, Takao Saotome, Penny L. Sappington, J. Vidya Sarma, Judy Savige, Francesco Paolo Schena, Eva Schepers, Miet Schetz, Gregory A. Schmidt, Nestor Schor, Nicola Schusterschitz, Giuseppe Segoloni, Nirva Shah, Shamik H. Shah, Sudhir V. Shah, Asif A. Sharfuddin, Andrew Shaw, Hidetoshi Shiga, Hisataka Shoji, Ashutosh Shukla, Fiona Simpson, Kai Singbartl, Mervyn Singer, Kim Solez, Kevin M. Sowinski, Mark Stafford-Smith, Jan Stange, Luca Stefanelli, Deborah M. Stein, Maurizio Stella, Giovanni Stellin, David A. Story, Sanjay Subramanian, Kristina Swärd, Jordan M. Symons, Kian Bun Tai, James Tattersall, Luisa Tedeschi, Isaac Teitelbaum, Vicente P. Castro Teixeira, Ciro Tetta, Charuhas V. Thakar, Hermann Theilen, Karl W. Thomas, Ashita Tolwani, Francesco Trepiccione, Giorgio Triolo, Jennifer L.Y. Tsang, Emre Tutal, Shigehiko Uchino, Mark Unruh, G. Matthew Vail, Massimo Valentino, Volker Vallon, Wim Van Biesen, Frank M. van der Sande, Dominique M. Vandijck, Raymond Vanholder, Sanju A. Varghese, Ramesh Venkataraman, Bala Venkatesh, Anton Verbine, Jean-Louis Vincent, Christophe Vinsonneau, Ravindran Visvanathan, Alexandra Voinescu, Scott Walters, Li Wan, Peter A. Ward, Richard A. Ward, Stephen Warrillow, Steve Webb, Kenneth Scott Whitlow, Anders Wieslander, Alan H. Wilkinson, Keith Wille, James Frank Winchester, Christine Wu, James Yassin, Jane Y. Yeun, Terence Pok-Siu Yip, Alex W. Yu, Miriam Zacchia, Najam Zaida, Nereo Zamperetti, Michael Zappitelli, and Alexander Zarbock

Published
2009

15. Chapter 6 Renal Toxicities Associated with Immunomodulatory Drugs

Author

Alan D. Salama

Subjects
Autoimmune disease, Kidney, business.industry, medicine.medical_treatment, medicine.disease, medicine.disease_cause, Autoimmunity, medicine.anatomical_structure, Immunosuppressive drug, Immunity, Immunology, Toxicity, medicine, Adverse effect, business, Adjuvant
Abstract

Publisher Summary This chapter discusses the renal toxicities associated with immunomodulatory drugs. Immunosuppressive drug therapy remains an essential cornerstone of treatment in autoimmunity. Re-establishing immunological tolerance to particular auto-antigens, although highly desirable, is not yet achievable in a reproducible manner. The net effect is that although the autoimmune disease is treated, the patients may experience to adverse effects related to their loss of defensive immunity to pathogens and to malignantly transformed cells. This chapter reviews the renal toxicity associated with currently used immunosuppressants, immune modulators, and some adjuvant therapies frequently utilized with these agents. It highlights the explanation for these effects. This chapter discusses some of the novel agents that are becoming available and what is expected in the future regarding their use and their adverse effects on the kidney. This chapter also discusses the effects according to the renal compartments affected, as well as according to the agent used.

Published
2007

16. Treatment with Quinoline-3-carboxamide does not successfully prevent immune-mediated glomerulonephritis in mice

Author

Juliana Draibe, Alan D. Salama, and Ruth J. Pepper

Subjects
0301 basic medicine, Male, Kidney Glomerulus, lcsh:RC870-923, S100A9, Nephrotoxicity, S100A8, 03 medical and health sciences, chemistry.chemical_compound, Mice, 0302 clinical medicine, Immune system, Glomerulonephritis, Calprotectina, medicine, Animals, Animal model, Creatinine, Calprotectin, business.industry, Modelo animal, Glomerulonefritis, Animal models in research, medicine.disease, lcsh:Diseases of the genitourinary system. Urology, Mice, Inbred C57BL, 030104 developmental biology, chemistry, Nephrology, Immunology, Quinolines, Paquinimod, Models animals en la investigació, business, Nephritis, 030217 neurology & neurosurgery
Abstract

Introduction: Quinoline-3-carboximide compounds, such as paquinimod, which targets the protein S100A9, have demonstrated efficacy in treating autoimmune diseases. S100A9, in association with S100A8, forms the heterodimer S100A8/S100A9, known as calprotectin; that has been shown to be upregulated in numerous inflammatory disorders. We had previously demonstrated protection from glomerular disease in S100A9-deficient mice. The aim of this study was to assess the efficacy of paquinimod in the prevention and treatment of experimental glomerulonephritis. Methods: Nephrotoxic nephritis (NTN) was induced in C57BL/6 mice according to our standard protocol. Mice were treated with different doses of paquinimod either at disease induction (prevention group) or two days following induction (therapeutic group) and sacrificed 8 days following induction. Disease was assessed histologically (number of glomerular crescents, degree of glomerular thrombosis, number of infiltrating leucocytes and calprotectin expression) and biochemically (serum creatinine and urea levels, and urinary levels of protein). Results: Neither treatment with low (0.5 mg/kg) or high (25 mg/kg) doses of paquinimod, given preventatively or therapeutically, led to disease attenuation, as assessed by biochemical or histological parameters. Additionally, we found trends for an increase in renal glomerular calprotectin expression in the high dose groups, suggesting a possible feedback regulation of calprotectin expression. Conclusions: Our results show that paquinimod does not successfully prevent or treat mice with NTN. Other models of immune-mediated glomerulonephritis need to be tested to investigate the therapeutic potential of this compound in renal disease. (C) 2016 Sociedad Espanola de Nefrologia. Published by Elsevier Espana, S.L.U.

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