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113 results on '"Barros, Xoana"'

1. Phase 2 Trial of Cemdisiran in Adult Patients with IgA Nephropathy: A Randomized Controlled Trial

Author

Barratt, Jonathan, Liew, Adrian, Yeo, See Cheng, Fernström, Anders, Barbour, Sean J., Sperati, C. John, Villanueva, Russell, Wu, Ming-Ju, Wang, Dazhe, Borodovsky, Anna, Badri, Prajakta, Yureneva, Elena, Bhan, Ishir, Cattran, Daniel, Achanti, Anand, Budisavljevic, Milos, Walker, Linda, Aggarwal, Naresh, Andres, Stephanie, Navarro, Marie Stella, Gabuay, Haydee, Barany, Peter, Heimbürger, Olof, Durgé, Ulrika Jensen, Barbour, Sean, Sheriff, Zainab, MacLeod, Paula, Barratt, Jonathan, Cheung, Chee Kay, Selvaskandan, Haresh, Sklarzewicz, Justyna, Cattran, Daniel, Reich, Heather N., Ling, Paul, Jauhal, Arenn, Chantrel, Francois, Grellier, Jimmy, Alzina, Camille, Chen, Jin Bor, Chen, Kuan-Hsing, Hsu, Hsiang-Hao, Yang, Huang-Yu, Tu, Kun-Hua, Encarnacion, Montserrat Diaz, Rusiñol, Helena Marco, San Miguel Amigo, Luz, Bardaju de Quixano, Beatriz, Torres, Irene Silva, Espinosa, Mario, López-López, Isabel, Regalado, Rocío, Fernström, Anders, Gylling, Micael, Uhlin, Fredrik, Fervenza, Fernando, Goh, Bak Leong, Ibrahim, Fairol H., Alias, Aida Azlin, Lian, Tay Li, Hour, Billy, Rosales, Tyrone, Macias, Veronica, Kaskas, Marwan, Lanot, Antoine, Gueutin, Victor, Brucato, Sylvie, Legrand, Eric, Cabantous, Julie, Martin, Nadia, Barros, Xoana, Martínez, Cristina, Capdevila, Montserrat, Rovira, Irene, Mohamad Nor, Fariz Safhan, Ahmad, Mohd Kamil, Syahril Rozli Wan Ali, Wan Ahmad, Ng, Tze Jian, Atira Hisham, ‘Izzah’, Kamaronzaman, Nur Liyana, Mohamed Asri, Nadia Shahirah, Abu Othman, Mohamad Haziq, Mohd, Mohd Shahril, Moranne, Olivier, Ng, Kok Peng, Ooi, Shok Hoon, Ambros, Joan Torras, Coloma, Ana, Draibe, Juliana, Galofre, Claudia, Troyanov, Stephan, Marcotte, Guylaine, Villanueva, Russell, De Leon, Donnah Franceska, Wu, Ming-Ju, Lee, Shan, Yahya, Rosnawati, Yee, Seow Yeing, Wan Mohamad, Wan Hazlina, Nordin, Nurul Zaynah, Abdul Wahab, Muhamad Zaimi, Rohani, Zurina Che, Mod Baharuddin, Mohd Alfaisal, Asswad Kassim, Muhamad Nur, Zuhafifah Mohd Zaki, Siti Nur, Yeo, See Cheng, Lim, Ru Sin, Soh, Siew Hwa, Lee, Felicia, Jiao, Hongli, Lim, Rosa, Lin, Kai Yan, Zaoui, Philippe, Carron, Pierre-Louis, Tartry, David, Bugnazet, Mathilde, Imerzoukene, Farida, Theo, Florence, Dhion, Séverine, Argoud, Meryll, Vial, Gaëlle, Lehman, Audrey, and Romanet, Thierry

Published
2024
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2. Diagnosis and Treatment of Renal ANCA Vasculitis: A Summary of the Consensus Document of the Catalan Group for the Study of Glomerular Diseases (GLOMCAT).

Author

Draibe, Juliana Bordignon, Marco, Helena, Ibernon, Meritxell, Agraz, Irene, Arcal, Carola, Barros, Xoana, Cabrera, Victoria, Da Silva, Iara, Díaz, Montserrat, Fulladosa, Xavier, Guillén, Elena, Lescano, Patricia, Valenzuela, Laura Martínez, Márquez, Eva, Martín, Nadia, Merino, Ana, Navarro, Maru, Rodríguez, Eva, Soler, Mª José, and Torras, Joan

Abstract

The document provides a comprehensive overview of the diagnosis, monitoring, and treatment of anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV) with renal involvement, focusing on granulomatosis with polyangiitis (GPA) and microscopic polyangiitis (MPA). It outlines the definitions, clinical presentation, histopathological classification, monitoring strategies, induction and maintenance treatments, as well as special considerations for relapsing, refractory, and frail patients with renal AAV. The document was prepared by the Catalan Group for the Study of Glomerular Diseases (GLOMCAT), which comprises nephrologists with extensive experience in the diagnosis and treatment of AAV patients. Several virtual and face-to-face meetings were held for coordination, section assignments, and content discussion. An exhaustive and systematic search of the literature was carried out, which included, among others, the following databases: PubMed, EMBASE, Cochrane Library, Google Scholar, and ClinicalTrials.gov, as well as the abstract books of national and international congresses. Overall, the document provides a comprehensive guide for clinicians managing patients with renal AAV, offering evidence-based recommendations for diagnosis, monitoring, and treatment across various clinical scenarios. [ABSTRACT FROM AUTHOR]

Published
2024
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3. Acute Myeloid Leukemia as a Trigger for Hemolytic–Uremic Syndrome.

Author

El Bachouti, Jonas, Domínguez-Guasch, Anna, Arce, Yolanda, Oñate, Guadalupe, Marco, Helena, Diaz, Montserrat, Guirado, Lluís, Torra, Roser, and Barros, Xoana

Subjects
HEMOLYTIC-uremic syndrome, ACUTE myeloid leukemia, KIDNEY physiology, ECULIZUMAB, DIAGNOSIS
Abstract

Acute myeloid leukemia (AML) has not been identified as a cause of secondary hemolytic–uremic syndrome (HUS). This case report describes a woman who developed severe HUS at the time of AML diagnosis and responded favorably to initial treatment with eculizumab, which stabilized her condition and allowed for treatment of the AML. After one year, with stable renal function and genetic studies reported as normal, eculizumab was successfully discontinued. The prompt use of eculizumab was critical to the patient's survival and improvement in renal function, highlighting the efficacy of early eculizumab treatment in secondary HUS. [ABSTRACT FROM AUTHOR]

Published
2024
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4. #1803 Is class II lupus nephritis as benign as one thinks?

Author

Gonçalves, Pedro Lisboa, primary, Redondo, Gerson Berná, additional, Arce, Yolanda, additional, Magallares, Berta, additional, Castellvi, Ivan, additional, Pasache, Hans Kevin, additional, Dominguez, Anna, additional, Barros, Xoana, additional, Rusiñol, Helena Marco, additional, and Encarnacion, Montserrat Mercedes Diaz, additional

Published
2024
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6. #198 Different patterns of renal thrombotic microangiopathy

Author

Guasch, Anna Domínguez, primary, Arce, Yolanda, additional, Bachouti, Jonas E l, additional, Tinoco, Adria, additional, Pasache, Hans Kevin, additional, Basantes, Andrea Catalina, additional, Marco, Helena, additional, Torra, Roser, additional, Guirado, Lluis, additional, Encarnacion, Montserrat Mercedes Diaz, additional, and Barros, Xoana, additional

Published
2024
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7. Clinical profiles and patterns of kidney disease progression in C3 glomerulopathy

Author

Instituto de Salud Carlos III, European Commission, Red Española de Investigación Renal, Comunidad de Madrid, Ministerio de Economía y Competitividad (España), Caravaca-Fontán, Fernando [0000-0002-5830-9663], Cavero, Teresa [0000-0001-5187-9906], Díaz-Encarnación, Montserrat M. [0000-0001-5172-3370], Ariceta, Gema [0000-0003-1763-1098], Quintana, Luis F. [0000-0001-7582-8476], Barros, Xoana [0000-0001-9690-9769], Ramos, Natalia [0000-0001-9832-326X], Rodríguez-Mendiola, Nuria [0000-0001-6994-7161], Fernández-Juárez, Gema [0000-0001-6641-7763], Pérez de José, Ana [0000-0002-6952-1459], Pérez Gómez, Vanessa [0000-0003-4558-5236], Allende, Natalia [0000-0001-9857-793X], Sánchez de la Nieta, María Dolores [0000-0001-8574-0013], Rivas, Begoña [0000-0002-5886-9943], Melgosa, Marta [0000-0001-6236-414X], Huerta, Ana [0000-0003-3342-7628], Miquel, Rosa [0000-0002-0298-7342], Mon, Carmen [0000-0001-9081-8428], de Lorenzo, Alberto [0000-0001-8847-083X], Draibe, Juliana [0000-0002-2819-8560], González, Fayna [0000-0002-2313-2511], Shabaka, Amir [0000-0001-7039-4701], Martín-Penagos, L. [0000-0003-0159-7358], Rodríguez de Córdoba, Santiago [0000-0001-6401-1874], Goicoechea de Jorge, Elena [0000-0002-4978-2483], Praga, Manuel [0000-0001-9270-1071], Caravaca-Fontán, Fernando, Cavero, Teresa, Díaz-Encarnación, Montserrat M., Cabello-Chaves, Virginia, Ariceta, Gema, Quintana, Luis F., Marco, Helena, Barros, Xoana, Ramos, Natalia, Rodríguez-Mendiola, Nuria, Cruz, Sonia, Fernández-Juárez, Gema, Rodríguez, Adela, Pérez de José, Ana, Rabasco, Cristina, Rodado, Raquel, Fernández, Loreto, Pérez Gómez, Vanessa, Ávila, Ana, Bravo, Luis, Espinosa, Natalia, Allende, Natalia, Sánchez de la Nieta, María Dolores, Rodríguez, Eva, Rivas, Begoña, Melgosa, Marta, Huerta, Ana, Miquel, Rosa, Mon, Carmen, Fraga, Gloria, de Lorenzo, Alberto, Draibe, Juliana, González, Fayna, Shabaka, Amir, López-Rubio, María Esperanza, Fenollosa, María Ángeles, Martín-Penagos, L., Da Silva, Iara, Alonso Titos, Juana, Rodríguez de Córdoba, Santiago, Goicoechea de Jorge, Elena, Praga, Manuel, Instituto de Salud Carlos III, European Commission, Red Española de Investigación Renal, Comunidad de Madrid, Ministerio de Economía y Competitividad (España), Caravaca-Fontán, Fernando [0000-0002-5830-9663], Cavero, Teresa [0000-0001-5187-9906], Díaz-Encarnación, Montserrat M. [0000-0001-5172-3370], Ariceta, Gema [0000-0003-1763-1098], Quintana, Luis F. [0000-0001-7582-8476], Barros, Xoana [0000-0001-9690-9769], Ramos, Natalia [0000-0001-9832-326X], Rodríguez-Mendiola, Nuria [0000-0001-6994-7161], Fernández-Juárez, Gema [0000-0001-6641-7763], Pérez de José, Ana [0000-0002-6952-1459], Pérez Gómez, Vanessa [0000-0003-4558-5236], Allende, Natalia [0000-0001-9857-793X], Sánchez de la Nieta, María Dolores [0000-0001-8574-0013], Rivas, Begoña [0000-0002-5886-9943], Melgosa, Marta [0000-0001-6236-414X], Huerta, Ana [0000-0003-3342-7628], Miquel, Rosa [0000-0002-0298-7342], Mon, Carmen [0000-0001-9081-8428], de Lorenzo, Alberto [0000-0001-8847-083X], Draibe, Juliana [0000-0002-2819-8560], González, Fayna [0000-0002-2313-2511], Shabaka, Amir [0000-0001-7039-4701], Martín-Penagos, L. [0000-0003-0159-7358], Rodríguez de Córdoba, Santiago [0000-0001-6401-1874], Goicoechea de Jorge, Elena [0000-0002-4978-2483], Praga, Manuel [0000-0001-9270-1071], Caravaca-Fontán, Fernando, Cavero, Teresa, Díaz-Encarnación, Montserrat M., Cabello-Chaves, Virginia, Ariceta, Gema, Quintana, Luis F., Marco, Helena, Barros, Xoana, Ramos, Natalia, Rodríguez-Mendiola, Nuria, Cruz, Sonia, Fernández-Juárez, Gema, Rodríguez, Adela, Pérez de José, Ana, Rabasco, Cristina, Rodado, Raquel, Fernández, Loreto, Pérez Gómez, Vanessa, Ávila, Ana, Bravo, Luis, Espinosa, Natalia, Allende, Natalia, Sánchez de la Nieta, María Dolores, Rodríguez, Eva, Rivas, Begoña, Melgosa, Marta, Huerta, Ana, Miquel, Rosa, Mon, Carmen, Fraga, Gloria, de Lorenzo, Alberto, Draibe, Juliana, González, Fayna, Shabaka, Amir, López-Rubio, María Esperanza, Fenollosa, María Ángeles, Martín-Penagos, L., Da Silva, Iara, Alonso Titos, Juana, Rodríguez de Córdoba, Santiago, Goicoechea de Jorge, Elena, and Praga, Manuel

Abstract

Background C3 glomerulopathy is a rare kidney disease, which makes it difficult to collect large cohorts of patients to better understand its variability. The aims of this study were to describe the clinical profiles and patterns of progression of kidney disease., Methods This was a retrospective, observational cohort study. Patients diagnosed with C3 glomerulopathy between 1995 and 2020 were enrolled. Study population was divided into clinical profiles by combining the following predictors: eGFR under/above 30 ml/min per 1.73 m2, proteinuria under/above 3.5 g/d, and histologic chronicity score under/above 4. The change in eGFR and proteinuria over time was evaluated in a subgroup with consecutive measurements of eGFR and proteinuria., Results One hundred and fifteen patients with a median age of 30 years (interquartile range 19–50) were included. Patients were divided into eight clinical profiles. Kidney survival was significantly higher in patients with a chronicity score <4 and proteinuria <3.5 g/d, both in those presenting with an eGFR under/above 30 ml/min per 1.73 m2. The median eGFR slope of patients who reached kidney failure was −6.5 ml/min per 1.73 m2 per year (interquartile range −1.6 to −17). Patients who showed a reduction in proteinuria over time did not reach kidney failure. On the basis of the rate of eGFR decline, patients were classified as faster eGFR decline (≥5 ml/min per 1.73 m2 per year), slower (<5 ml/min per 1.73 m2 per year), and those without decline. A faster eGFR decline was associated with higher probability of kidney failure., Conclusions Kidney survival is significantly higher in patients with a chronicity score <4 and proteinuria <3.5 g/d regardless of baseline eGFR, and a faster rate of decline in eGFR is associated with higher probability of kidney failure.

Published
2023

8. Thrombotic microangiopathy in patients with malignant hypertension

Author

Instituto de Salud Carlos III, Ministerio de Economía y Competitividad (España), Ministerio de Ciencia, Innovación y Universidades (España), Comunidad de Madrid, Red Española de Investigación Renal, Cavero, Teresa [0000-0001-5187-9906], Auñón, Pilar [0000-0001-8017-0090], Caravaca-Fontán, Fernando [0000-0002-5830-9663], Trujillo, Hernando [0000-0002-3520-1422], Arjona, Emilia [0000-0002-0753-3657], Morales, Enrique [0000-0002-5824-6973], Guillén, Elena [0000-0002-5687-5549], Blasco, Miquel [0000-0003-0789-7992], Cao, Mercedes [0000-0002-8389-1800], Huerta, Ana [0000-0003-3342-7628], Rubio, Esther [0000-0002-6038-2827], Barros, Xoana [0000-0001-9690-9769], Goicoechea de Jorge, Elena [0000-0002-4978-2483], Rodríguez de Córdoba, Santiago [0000-0001-6401-1874], Praga, Manuel [0000-0001-9270-1071], Cavero, Teresa, Auñón, Pilar, Caravaca-Fontán, Fernando, Trujillo, Hernando, Arjona, Emilia, Morales, Enrique, Guillén, Elena, Blasco, Miquel, Rabasco, Cristina, Espinosa, Mario, Blanco, Marta, Rodríguez-Magariños, Catuxa, Cao, Mercedes, Ávila, Ana, Huerta, Ana, Rubio, Esther, Cabello-Chaves, Virginia, Barros, Xoana, Goicoechea de Jorge, Elena, Rodríguez de Córdoba, Santiago, Praga, Manuel, Instituto de Salud Carlos III, Ministerio de Economía y Competitividad (España), Ministerio de Ciencia, Innovación y Universidades (España), Comunidad de Madrid, Red Española de Investigación Renal, Cavero, Teresa [0000-0001-5187-9906], Auñón, Pilar [0000-0001-8017-0090], Caravaca-Fontán, Fernando [0000-0002-5830-9663], Trujillo, Hernando [0000-0002-3520-1422], Arjona, Emilia [0000-0002-0753-3657], Morales, Enrique [0000-0002-5824-6973], Guillén, Elena [0000-0002-5687-5549], Blasco, Miquel [0000-0003-0789-7992], Cao, Mercedes [0000-0002-8389-1800], Huerta, Ana [0000-0003-3342-7628], Rubio, Esther [0000-0002-6038-2827], Barros, Xoana [0000-0001-9690-9769], Goicoechea de Jorge, Elena [0000-0002-4978-2483], Rodríguez de Córdoba, Santiago [0000-0001-6401-1874], Praga, Manuel [0000-0001-9270-1071], Cavero, Teresa, Auñón, Pilar, Caravaca-Fontán, Fernando, Trujillo, Hernando, Arjona, Emilia, Morales, Enrique, Guillén, Elena, Blasco, Miquel, Rabasco, Cristina, Espinosa, Mario, Blanco, Marta, Rodríguez-Magariños, Catuxa, Cao, Mercedes, Ávila, Ana, Huerta, Ana, Rubio, Esther, Cabello-Chaves, Virginia, Barros, Xoana, Goicoechea de Jorge, Elena, Rodríguez de Córdoba, Santiago, and Praga, Manuel

Abstract

Background: Thrombotic microangiopathy (TMA) is a complication of malignant hypertension (mHTN) attributed to high blood pressure (BP). However, no studies have investigated in patients with mHTN of different aetiologies whether the presence of TMA is associated with specific causes of mHTN., Methods: We investigated the presence of TMA (microangiopathic haemolytic anaemia and thrombocytopenia) in a large and well-characterized cohort of 199 patients with mHTN of different aetiologies [primary HTN 44%, glomerular diseases 16.6%, primary atypical haemolytic uraemic syndrome (aHUS) 13.1%, renovascular HTN 9.5%, drug-related HTN 7%, systemic diseases 5.5%, endocrine diseases 4.5%]. Outcomes of the study were kidney recovery and kidney failure., Results: Patients with TMA [40 cases (20.1%)] were younger, were more likely female and had lower BP levels and worse kidney function at presentation. Their underlying diseases were primary aHUS (60%), drug-related mHTN (15%), glomerular diseases [all of them immunoglobulin A nephropathy (IgAN); 10%], systemic diseases (10%) and primary HTN (5%). The presence of TMA was 92.3% in primary aHUS, 42.9% in drug-related HTN, 36.4% in systemic diseases, 12.1% in glomerular diseases and 2.3% in primary HTN. No patient with renovascular HTN or mHTN caused by endocrine diseases developed TMA, despite BP levels as high as patients with TMA. A higher proportion of TMA patients developed kidney failure as compared with patients without TMA (56.4% versus 38.9%, respectively)., Conclusions: The presence of TMA in patients with mHTN should guide the diagnosis towards primary aHUS, drug-related mHTN, some systemic diseases and IgAN, while it is exceptional in other causes of mHTN.

Published
2023

9. Clinical profiles and patterns of kidney disease progression in C3 glomerulopathy

Author

Caravaca-Fontán, Fernando, Cavero, Teresa, Díaz-Encarnación, Montserrat M., Cabello-Chaves, Virginia, Ariceta, Gema, Quintana, Luis F., Marco, Helena, Barros, Xoana, Ramos, Natalia, Rodríguez-Mendiola, Nuria, Cruz, Sonia, Fernández-Juárez, Gema, Rodríguez, Adela, Pérez de José, Ana, Rabasco, Cristina, Rodado, Raquel, Fernández, Loreto, Pérez Gómez, Vanessa, Ávila, Ana, Bravo, Luis, Espinosa, Natalia, Allende, Natalia, Sánchez de la Nieta, María Dolores, Rodríguez, Eva, Rivas, Begoña, Melgosa, Marta, Huerta, Ana, Miquel, Rosa, Mon, Carmen, Fraga, Gloria, de Lorenzo, Alberto, Draibe, Juliana, González, Fayna, Shabaka, Amir, López-Rubio, María Esperanza, Fenollosa, María Ángeles, Martín-Penagos, L., Da Silva, Iara, Alonso Titos, Juana, Rodríguez de Córdoba, Santiago, Goicoechea de Jorge, Elena, Praga, Manuel, Instituto de Salud Carlos III, European Commission, Red de Investigación Renal (España), Comunidad de Madrid, Ministerio de Economía y Competitividad (España), Caravaca-Fontán, Fernando, Cavero, Teresa, Díaz-Encarnación, Montserrat M., Ariceta, Gema, Quintana, Luis F., Barros, Xoana, Ramos, Natalia, Rodríguez-Mendiola, Nuria, Fernández-Juárez, Gema, Pérez de José, Ana, Pérez Gómez, Vanessa, Allende, Natalia, Sánchez de la Nieta, María Dolores, Rivas, Begoña, Melgosa, Marta, Huerta, Ana, Miquel, Rosa, Mon, Carmen, de Lorenzo, Alberto, Draibe, Juliana, González, Fayna, Shabaka, Amir, Martín-Penagos, L., Rodríguez de Córdoba, Santiago, Goicoechea de Jorge, Elena, and Praga, Manuel

Abstract

14 p.-4 fig.-3 tab., Background C3 glomerulopathy is a rare kidney disease, which makes it difficult to collect large cohorts of patients to better understand its variability. The aims of this study were to describe the clinical profiles and patterns of progression of kidney disease., Methods This was a retrospective, observational cohort study. Patients diagnosed with C3 glomerulopathy between 1995 and 2020 were enrolled. Study population was divided into clinical profiles by combining the following predictors: eGFR under/above 30 ml/min per 1.73 m2, proteinuria under/above 3.5 g/d, and histologic chronicity score under/above 4. The change in eGFR and proteinuria over time was evaluated in a subgroup with consecutive measurements of eGFR and proteinuria., Results One hundred and fifteen patients with a median age of 30 years (interquartile range 19–50) were included. Patients were divided into eight clinical profiles. Kidney survival was significantly higher in patients with a chronicity score, Conclusions Kidney survival is significantly higher in patients with a chronicity score, Work in this study was supported by the Instituto de Salud Carlos III/Fondo Europeo de Desarrollo Regional (ISCIII/FEDER) grant PI16/01685 and PI19/1624, and Red de Investigación Renal (RedInRen) (RD12/0021/0029) (to MP), the Autonomous Region of Madrid (S2017/BMD-3673) (to MP). SRdeC is supported by Ministerio de Economia y Competitividad grant PID2019-104912RB-I00 y Autonomous Region of Madrid grant S2017/BMD-3673.

Published
2023

10. Development and validation of a nomogram to predict kidney survival at baseline in patients with C3 glomerulopathy

Author

Instituto de Salud Carlos III, Red Española de Investigación Renal, Comunidad de Madrid, Ministerio de Economía y Competitividad (España), Caravaca-Fontán, Fernando [0000-0002-5830-9663], Cavero, Teresa [0000-0001-5187-9906], Díaz-Encarnación, Montserrat M. [0000-0001-5172-3370], Ariceta, Gema [0000-0003-1763-1098], Quintana, Luis F. [0000-0001-7582-8476], Barros, Xoana [0000-0001-9690-9769], Ramos, Natalia [0000-0001-9832-326X], Rodríguez-Mendiola, Nuria [0000-0001-6994-7161], Fernández-Juárez, Gema [0000-0001-6641-7763], Pérez de José, Ana [0000-0002-6952-1459], Pérez Gómez, Vanessa [0000-0003-4558-5236], Allende, Natalia [0000-0001-9857-793X], Sánchez de la Nieta, María Dolores [0000-0001-8574-0013], Olea, Teresa [0000-0003-2370-1048], Melgosa, Marta [0000-0001-6236-414X], Huerta, Ana [0000-0003-3342-7628], Mon, Carmen [0000-0001-9081-8428], de Lorenzo, Alberto [0000-0001-8847-083X], Draibe, Juliana [0000-0002-2819-8560], González, Fayna [0000-0002-2313-2511], Shabaka, Amir [0000-0001-7039-4701], Martín-Penagos, L. [0000-0003-0159-7358], Rodríguez de Córdoba, Santiago [0000-0001-6401-1874], Goicoechea de Jorge, Elena [0000-0002-4978-2483], Praga, Manuel [0000-0001-9270-1071], Caravaca-Fontán, Fernando, Rivero, Marta, Cavero, Teresa, Díaz-Encarnación, Montserrat M., Cabello-Chaves, Virginia, Ariceta, Gema, Quintana, Luis F., Marco, Helena, Barros, Xoana, Ramos, Natalia, Rodríguez-Mendiola, Nuria, Cruz, Sonia, Fernández-Juárez, Gema, Rodríguez, Adela, Pérez de José, Ana, Rabasco, Cristina, Rodado, Raquel, Fernández, Loreto, Pérez Gómez, Vanessa, Ávila, Ana, Bravo, Luis, Espinosa, Natalia, Allende, Natalia, Sánchez de la Nieta, María Dolores, Rodríguez, Eva, Olea, Teresa, Melgosa, Marta, Huerta, Ana, Miquel, Rosa, Mon, Carmen, Fraga, Gloria, de Lorenzo, Alberto, Draibe, Juliana, González, Fayna, Shabaka, Amir, López-Rubio, María Esperanza, Fenollosa, María Ángeles, Martín-Penagos, L., Da Silva, Iara, Alonso Titos, Juana, Rodríguez de Córdoba, Santiago, Goicoechea de Jorge, Elena, Praga, Manuel, Instituto de Salud Carlos III, Red Española de Investigación Renal, Comunidad de Madrid, Ministerio de Economía y Competitividad (España), Caravaca-Fontán, Fernando [0000-0002-5830-9663], Cavero, Teresa [0000-0001-5187-9906], Díaz-Encarnación, Montserrat M. [0000-0001-5172-3370], Ariceta, Gema [0000-0003-1763-1098], Quintana, Luis F. [0000-0001-7582-8476], Barros, Xoana [0000-0001-9690-9769], Ramos, Natalia [0000-0001-9832-326X], Rodríguez-Mendiola, Nuria [0000-0001-6994-7161], Fernández-Juárez, Gema [0000-0001-6641-7763], Pérez de José, Ana [0000-0002-6952-1459], Pérez Gómez, Vanessa [0000-0003-4558-5236], Allende, Natalia [0000-0001-9857-793X], Sánchez de la Nieta, María Dolores [0000-0001-8574-0013], Olea, Teresa [0000-0003-2370-1048], Melgosa, Marta [0000-0001-6236-414X], Huerta, Ana [0000-0003-3342-7628], Mon, Carmen [0000-0001-9081-8428], de Lorenzo, Alberto [0000-0001-8847-083X], Draibe, Juliana [0000-0002-2819-8560], González, Fayna [0000-0002-2313-2511], Shabaka, Amir [0000-0001-7039-4701], Martín-Penagos, L. [0000-0003-0159-7358], Rodríguez de Córdoba, Santiago [0000-0001-6401-1874], Goicoechea de Jorge, Elena [0000-0002-4978-2483], Praga, Manuel [0000-0001-9270-1071], Caravaca-Fontán, Fernando, Rivero, Marta, Cavero, Teresa, Díaz-Encarnación, Montserrat M., Cabello-Chaves, Virginia, Ariceta, Gema, Quintana, Luis F., Marco, Helena, Barros, Xoana, Ramos, Natalia, Rodríguez-Mendiola, Nuria, Cruz, Sonia, Fernández-Juárez, Gema, Rodríguez, Adela, Pérez de José, Ana, Rabasco, Cristina, Rodado, Raquel, Fernández, Loreto, Pérez Gómez, Vanessa, Ávila, Ana, Bravo, Luis, Espinosa, Natalia, Allende, Natalia, Sánchez de la Nieta, María Dolores, Rodríguez, Eva, Olea, Teresa, Melgosa, Marta, Huerta, Ana, Miquel, Rosa, Mon, Carmen, Fraga, Gloria, de Lorenzo, Alberto, Draibe, Juliana, González, Fayna, Shabaka, Amir, López-Rubio, María Esperanza, Fenollosa, María Ángeles, Martín-Penagos, L., Da Silva, Iara, Alonso Titos, Juana, Rodríguez de Córdoba, Santiago, Goicoechea de Jorge, Elena, and Praga, Manuel

Abstract

Background: C3 glomerulopathy is a rare and heterogeneous complement-driven disease. It is often challenging to accurately predict in clinical practice the individual kidney prognosis at baseline. We herein sought to develop and validate a prognostic nomogram to predict long-term kidney survival., Methods: We conducted a retrospective, multicenter observational cohort study in 35 nephrology departments belonging to the Spanish Group for the Study of Glomerular Diseases. The dataset was randomly divided into a training group (n = 87) and a validation group (n = 28). The least absolute shrinkage and selection operator (LASSO) regression was used to screen the main predictors of kidney outcome and to build the nomogram. The accuracy of the nomogram was assessed by discrimination and risk calibration in the training and validation sets., Results: The study group comprised 115 patients, of whom 46 (40%) reached kidney failure in a median follow-up of 49 months (range 24–112). No significant differences were observed in baseline estimated glomerular filtration rate (eGFR), proteinuria or total chronicity score of kidney biopsies, between patients in the training versus those in the validation set. The selected variables by LASSO were eGFR, proteinuria and total chronicity score. Based on a Cox model, a nomogram was developed for the prediction of kidney survival at 1, 2, 5 and 10 years from diagnosis. The C-index of the nomogram was 0.860 (95% confidence interval 0.834–0.887) and calibration plots showed optimal agreement between predicted and observed outcomes., Conclusions: We constructed and validated a practical nomogram with good discrimination and calibration to predict the risk of kidney failure in C3 glomerulopathy patients at 1, 2, 5 and 10 years.

Published
2022

11. #5009 GESTATIONAL COUNSELING DURING PREGNANCY IN PATIENTS WITH KIDNEY DISEASE: EXPERIENCE OF A MULTIDISCIPLINARY TEAM

Author

Brito, María Verónica Coll, primary, Redondo, Gerson Berna, additional, Lopez, Berta Magallares, additional, Olivé, Elisa Llurba, additional, Barros, Xoana, additional, Dominguez, Anna, additional, Bardaji, Beatriz, additional, Guirado, Lluis, additional, Encarnacion, Monserrat Diaz, additional, and Rusiñol, Helena Marco, additional

Published
2023
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13. The coexistence of diabetic retinopathy and diabetic nephropathy is associated with worse kidney outcomes.

Author

Bermejo, Sheila, González, Ester, López-Revuelta, Katia, Ibernon, Meritxell, López, Diana, Martín-Gómez, Adoración, Garcia-Osuna, Rosa, Linares, Tania, Díaz, Montserrat, Martín, Nàdia, Barros, Xoana, Marco, Helena, Navarro, Maruja Isabel, Esparza, Noemí, Elias, Sandra, Coloma, Ana, Robles, Nicolás Roberto, Agraz, Irene, Poch, Esteban, and Rodas, Lida

Subjects
DIABETIC retinopathy, DIABETIC nephropathies, RENAL replacement therapy, DIABETES complications, RENAL biopsy, KIDNEY failure
Abstract

Background Up to 50–60% of patients with diabetes have non-diabetic kidney disease (NDKD) on kidney biopsy. Diabetic retinopathy (DR) is a microvascular complication of diabetes frequently associated with diabetic nephropathy (DN). The objective of the current study was to investigate the kidney outcomes and survival in patients with biopsy diagnoses of DN and NDKD according to the presence of DR. Methods We conducted an observational, multicentre and retrospective study of the pathological findings of renal biopsies from 832 consecutive patients with diabetes from 2002 to 2014 from 18 nephrology departments. The association of DR with kidney replacement therapy (KRT) or survival was assessed by Kaplan–Meier and Cox regression analyses. Results Of 832 patients with diabetes and renal biopsy, 768 had a retinal examination and 221/768 (22.6%) had DR. During a follow-up of 10 years, 288/760 (37.9%) patients with follow-up data needed KRT and 157/760 (20.7%) died. The incidence of KRT was higher among patients with DN (alone or with NDKD) and DR [103/175 (58.9%)] than among patients without DR [88/216 (40.7%), P  < .0001]. The incidence of KRT was also higher among patients with only NDKD and DR than among those without DR [18/46 (39.1%) versus 79/331 (23.9%), P  < .0001]. In multivariate analysis, DR or DN were independent risk factors for KRT {hazard ratio [HR] 2.48 [confidence interval (CI) 1.85–3.31], P  < .001}. DN (with or without DR) was also identified as an independent risk factor for mortality [HR 1.81 (CI 1.26–2.62), P  = .001]. Conclusions DR is associated with a higher risk of progression to kidney failure in patients with histological DN and in patients with NDKD. [ABSTRACT FROM AUTHOR]

Published
2023
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15. Longitudinal change in proteinuria and kidney outcomes in C3 glomerulopathy

Author

Instituto de Salud Carlos III, European Commission, Red Española de Investigación Renal, Comunidad de Madrid, Ministerio de Ciencia, Innovación y Universidades (España), Ministerio de Economía y Competitividad (España), Caravaca-Fontán, Fernando [0000-0002-5830-9663], Díaz-Encarnación, Montserrat M. [0000-0001-5172-3370], Cabello, Virginia [0000-0002-0877-5498], Ariceta, Gema [0000-0003-1763-1098], Quintana, Luis F. [0000-0001-7582-8476], Barros, Xoana [0000-0001-9690-9769], Ramos, Natalia [0000-0001-9832-326X], Rodríguez-Mendiola, Nuria [0000-0001-6994-7161], Fernández-Juárez, Gema [0000-0001-6641-7763], Pérez de José, Ana [0000-0002-6952-1459], Pérez Gómez, Vanessa [0000-0003-4558-5236], Sánchez de la Nieta, María Dolores [0000-0001-8574-0013], Olea, Teresa [0000-0003-2370-1048], Melgosa, Marta [0000-0001-6236-414X], Huerta, Ana [0000-0003-3342-7628], de Lorenzo, Alberto [0000-0001-8847-083X], Draibe, Juliana [0000-0002-2819-8560], González, Fayna [0000-0002-2313-2511], Shabaka, Amir [0000-0001-7039-4701], Martín-Penagos, L. [0000-0003-0159-7358], Rodríguez de Córdoba, Santiago [0000-0001-6401-1874], Goicoechea de Jorge, Elena [0000-0002-4978-2483], Praga, Manuel [0000-0001-9270-1071], Caravaca-Fontán, Fernando, Díaz-Encarnación, Montserrat M., Cabello, Virginia, Ariceta, Gema, Quintana, Luis F., Marco, Helena, Barros, Xoana, Ramos, Natalia, Rodríguez-Mendiola, Nuria, Cruz, Sonia, Fernández-Juárez, Gema, Rodríguez, Adela, Pérez de José, Ana, Rabasco, Cristina, Rodado, Raquel, Fernández, Loreto, Pérez Gómez, Vanessa, Ávila, Ana, Bravo, Luis, Espinosa, Natalia, Allende, Natalia, Sánchez de la Nieta, María Dolores, Rodríguez, Eva, Olea, Teresa, Melgosa, Marta, Huerta, Ana, Miquel, Rosa, Mon, Carmen, Fraga, Gloria, de Lorenzo, Alberto, Draibe, Juliana, Cano-Megías, Marta, González, Fayna, Shabaka, Amir, López-Rubio, María Esperanza, Fenollosa, María Ángeles, Martín-Penagos, L., Da Silva, Iara, Alonso Titos, Juana, Rodríguez de Córdoba, Santiago, Goicoechea de Jorge, Elena, Praga, Manuel, Spanish Group for the Study of Glomerular Diseases (GLOSEN), Instituto de Salud Carlos III, European Commission, Red Española de Investigación Renal, Comunidad de Madrid, Ministerio de Ciencia, Innovación y Universidades (España), Ministerio de Economía y Competitividad (España), Caravaca-Fontán, Fernando [0000-0002-5830-9663], Díaz-Encarnación, Montserrat M. [0000-0001-5172-3370], Cabello, Virginia [0000-0002-0877-5498], Ariceta, Gema [0000-0003-1763-1098], Quintana, Luis F. [0000-0001-7582-8476], Barros, Xoana [0000-0001-9690-9769], Ramos, Natalia [0000-0001-9832-326X], Rodríguez-Mendiola, Nuria [0000-0001-6994-7161], Fernández-Juárez, Gema [0000-0001-6641-7763], Pérez de José, Ana [0000-0002-6952-1459], Pérez Gómez, Vanessa [0000-0003-4558-5236], Sánchez de la Nieta, María Dolores [0000-0001-8574-0013], Olea, Teresa [0000-0003-2370-1048], Melgosa, Marta [0000-0001-6236-414X], Huerta, Ana [0000-0003-3342-7628], de Lorenzo, Alberto [0000-0001-8847-083X], Draibe, Juliana [0000-0002-2819-8560], González, Fayna [0000-0002-2313-2511], Shabaka, Amir [0000-0001-7039-4701], Martín-Penagos, L. [0000-0003-0159-7358], Rodríguez de Córdoba, Santiago [0000-0001-6401-1874], Goicoechea de Jorge, Elena [0000-0002-4978-2483], Praga, Manuel [0000-0001-9270-1071], Caravaca-Fontán, Fernando, Díaz-Encarnación, Montserrat M., Cabello, Virginia, Ariceta, Gema, Quintana, Luis F., Marco, Helena, Barros, Xoana, Ramos, Natalia, Rodríguez-Mendiola, Nuria, Cruz, Sonia, Fernández-Juárez, Gema, Rodríguez, Adela, Pérez de José, Ana, Rabasco, Cristina, Rodado, Raquel, Fernández, Loreto, Pérez Gómez, Vanessa, Ávila, Ana, Bravo, Luis, Espinosa, Natalia, Allende, Natalia, Sánchez de la Nieta, María Dolores, Rodríguez, Eva, Olea, Teresa, Melgosa, Marta, Huerta, Ana, Miquel, Rosa, Mon, Carmen, Fraga, Gloria, de Lorenzo, Alberto, Draibe, Juliana, Cano-Megías, Marta, González, Fayna, Shabaka, Amir, López-Rubio, María Esperanza, Fenollosa, María Ángeles, Martín-Penagos, L., Da Silva, Iara, Alonso Titos, Juana, Rodríguez de Córdoba, Santiago, Goicoechea de Jorge, Elena, Praga, Manuel, and Spanish Group for the Study of Glomerular Diseases (GLOSEN)

Abstract

Introduction: The association between a change in proteinuria over time and its impact in kidney prognosis has not been analyzed in C3 glomerulopathy. This study aims to investigate the association between the longitudinal change in proteinuria and the risk of kidney failure., Methods: Retrospective, multicenter observational cohort study in 35 nephrology departments belonging to the Spanish Group for the Study of Glomerular Diseases (GLOSEN). Patients diagnosed with C3 glomerulopathy between 1995 and 2020 were enrolled. A joint modeling of linear mixed-effects models was applied to assess the underlying trajectory of a repeatedly measured proteinuria, and a Cox model to evaluate the association of this trajectory with the risk of kidney failure., Results: The study group consisted of 85 patients, 70 C3 glomerulonephritis and 15 dense deposit disease, with a median age of 26 years (range 13-41). During a median follow-up of 42 months, 25 patients reached kidney failure. The longitudinal change in proteinuria showed a strong association with the risk of this outcome, with a doubling of proteinuria levels resulting in a 2.5-fold increase of the risk. A second model showed that a ≥ 50% proteinuria reduction over time was significantly associated with a lower risk of kidney failure (HR: 0.79; 95% CI : 0.56-0.97; p < 0.001). This association was also found when the ≥50% proteinuria reduction was observed within the first 6 and 12 months of follow-up., Conclusion: The longitudinal change in proteinuria is strongly associated with the risk of kidney failure. The change in proteinuria over time can provide clinicians a dynamic prediction of kidney outcomes.

Published
2021

18. Longitudinal change in proteinuria and kidney outcomes in C3 glomerulopathy

Author

Caravaca-Fontán, Fernando, Díaz-Encarnación, Montserrat M., Cabello, Virginia, Ariceta, Gema, Quintana, Luis F., Marco, Helena, Barros, Xoana, Ramos, Natalia, Rodríguez-Mendiola, Nuria, Cruz, Sonia, Fernández-Juárez, Gema, Rodríguez, Adela, Pérez de José, Ana, Rabasco, Cristina, Rodado, Raquel, Fernández, Loreto, Pérez Gómez, Vanessa, Ávila, Ana, Bravo, Luis, Espinosa, Natalia, Allende, Natalia, Sánchez de la Nieta, María Dolores, Rodríguez, Eva, Olea, Teresa, Melgosa, Marta, Huerta, Ana, Miquel, Rosa, Mon, Carmen, Fraga, Gloria, de Lorenzo, Alberto, Draibe, Juliana, Cano-Megías, Marta, González, Fayna, Shabaka, Amir, López-Rubio, María Esperanza, Fenollosa, María Ángeles, Martín-Penagos, L., Da Silva, Iara, Alonso Titos, Juana, Rodríguez de Córdoba, Santiago, Goicoechea de Jorge, Elena, Praga, Manuel, Spanish Group for the Study of Glomerular Diseases (GLOSEN), Instituto de Salud Carlos III, European Commission, Red Española de Investigación Renal, Comunidad de Madrid, Ministerio de Ciencia, Innovación y Universidades (España), Ministerio de Economía y Competitividad (España), Caravaca-Fontán, Fernando [0000-0002-5830-9663], Díaz-Encarnación, Montserrat M. [0000-0001-5172-3370], Cabello, Virginia [0000-0002-0877-5498], Ariceta, Gema [0000-0003-1763-1098], Quintana, Luis F. [0000-0001-7582-8476], Barros, Xoana [0000-0001-9690-9769], Ramos, Natalia [0000-0001-9832-326X], Rodríguez-Mendiola, Nuria [0000-0001-6994-7161], Fernández-Juárez, Gema [0000-0001-6641-7763], Pérez de José, Ana [0000-0002-6952-1459], Pérez Gómez, Vanessa [0000-0003-4558-5236], Sánchez de la Nieta, María Dolores [0000-0001-8574-0013], Olea, Teresa [0000-0003-2370-1048], Melgosa, Marta [0000-0001-6236-414X], Huerta, Ana [0000-0003-3342-7628], de Lorenzo, Alberto [0000-0001-8847-083X], Draibe, Juliana [0000-0002-2819-8560], González, Fayna [0000-0002-2313-2511], Shabaka, Amir [0000-0001-7039-4701], Martín-Penagos, L. [0000-0003-0159-7358], Rodríguez de Córdoba, Santiago [0000-0001-6401-1874], Goicoechea de Jorge, Elena [0000-0002-4978-2483], Praga, Manuel [0000-0001-9270-1071], Caravaca-Fontán, Fernando, Díaz-Encarnación, Montserrat M., Cabello, Virginia, Ariceta, Gema, Quintana, Luis F., Barros, Xoana, Ramos, Natalia, Rodríguez-Mendiola, Nuria, Fernández-Juárez, Gema, Pérez de José, Ana, Pérez Gómez, Vanessa, Sánchez de la Nieta, María Dolores, Olea, Teresa, Melgosa, Marta, Huerta, Ana, de Lorenzo, Alberto, Draibe, Juliana, González, Fayna, Shabaka, Amir, Martín-Penagos, L., Rodríguez de Córdoba, Santiago, Goicoechea de Jorge, Elena, and Praga, Manuel

Subjects
Nephrology, Adult, medicine.medical_specialty, Adolescent, Glomerulonephritis, Membranoproliferative, 030232 urology & nephrology, Kidney failure, 030204 cardiovascular system & hematology, Lower risk, Kidney, 03 medical and health sciences, Joint models, Young Adult, 0302 clinical medicine, Glomerulonephritis, Glomerulopathy, Internal medicine, medicine, Humans, C3 glomerulopathy, Retrospective Studies, Transplantation, Proteinuria, business.industry, Proportional hazards model, urogenital system, Complement C3, medicine.disease, medicine.anatomical_structure, Kidney Failure, Chronic, medicine.symptom, business, Cohort study
Abstract

11 p.-4 fig.-4 tab., Introduction: The association between a change in proteinuria over time and its impact in kidney prognosis has not been analyzed in C3 glomerulopathy. This study aims to investigate the association between the longitudinal change in proteinuria and the risk of kidney failure., Methods: Retrospective, multicenter observational cohort study in 35 nephrology departments belonging to the Spanish Group for the Study of Glomerular Diseases (GLOSEN). Patients diagnosed with C3 glomerulopathy between 1995 and 2020 were enrolled. A joint modeling of linear mixed-effects models was applied to assess the underlying trajectory of a repeatedly measured proteinuria, and a Cox model to evaluate the association of this trajectory with the risk of kidney failure., Results: The study group consisted of 85 patients, 70 C3 glomerulonephritis and 15 dense deposit disease, with a median age of 26 years (range 13-41). During a median follow-up of 42 months, 25 patients reached kidney failure. The longitudinal change in proteinuria showed a strong association with the risk of this outcome, with a doubling of proteinuria levels resulting in a 2.5-fold increase of the risk. A second model showed that a ≥ 50% proteinuria reduction over time was significantly associated with a lower risk of kidney failure (HR: 0.79; 95% CI : 0.56-0.97; p < 0.001). This association was also found when the ≥50% proteinuria reduction was observed within the first 6 and 12 months of follow-up., Conclusion: The longitudinal change in proteinuria is strongly associated with the risk of kidney failure. The change in proteinuria over time can provide clinicians a dynamic prediction of kidney outcomes., This study was supported by the Instituto de Salud Carlos III/Fondo Europeo de Desarrollo Regional (ISCIII/FEDER) grant PI16/01685 and PI19/1624, and Red de Investigación Renal (RedInRen) (RD12/0021/0029) (to M.P.), the Autonomous Region of Madrid (S2017/BMD-3673) (to M.P.); E.G.d.J. was supported by the Spanish ‘Ministerio de Ciencia, Innovación y Universidades’ (RYC-2013-13395 and RTI2018-095955-B-100); S.R.d.C. was supported by Ministerio de Economía y Competitividad/FEDER grant SAF2015-66287R and Autonomous Region of Madrid grant S2017/BMD3673.

Published
2021

19. Thrombotic microangiopathy in patients with malignant hypertension

Author

Cavero, Teresa, primary, Auñón, Pilar, additional, Caravaca-Fontán, Fernando, additional, Trujillo, Hernando, additional, Arjona, Emi, additional, Morales, Enrique, additional, Guillén, Elena, additional, Blasco, Miquel, additional, Rabasco, Cristina, additional, Espinosa, Mario, additional, Blanco, Marta, additional, Rodríguez-Magariños, Catuxa, additional, Cao, Mercedes, additional, Ávila, Ana, additional, Huerta, Ana, additional, Rubio, Esther, additional, Cabello, Virginia, additional, Barros, Xoana, additional, Goicoechea de Jorge, Elena, additional, Rodríguez de Córdoba, Santiago, additional, and Praga, Manuel, additional

Published
2022
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20. Mycophenolate Mofetil in C3 glomerulopathy and pathogenic drivers of the disease

Author

Instituto de Salud Carlos III, Red Española de Investigación Renal, Comunidad de Madrid, Ministerio de Ciencia, Innovación y Universidades (España), Ministerio de Economía y Competitividad (España), Caravaca-Fontán, Fernando [0000-0002-5830-9663], Díaz-Encarnación, Montserrat M. [0000-0001-5172-3370], Lucientes, Laura [0000-0001-5596-370X], Cavero, Teresa [0000-0001-5187-9906], Ariceta, Gema [0000-0003-1763-1098], Quintana, Luis F. [0000-0001-7582-8476], Barros, Xoana [0000-0001-9690-9769], Ramos, Natalia [0000-0001-9832-326X], Rodríguez-Mendiola, Nuria [0000-0001-6994-7161], Fernández-Juárez, Gema [0000-0001-6641-7763], Pérez de José, Ana [0000-0002-6952-1459], Pérez Gómez, Vanessa [0000-0003-4558-5236], Lumbreras, Javier [0000-0003-1855-0724], Sánchez de la Nieta, María Dolores [0000-0001-8574-0013], Olea, Teresa [0000-0003-2370-1048], Melgosa, Marta [0000-0001-6236-414X], Huerta, Ana [0000-0003-3342-7628], de Lorenzo, Alberto [0000-0001-8847-083X], Draibe, Juliana [0000-0002-2819-8560], González, Fayna [0000-0002-2313-2511], Shabaka, Amir [0000-0001-7039-4701], Martín-Penagos, L. [0000-0003-0159-7358], Rodríguez de Córdoba, Santiago [0000-0001-6401-1874], Praga, Manuel [0000-0001-9270-1071], Goicoechea de Jorge, Elena [0000-0002-4978-2483], Caravaca-Fontán, Fernando, Díaz-Encarnación, Montserrat M., Lucientes, Laura, Cavero, Teresa, Cabello-Chaves, Virginia, Ariceta, Gema, Quintana, Luis F., Marco, Helena, Barros, Xoana, Ramos, Natalia, Rodríguez-Mendiola, Nuria, Cruz, Sonia, Fernández-Juárez, Gema, Rodríguez, Adela, Pérez de José, Ana, Rabasco, Cristina, Rodado, Raquel, Fernández, Loreto, Pérez Gómez, Vanessa, Ávila, Ana, Bravo, Luis, Lumbreras, Javier, Allende, Natalia, Sánchez de la Nieta, María Dolores, Rodríguez, Eva, Olea, Teresa, Melgosa, Marta, Huerta, Ana, Miquel, Rosa, Mon, Carmen, Fraga, Gloria, de Lorenzo, Alberto, Cano-Megías, Marta, González, Fayna, Shabaka, Amir, López-Rubio, María Esperanza, Fenollosa, María Ángeles, Martín-Penagos, L., Da Silva, Iara, Alonso Titos, Juana, Rodríguez de Córdoba, Santiago, Goicoechea de Jorge, Elena, Praga, Manuel, Instituto de Salud Carlos III, Red Española de Investigación Renal, Comunidad de Madrid, Ministerio de Ciencia, Innovación y Universidades (España), Ministerio de Economía y Competitividad (España), Caravaca-Fontán, Fernando [0000-0002-5830-9663], Díaz-Encarnación, Montserrat M. [0000-0001-5172-3370], Lucientes, Laura [0000-0001-5596-370X], Cavero, Teresa [0000-0001-5187-9906], Ariceta, Gema [0000-0003-1763-1098], Quintana, Luis F. [0000-0001-7582-8476], Barros, Xoana [0000-0001-9690-9769], Ramos, Natalia [0000-0001-9832-326X], Rodríguez-Mendiola, Nuria [0000-0001-6994-7161], Fernández-Juárez, Gema [0000-0001-6641-7763], Pérez de José, Ana [0000-0002-6952-1459], Pérez Gómez, Vanessa [0000-0003-4558-5236], Lumbreras, Javier [0000-0003-1855-0724], Sánchez de la Nieta, María Dolores [0000-0001-8574-0013], Olea, Teresa [0000-0003-2370-1048], Melgosa, Marta [0000-0001-6236-414X], Huerta, Ana [0000-0003-3342-7628], de Lorenzo, Alberto [0000-0001-8847-083X], Draibe, Juliana [0000-0002-2819-8560], González, Fayna [0000-0002-2313-2511], Shabaka, Amir [0000-0001-7039-4701], Martín-Penagos, L. [0000-0003-0159-7358], Rodríguez de Córdoba, Santiago [0000-0001-6401-1874], Praga, Manuel [0000-0001-9270-1071], Goicoechea de Jorge, Elena [0000-0002-4978-2483], Caravaca-Fontán, Fernando, Díaz-Encarnación, Montserrat M., Lucientes, Laura, Cavero, Teresa, Cabello-Chaves, Virginia, Ariceta, Gema, Quintana, Luis F., Marco, Helena, Barros, Xoana, Ramos, Natalia, Rodríguez-Mendiola, Nuria, Cruz, Sonia, Fernández-Juárez, Gema, Rodríguez, Adela, Pérez de José, Ana, Rabasco, Cristina, Rodado, Raquel, Fernández, Loreto, Pérez Gómez, Vanessa, Ávila, Ana, Bravo, Luis, Lumbreras, Javier, Allende, Natalia, Sánchez de la Nieta, María Dolores, Rodríguez, Eva, Olea, Teresa, Melgosa, Marta, Huerta, Ana, Miquel, Rosa, Mon, Carmen, Fraga, Gloria, de Lorenzo, Alberto, Cano-Megías, Marta, González, Fayna, Shabaka, Amir, López-Rubio, María Esperanza, Fenollosa, María Ángeles, Martín-Penagos, L., Da Silva, Iara, Alonso Titos, Juana, Rodríguez de Córdoba, Santiago, Goicoechea de Jorge, Elena, and Praga, Manuel

Abstract

BACKGROUND AND OBJECTIVES: C3 glomerulopathy is a complement-mediated disease arising from abnormalities in complement genes and/or antibodies against complement components. Previous studies showed that treatment with corticosteroids plus mycophenolate mofetil (MMF) was associated with improved outcomes, although the genetic profile of these patients was not systematically analyzed. This study aims to analyze the main determinants of disease progression and response to this therapeutic regimen., DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: We conducted a retrospective, multicenter, observational cohort study in 35 nephrology departments belonging to the Spanish Group for the Study of Glomerular Diseases. Patients diagnosed with C3 glomerulopathy (n=81) or dense deposit disease (n=16) between January 1995 and March 2018 were enrolled. Multivariable and propensity score matching analyses were used to evaluate the association of clinical and genetic factors with response to treatment with corticosteroids and MMF as measured by proportion of patients with disease remission and kidney survival (status free of kidney failure)., RESULTS: The study group comprised 97 patients (84% C3 glomerulopathy, 16% dense deposit disease). Forty-two patients were treated with corticosteroids plus MMF, and this treatment was associated with a higher rate of remission and lower probability of kidney failure (79% and 14%, respectively) compared with patients treated with other immunosuppressives (24% and 59%, respectively), or ecluzimab (33% and 67%, respectively), or conservative management (18% and 65%, respectively). The therapeutic superiority of corticosteroids plus MMF was observed both in patients with complement abnormalities and with autoantibodies. However, patients with pathogenic variants in complement genes only achieved partial remission, whereas complete remissions were common among patients with autoantibody-mediated forms. The main determinant of no remission was baseline proteinuria. Relapses occurred after treatment discontinuation in 33% of the patients who had achieved remission with corticosteroids plus MMF, and a longer treatment length of MMF was associated with a lower risk of relapse., CONCLUSIONS: The beneficial response to corticosteroids plus MMF treatment in C3 glomerulopathy appears independent of the pathogenic drivers analyzed in this study.

Published
2020

21. Thrombotic microangiopathy in patients with malignant hypertension.

Author

Cavero, Teresa, Auñón, Pilar, Caravaca-Fontán, Fernando, Trujillo, Hernando, Arjona, Emi, Morales, Enrique, Guillén, Elena, Blasco, Miquel, Rabasco, Cristina, Espinosa, Mario, Blanco, Marta, Rodríguez-Magariños, Catuxa, Cao, Mercedes, Ávila, Ana, Huerta, Ana, Rubio, Esther, Cabello, Virginia, Barros, Xoana, Jorge, Elena Goicoechea de, and Córdoba, Santiago Rodríguez de

Subjects
HEMOLYTIC-uremic syndrome, HYPERTENSION, KIDNEY glomerulus diseases, ENDOCRINE diseases, IGA glomerulonephritis, THROMBOTIC thrombocytopenic purpura, KIDNEY failure
Abstract

Background Thrombotic microangiopathy (TMA) is a complication of malignant hypertension (mHTN) attributed to high blood pressure (BP). However, no studies have investigated in patients with mHTN of different aetiologies whether the presence of TMA is associated with specific causes of mHTN. Methods We investigated the presence of TMA (microangiopathic haemolytic anaemia and thrombocytopenia) in a large and well-characterized cohort of 199 patients with mHTN of different aetiologies [primary HTN 44%, glomerular diseases 16.6%, primary atypical haemolytic uraemic syndrome (aHUS) 13.1%, renovascular HTN 9.5%, drug-related HTN 7%, systemic diseases 5.5%, endocrine diseases 4.5%]. Outcomes of the study were kidney recovery and kidney failure. Results Patients with TMA [40 cases (20.1%)] were younger, were more likely female and had lower BP levels and worse kidney function at presentation. Their underlying diseases were primary aHUS (60%), drug-related mHTN (15%), glomerular diseases [all of them immunoglobulin A nephropathy (IgAN); 10%], systemic diseases (10%) and primary HTN (5%). The presence of TMA was 92.3% in primary aHUS, 42.9% in drug-related HTN, 36.4% in systemic diseases, 12.1% in glomerular diseases and 2.3% in primary HTN. No patient with renovascular HTN or mHTN caused by endocrine diseases developed TMA, despite BP levels as high as patients with TMA. A higher proportion of TMA patients developed kidney failure as compared with patients without TMA (56.4% versus 38.9%, respectively). Conclusions The presence of TMA in patients with mHTN should guide the diagnosis towards primary aHUS, drug-related mHTN, some systemic diseases and IgAN, while it is exceptional in other causes of mHTN. [ABSTRACT FROM AUTHOR]

Published
2023
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23. MO256: IGM in Fibrillary Glomerulopathy Linked to Monoclonal Gammopathy

Author

Fayos de Arizón, Leonor, primary, Mercedes Diaz Encarnacion, Montserrat, additional, Arce, Yolanda, additional, Marco Rusiñol, Helena, additional, Coll Brito, Verónica, additional, Arana Aliaga, Carolt, additional, Barros, Xoana, additional, Soledad García-Cuerva, Maria, additional, Berna Redondo, Gerson, additional, and Guirado, Lluis, additional

Published
2022
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24. Development and validation of a nomogram to predict kidney survival at baseline in patients with C3 glomerulopathy

Author

Caravaca-Fontán, Fernando, primary, Rivero, Marta, additional, Cavero, Teresa, additional, Díaz-Encarnación, Montserrat, additional, Cabello, Virginia, additional, Ariceta, Gema, additional, Quintana, Luis F, additional, Marco, Helena, additional, Barros, Xoana, additional, Ramos, Natalia, additional, Rodríguez-Mendiola, Nuria, additional, Cruz, Sonia, additional, Fernández-Juárez, Gema, additional, Rodríguez, Adela, additional, Pérez de José, Ana, additional, Rabasco, Cristina, additional, Rodado, Raquel, additional, Fernández, Loreto, additional, Pérez-Gómez, Vanessa, additional, Ávila, Ana, additional, Bravo, Luis, additional, Espinosa, Natalia, additional, Allende, Natalia, additional, Sanchez de la Nieta, Maria Dolores, additional, Rodríguez, Eva, additional, Olea, Teresa, additional, Melgosa, Marta, additional, Huerta, Ana, additional, Miquel, Rosa, additional, Mon, Carmen, additional, Fraga, Gloria, additional, de Lorenzo, Alberto, additional, Draibe, Juliana, additional, González, Fayna, additional, Shabaka, Amir, additional, López-Rubio, Maria Esperanza, additional, Fenollosa, María Ángeles, additional, Martín-Penagos, Luis, additional, Da Silva, Iara, additional, Alonso Titos, Juana, additional, Rodríguez de Córdoba, Santiago, additional, Goicoechea de Jorge, Elena, additional, and Praga, Manuel, additional

Published
2022
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25. Severe and malignant hypertension are common in primary atypical hemolytic uremic syndrome

Author

Instituto de Salud Carlos III, European Commission, Ministerio de Economía y Competitividad (España), Cavero, Teresa [0000-0001-5187-9906], Arjona, Emilia [0000-0002-0753-3657], Soto, Karina [0000-0002-6977-9361], Caravaca-Fontán, Fernando [0000-0002-5830-9663], Blasco, Miquel [0000-0003-0789-7992], Huerta, Ana [0000-0003-3342-7628], Fulladosa, Xavier [0000-0003-1974-9874], Ramos, Natalia [0000-0001-9832-326X], Morales-Ruiz, E. [0000-0002-5824-6973], Draibe, Juliana [0000-0002-2819-8560], Quintana, Luis F. [0000-0001-7582-8476], Barros, Xoana [0000-0001-9690-9769], Cao, Mercedes [0000-0002-8389-1800], Rodríguez de Córdoba, Santiago [0000-0001-6401-1874], Praga, Manuel [0000-0001-9270-1071], Cavero, Teresa, Arjona, Emilia, Soto, Karina, Caravaca-Fontán, Fernando, Rabasco, Cristina, Bravo, Luis, de la Cerda, Francisco, Martín, Nadia, Blasco, Miquel, Ávila, Ana, Huerta, Ana, Cabello-Chaves, Virginia, Jarque, Ana, Alcázar, Concepción, Fulladosa, Xavier, Carbayo, Javier, Anaya, Sara, Cobelo, Carmen, Ramos, Natalia, Iglesias, Elena, Baltar, José, Martínez-Gallardo, Rocío, Pérez, Lourdes, Morales-Ruiz, E., González, Roberto, Macía, Manuel, Draibe, Juliana, Pallardó, Luis, Quintana, Luis F., Espinosa, Mario, Barros, Xoana, Pereira, Fernando, Cao, Mercedes, Moreno, Juan Antonio, Rodríguez de Córdoba, Santiago, Praga, Manuel, Instituto de Salud Carlos III, European Commission, Ministerio de Economía y Competitividad (España), Cavero, Teresa [0000-0001-5187-9906], Arjona, Emilia [0000-0002-0753-3657], Soto, Karina [0000-0002-6977-9361], Caravaca-Fontán, Fernando [0000-0002-5830-9663], Blasco, Miquel [0000-0003-0789-7992], Huerta, Ana [0000-0003-3342-7628], Fulladosa, Xavier [0000-0003-1974-9874], Ramos, Natalia [0000-0001-9832-326X], Morales-Ruiz, E. [0000-0002-5824-6973], Draibe, Juliana [0000-0002-2819-8560], Quintana, Luis F. [0000-0001-7582-8476], Barros, Xoana [0000-0001-9690-9769], Cao, Mercedes [0000-0002-8389-1800], Rodríguez de Córdoba, Santiago [0000-0001-6401-1874], Praga, Manuel [0000-0001-9270-1071], Cavero, Teresa, Arjona, Emilia, Soto, Karina, Caravaca-Fontán, Fernando, Rabasco, Cristina, Bravo, Luis, de la Cerda, Francisco, Martín, Nadia, Blasco, Miquel, Ávila, Ana, Huerta, Ana, Cabello-Chaves, Virginia, Jarque, Ana, Alcázar, Concepción, Fulladosa, Xavier, Carbayo, Javier, Anaya, Sara, Cobelo, Carmen, Ramos, Natalia, Iglesias, Elena, Baltar, José, Martínez-Gallardo, Rocío, Pérez, Lourdes, Morales-Ruiz, E., González, Roberto, Macía, Manuel, Draibe, Juliana, Pallardó, Luis, Quintana, Luis F., Espinosa, Mario, Barros, Xoana, Pereira, Fernando, Cao, Mercedes, Moreno, Juan Antonio, Rodríguez de Córdoba, Santiago, and Praga, Manuel

Abstract

Malignant hypertension is listed among the causes of secondary thrombotic microangiopathy (TMA), but pathogenic mutations in complement genes have been reported in patients with hypertension-induced TMA. Here we investigated the frequency and severity of hypertension in 55 patients with primary atypical hemolytic uremic syndrome (aHUS). A genetic analysis was performed in all patients, and funduscopic examination was performed in all the patients with Grades 2 and 3 hypertension. A cohort of 110 patients with malignant hypertension caused by diseases other than aHUS served as control. Thirty-six patients with aHUS presented Grade 2 or Grade 3 hypertension and funduscopic examination showed malignant hypertension in 19. Genetic abnormalities in complement were found in 19 patients (37% among patients with malignant hypertension). Plasmapheresis was performed in 46 patients and 26 received eculizumab. Renal and hematological responses were significantly lower after plasmapheresis (24%) than after eculizumab (81%). Renal survival was significantly higher in patients treated with eculizumab (85% at one, three and five years) compared to patients who did not receive this treatment (54%, 46% and 41%), respectively. Response to eculizumab was independent of hypertension severity and the presence of complement genetic abnormalities. Among patients with malignant hypertension caused by other diseases the prevalence of TMA was very low (5%). Thus, severe and malignant hypertension are common among patients with aHUS and eculizumab treatment leads to a higher renal survival when compared to plasmapheresis. However, TMA is uncommon among patients presenting with malignant hypertension caused by diseases other than aHUS.

Published
2019

26. Severe and malignant hypertension are common in primary atypical hemolytic uremic syndrome

Author

Cavero, Teresa, Arjona, Emilia, Soto, Karina, Caravaca-Fontán, Fernando, Rabasco, Cristina, Bravo, Luis, de la Cerda, Francisco, Martín, Nadia, Blasco, Miquel, Ávila, Ana, Huerta, Ana, Cabello, Virginia, Jarque, Ana, Alcázar, Concepción, Fulladosa, Xavier, Carbayo, Javier, Anaya, Sara, Cobelo, Carmen, Ramos, Natalia, Iglesias, Elena, Baltar, José, Martínez-Gallardo, Rocío, Pérez, Lourdes, Morales, Enrique, González, Roberto, Macía, Manuel, Draibe, Juliana, Pallardó, Luis, Quintana, Luis F, Espinosa, Mario, Barros, Xoana, Pereira, Fernando, Cao, Mercedes, Moreno, Juan Antonio, Rodríguez de Córdoba, Santiago, Praga, Manuel, Spanish Group for the Study of Glomerular Diseases (GLOSEN), Instituto de Salud Carlos III, European Commission, Ministerio de Economía y Competitividad (España), Cavero, Teresa, Arjona, Emilia, Soto, Karina, Caravaca-Fontán, Fernando, Blasco, Miquel, Huerta, Ana, Fulladosa, Xavier, Ramos, Natalia, Morales-Ruiz, E., Draibe, Juliana, Quintana, Luis F., Barros, Xoana, Cao, Mercedes, Rodríguez de Córdoba, Santiago, Praga, Manuel, Cavero, Teresa [0000-0001-5187-9906], Arjona, Emilia [0000-0002-0753-3657], Soto, Karina [0000-0002-6977-9361], Caravaca-Fontán, Fernando [0000-0002-5830-9663], Blasco, Miquel [0000-0003-0789-7992], Huerta, Ana [0000-0003-3342-7628], Fulladosa, Xavier [0000-0003-1974-9874], Ramos, Natalia [0000-0001-9832-326X], Morales-Ruiz, E. [0000-0002-5824-6973], Draibe, Juliana [0000-0002-2819-8560], Quintana, Luis F. [0000-0001-7582-8476], Barros, Xoana [0000-0001-9690-9769], Cao, Mercedes [0000-0002-8389-1800], Rodríguez de Córdoba, Santiago [0000-0001-6401-1874], and Praga, Manuel [0000-0001-9270-1071]

Subjects
0301 basic medicine, Adult, Male, medicine.medical_specialty, Thrombotic microangiopathy, Malignant hypertension, medicine.medical_treatment, 030232 urology & nephrology, Complement, urologic and male genital diseases, Antibodies, Monoclonal, Humanized, Gastroenterology, Severity of Illness Index, Hypertension, Malignant, 03 medical and health sciences, Young Adult, 0302 clinical medicine, Internal medicine, hemic and lymphatic diseases, Atypical hemolytic uremic syndrome, medicine, Humans, In patient, complement, malignant hypertension, Atypical Hemolytic Uremic Syndrome, Retrospective Studies, business.industry, atypical hemolytic uremic syndrome, Incidence, Complement System Proteins, Plasmapheresis, Eculizumab, Middle Aged, medicine.disease, 030104 developmental biology, Complement Inactivating Agents, Nephrology, Cohort, eculizumab, Female, Renal survival, business, medicine.drug
Abstract

Malignant hypertension is listed among the causes of secondary thrombotic microangiopathy (TMA), but pathogenic mutations in complement genes have been reported in patients with hypertension-induced TMA. Here we investigated the frequency and severity of hypertension in 55 patients with primary atypical hemolytic uremic syndrome (aHUS). A genetic analysis was performed in all patients, and funduscopic examination was performed in all the patients with Grades 2 and 3 hypertension. A cohort of 110 patients with malignant hypertension caused by diseases other than aHUS served as control. Thirty-six patients with aHUS presented Grade 2 or Grade 3 hypertension and funduscopic examination showed malignant hypertension in 19. Genetic abnormalities in complement were found in 19 patients (37% among patients with malignant hypertension). Plasmapheresis was performed in 46 patients and 26 received eculizumab. Renal and hematological responses were significantly lower after plasmapheresis (24%) than after eculizumab (81%). Renal survival was significantly higher in patients treated with eculizumab (85% at one, three and five years) compared to patients who did not receive this treatment (54%, 46% and 41%), respectively. Response to eculizumab was independent of hypertension severity and the presence of complement genetic abnormalities. Among patients with malignant hypertension caused by other diseases the prevalence of TMA was very low (5%). Thus, severe and malignant hypertension are common among patients with aHUS and eculizumab treatment leads to a higher renal survival when compared to plasmapheresis. However, TMA is uncommon among patients presenting with malignant hypertension caused by diseases other than aHUS., Work in this study was supported by the Instituto de Salud Carlos III /Fondo Europeo de Desarrollo Regional (ISCIII/FEDER) grants PI13/02502, PICI14/00350, and PI16/01685 (to MP), and grants PI13/00802, PI14/00883 and PI17/00130 (to JAM.); the ISCIII/FEDER Programa Miguel Servet, grants CP10/00479 and CPII16/00017 (to JAM); the Spanish “Ministerio de Economía y Competitividad/FEDER” [SAF2015-66287-R] (to SRdeC); the Autonomous Region of Madrid (S2017/BMD-3673) (to SRdeC, EA and MP); Red de Investigación Renal (RedInRen) (RD12/0021/0029) (to MP), the “Fundación Inocente” (Madrid, Spain).] (to SRdC), and the Spanish Society of Nephrology and Fundación Renal Ínigo Álvarez de Toledo (FRIAT) (to JAM).

Published
2019

28. Validation of a Histologic Scoring Index for C3 Glomerulopathy

Author

Caravaca-Fontán, Fernando, primary, Trujillo, Hernando, additional, Alonso, Marina, additional, Díaz-Encarnación, Montserrat, additional, Cabello, Virginia, additional, Ariceta, Gema, additional, Quintana, Luis F., additional, Marco, Helena, additional, Barros, Xoana, additional, Ramos, Natalia, additional, Rodríguez-Mendiola, Nuria, additional, Cruz, Sonia, additional, Fernández-Juárez, Gema, additional, Rodríguez, Eva, additional, de la Cerda, Francisco, additional, Pérez de José, Ana, additional, López, Inmaculada, additional, Fernández, Loreto, additional, Pérez Gómez, Vanessa, additional, Ávila, Ana, additional, Bravo, Luis, additional, Lumbreras, Javier, additional, Allende, Natalia, additional, Sanchez de la Nieta, Maria Dolores, additional, Olea, Teresa, additional, Melgosa, Marta, additional, Huerta, Ana, additional, Miquel, Rosa, additional, Mon, Carmen, additional, Fraga, Gloria, additional, de Lorenzo, Alberto, additional, Draibe, Juliana, additional, González, Fayna, additional, Shabaka, Amir, additional, Illescas, Maria Luisa, additional, Calvo, Consuelo, additional, Oviedo, Victoria, additional, Da Silva, Iara, additional, Goicoechea de Jorge, Elena, additional, Caravaca, Francisco, additional, Praga, Manuel, additional, Cavero, Teresa, additional, Sevillano, Ángel, additional, Gutiérrez, Eduardo, additional, Morales, Enrique, additional, González, Lucia, additional, Camacho Galán, Rafael, additional, Gabaldón Domínguez, Alejandra, additional, Garrido, Marta, additional, Navarro, Alexandra, additional, Cortés, José Antonio, additional, Pascual Martin, Alejando, additional, Pérez-Ebri, M. Luisa, additional, Cabrera-Pérez, Rocío, additional, Panizo Santos, Ángel, additional, Yébenes Gregorio, Laura, additional, García Fernández, Maria Eugenia, additional, Gimeno, Javier, additional, Cannata Ortiz, Pablo, additional, Roselló Sastre, Esther, additional, Saiz, Ana, additional, Salido Ruiz, Eduardo, additional, Rodríguez, Rosa, additional, Corbacho Cuevas, Cesáreo, additional, Crespo, Francisco Díaz, additional, Arce, Yolanda, additional, Garcia-Cuerva Calvar, Maria Soledad, additional, Saus, Carles, additional, Guerrero Márquez, Carmen, additional, García-Herrera, Adriana, additional, Gomà Gallego, Montserrat, additional, López Álvarez, Dolores, additional, Meléndez Muñoz, Cristina, additional, Centeno, Macarena, additional, Ferri Ñíguez, Belén, additional, Mosquera Reboredo, Juan, additional, Vázquez Martul, Eduardo, additional, and Pérez Gutiérrez, Sofía, additional

Published
2021
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29. Longitudinal change in proteinuria and kidney outcomes in C3 glomerulopathy.

Author

Caravaca-Fontán, Fernando, Díaz-Encarnación, Montserrat, Cabello, Virginia, Ariceta, Gema, Quintana, Luis F, Marco, Helena, Barros, Xoana, Ramos, Natalia, Rodríguez-Mendiola, Nuria, Cruz, Sonia, Fernández-Juárez, Gema, Rodríguez, Adela, José, Ana Pérez de, Rabasco, Cristina, Rodado, Raquel, Fernández, Loreto, Gómez, Vanessa Pérez, Ávila, Ana, Bravo, Luis, and Espinosa, Natalia

Subjects
COMPLEMENT (Immunology), KIDNEY failure, PROTEINURIA, KIDNEY glomerulus diseases, KIDNEYS
Abstract

Introduction The association between a change in proteinuria over time and its impact on kidney prognosis has not been analysed in complement component 3 (C3) glomerulopathy. This study aims to investigate the association between the longitudinal change in proteinuria and the risk of kidney failure. Methods This was a retrospective, multicentre observational cohort study in 35 nephrology departments belonging to the Spanish Group for the Study of Glomerular Diseases. Patients diagnosed with C3 glomerulopathy between 1995 and 2020 were enrolled. A joint modelling of linear mixed-effects models was applied to assess the underlying trajectory of a repeatedly measured proteinuria, and a Cox model to evaluate the association of this trajectory with the risk of kidney failure. Results The study group consisted of 85 patients, 70 C3 glomerulonephritis and 15 dense deposit disease, with a median age of 26 years (range 13–41). During a median follow-up of 42 months, 25 patients reached kidney failure. The longitudinal change in proteinuria showed a strong association with the risk of this outcome, with a doubling of proteinuria levels resulting in a 2.5-fold increase of the risk. A second model showed that a ≥50% proteinuria reduction over time was significantly associated with a lower risk of kidney failure (hazard ratio 0.79; 95% confidence interval 0.56–0.97; P < 0.001). This association was also found when the ≥50% proteinuria reduction was observed within the first 6 and 12 months of follow-up. Conclusions The longitudinal change in proteinuria is strongly associated with the risk of kidney failure. The change in proteinuria over time can provide clinicians a dynamic prediction of kidney outcomes. [ABSTRACT FROM AUTHOR]

Published
2022
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31. Risk factors for non-diabetic renal disease in diabetic patients

Author

Bermejo, Sheila, primary, González, Ester, additional, López-Revuelta, Katia, additional, Ibernon, Meritxell, additional, López, Diana, additional, Martín-Gómez, Adoración, additional, Garcia-Osuna, Rosa, additional, Linares, Tania, additional, Díaz, Montserrat, additional, Martín, Nàdia, additional, Barros, Xoana, additional, Marco, Helena, additional, Navarro, Maruja Isabel, additional, Esparza, Noemí, additional, Elias, Sandra, additional, Coloma, Ana, additional, Robles, Nicolás Roberto, additional, Agraz, Irene, additional, Poch, Esteban, additional, Rodas, Lida, additional, Lozano, Víctor, additional, Fernández, Beatriz, additional, Hernández, Eduardo, additional, Martínez, Maria Isabel, additional, Stanescu, Ramona Ionela, additional, Moirón, José Pelayo, additional, García, Núria, additional, Goicoechea, Marian, additional, Calero, Francesca, additional, Bonet, Josep, additional, Galceran, Josep M, additional, Liaño, Fernando, additional, Pascual, Julio, additional, Praga, Manuel, additional, Fulladosa, Xavier, additional, and Soler, María José, additional

Published
2020
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32. Complement Activation and Thrombotic Microangiopathies

Author

Palomo, Marta, primary, Blasco, Miquel, additional, Molina, Patricia, additional, Lozano, Miquel, additional, Praga, Manuel, additional, Torramade-Moix, Sergi, additional, Martinez-Sanchez, Julia, additional, Cid, Joan, additional, Escolar, Gines, additional, Carreras, Enric, additional, Paules, Cristina, additional, Crispi, Fatima, additional, Quintana, Luis F., additional, Poch, Esteban, additional, Rodas, Lida, additional, Goma, Emma, additional, Morelle, Johann, additional, Espinosa, Mario, additional, Morales, Enrique, additional, Avila, Ana, additional, Cabello, Virginia, additional, Ariceta, Gema, additional, Chocron, Sara, additional, Manrique, Joaquin, additional, Barros, Xoana, additional, Martin, Nadia, additional, Huerta, Ana, additional, Fraga-Rodriguez, Gloria M., additional, Cao, Mercedes, additional, Martin, Marisa, additional, Romera, Ana Maria, additional, Moreso, Francesc, additional, Manonelles, Anna, additional, Gratacos, Eduard, additional, Pereira, Arturo, additional, Campistol, Josep M., additional, and Diaz-Ricart, Maribel, additional

Published
2019
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33. SP416DIABETIC PATIENTS WITH DIABETIC NEPHROPATHY HAVE WORSE RENAL PROGNOSIS. STUDY BIODIAB-GLOSEN-GEENDIAB

Author

Bermejo, Sheila, primary, González, Ester, additional, López, Katia, additional, Ibernón, Meritxell, additional, López, Diana, additional, Martín-Gómez, Adoración, additional, García, Rosa, additional, Linares, Tania, additional, Díaz, Montserrat, additional, Martín, Nadia, additional, Barros, Xoana, additional, Marco, Helena, additional, Navarro, Maruja Isabel, additional, Esparza, Noemí, additional, Elías, Sandra, additional, Coloma, Ana, additional, Robles, Nicolás Roberto, additional, Hernández, Eduardo, additional, Martínez, Maria Isabel, additional, Agraz, Irene, additional, Pelayo Moirón, José, additional, Goicoechea, Marian, additional, Bonet, Josep, additional, García, Núria, additional, Liaño, Fernando, additional, Pascual, Julio, additional, Praga, Manuel, additional, Fulladosa, Xavier, additional, and Soler, María José, additional

Published
2018
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34. SP425RENAL BIOPSY IN DIABETIC PATIENTS: PRELIMINARY RESULTS OF THE SPANISH MULTICENTER STUDY BIODIAB-GLOSEN-GEENDIAB

Author

Bermejo, Sheila, primary, González, Ester, additional, López, Katia, additional, Ibernón, Meritxell, additional, López, Diana, additional, Martín-Gómez, Adoración, additional, García, Rosa, additional, Linares, Tania, additional, Díaz, Montserrat, additional, Martin, Nadia, additional, Barros, Xoana, additional, Marco, Helena, additional, Navarro, Maruja Isabel, additional, Esparza, Noemi, additional, Elias, Sandra, additional, Coloma, Ana, additional, Robles, Nicolás Roberto, additional, Hernández, Eduardo, additional, García, Nuria, additional, Martínez, Maria Isabel, additional, Goicoechea, Marian, additional, Agraz, Irene, additional, Pelayo Moirón, José, additional, Bonet, Josep, additional, Liaño, Fernando, additional, Pascual, Julio, additional, Stanescu, Ramone-laIonela, additional, Praga, Manuel, additional, Fulladosa, Xavier, additional, and Soler, María José, additional

Published
2018
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36. Efficacy of mycophenolate treatment in adults with steroid-dependent/frequently relapsing idiopathic nephrotic syndrome

Author

Sandoval, Diego, primary, Poveda, Rafael, additional, Draibe, Juliana, additional, Pérez-Oller, Laureà, additional, Díaz, Montserrat, additional, Ballarín, José, additional, Saurina, Anna, additional, Marco, Helena, additional, Bonet, Josep, additional, Barros, Xoana, additional, Fulladosa, Xavier, additional, Torras, Joan, additional, and Cruzado, Josep M., additional

Published
2017
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37. Antiphospholipase 2 receptor antibody levels to predict complete spontaneous remission in primary membranous nephropathy.

Author

Rodas, Lida M, Matas-García, Ana, Barros, Xoana, Blasco, Miquel, Viñas, Odette, Llobell, Arturo, Martin, Nadia, and Quintana, Luis F

Abstract

Background M-type phospholipase A2 receptor (APLA2R) is considered the major antigen involved in the pathogenesis of adult primary membranous nephropathy (MN), which is the leading cause of non-diabetic nephrotic syndrome. Antibodies to this antigen have been proved to be an excellent biomarker of disease activity in primary MN. In fact, preliminary data suggest that the higher the antibody level the more proteinuria, and that a decrease in antibody level precedes the remission of proteinuria, but more solid evidence is needed. Methods The present work aims to characterize the predictive value of the level of antibodies against PLA2R as a biomarker of disease course and treatment response in a well-defined cohort of 62 patients from University Hospitals Clinic of Barcelona and Josep Trueta in Girona. The primary outcome was the appearance of a spontaneous complete remission (CR), defined as induction of a CR without the use of immunosuppressive agents. Results In common with other reports, this work confirms that spontaneous CR is more frequent in patients with low titre of APLA2R at diagnosis, but strikingly, in this cohort we found that spontaneous CR was achieved in patients with APLA2R levels <40 UI/mL. Furthermore, spontaneous CR were less frequently observed in patients with proteinuria >8 g/day. Conclusions In conclusion, these findings point out the important role of APLA2R as a tool to predict the disease course and establish personalized therapeutic options at the moment of diagnosis of primary MN. Specifically, patients with low titre of APLA2R (<40 UI/mL) and proteinuria <4/day could obtain benefit of a longer period of follow-up with conservative treatment after diagnosis. [ABSTRACT FROM AUTHOR]

Published
2019
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38. Manejo de la hipercalcemia tras el trasplante renal

Author

Torregrosa,José V. and Barros,Xoana

Subjects
Hiperparatiroidismo secundario, Trasplante renal, Paratiroidectomía, Hiperparatiroidismo terciario, Calcimiméticos, Cinacalcet, Hipercalcemia
Abstract

La hipercalcemia postrasplante debida a la persistencia del hiperparatiroidismo (HPT) secundario tiene una prevalencia elevada en los primeros 3 meses postrasplante, que va disminuyendo a lo largo del primer año, aunque en torno al 5-10 % de los trasplantados renales persiste en el tiempo. La mayor resorción ósea y la mayor reabsorción tubular de calcio debido a la acción de la hormona paratiroidea (PTH) parecen ser los mecanismos principalmente implicados en la hipercalcemia. La PTH en el momento del trasplante renal (TR) es el factor que determina el desarrollo de hipercalcemia pos-TR, aunque a veces se encuentre enmascarada en los pacientes bien controlados con tratamiento médico. Cada vez más los pacientes en diálisis reciben cinacalcet como tratamiento del HPT secundario. La retirada del calcimimético en el momento del trasplante renal da lugar a una mayor prevalencia de hipercalcemia e hiperparatiroidismo en estos pacientes. En los pacientes con PTH bien controlada con cinacalcet antes del trasplante, existe una relación directa entre la dosis y el desarrollo posterior de hipercalcemia, probablemente porque indica la presencia de un HPT secundario más severo. La hipercalcemia puede tener efectos deletéreos sobre el injerto renal dando lugar a calcificación tubulointersticial. La hipercalcemia persistente es una marcador de aumento del riesgo de empeoramiento de la patología ósea de estos pacientes. Hoy en día, la primera opción de tratamiento la constituye el cinacalcet, y ante la ausencia de respuesta se valorará la realización de una paratiroidectomía. En esta revisión proponemos un algoritmo de manejo de la hipercalcemia pos-TR.

Published
2013

39. Manejo de la hipercalcemia tras el trasplante renal

Author

Torregrosa, José V. and Barros, Xoana

Subjects
Hiperparatiroidismo secundario, Parathyroidectomy, Hypercalcaemia, Secondary hyperparathyroidism, Trasplante renal, Paratiroidectomía, Calcimimetics, Hiperparatiroidismo terciario, Calcimiméticos, Renal transplantation, Cinacalcet, Tertiary hyperparathyroidism, Hipercalcemia
Abstract

La hipercalcemia postrasplante debida a la persistencia del hiperparatiroidismo (HPT) secundario tiene una prevalencia elevada en los primeros 3 meses postrasplante, que va disminuyendo a lo largo del primer año, aunque en torno al 5-10 % de los trasplantados renales persiste en el tiempo. La mayor resorción ósea y la mayor reabsorción tubular de calcio debido a la acción de la hormona paratiroidea (PTH) parecen ser los mecanismos principalmente implicados en la hipercalcemia. La PTH en el momento del trasplante renal (TR) es el factor que determina el desarrollo de hipercalcemia pos-TR, aunque a veces se encuentre enmascarada en los pacientes bien controlados con tratamiento médico. Cada vez más los pacientes en diálisis reciben cinacalcet como tratamiento del HPT secundario. La retirada del calcimimético en el momento del trasplante renal da lugar a una mayor prevalencia de hipercalcemia e hiperparatiroidismo en estos pacientes. En los pacientes con PTH bien controlada con cinacalcet antes del trasplante, existe una relación directa entre la dosis y el desarrollo posterior de hipercalcemia, probablemente porque indica la presencia de un HPT secundario más severo. La hipercalcemia puede tener efectos deletéreos sobre el injerto renal dando lugar a calcificación tubulointersticial. La hipercalcemia persistente es una marcador de aumento del riesgo de empeoramiento de la patología ósea de estos pacientes. Hoy en día, la primera opción de tratamiento la constituye el cinacalcet, y ante la ausencia de respuesta se valorará la realización de una paratiroidectomía. En esta revisión proponemos un algoritmo de manejo de la hipercalcemia pos-TR. Post-transplant hypercalcemia due to persistent secondary hyperparathyroidism (HPT) has a high prevalence in the first 3 months after surgery and decreases during the first year, but it persists over time in around 5-10% of renal transplant patients. The increased bone resorption and tubular reabsorption of calcium due to the action of the parathyroid hormone (PTH) appear to be the main mechanisms involved in hypercalcemia. At the time of the renal transplantation (RT), PTH is the factor that determines the development of post-RT hypercalcemia, although it is sometimes masked in patients who are well controlled with medical treatment. The number of dialysis patients receiving treatment with cinacalcet for secondary HPT is increasing. The withdrawal of the calcimimetic at the time of renal transplantation results in a higher prevalence of hypercalcaemia and hyperparathyroidism in these patients. In patients with PTH well controlled with cinacalcet before transplantation, there is a direct relationship between the dose and the subsequent development of hypercalcemia, probably because it indicates the presence of a more severe secondary HPT. Hypercalcemia may have deleterious effects on the renal graft, resulting in tubulointerstitial calcification. Persistent hypercalcemia is a marker of an increased risk of bone disease deterioration in these patients. Nowadays, the first treatment option is cinacalcet and if there is no response, we consider performing a parathyroidectomy. In this review, we propose an algorithm for management of post-RT hypercalcemia.

Published
2013

40. Seasonal variations in the onset of positive and negative renal ANCA-associated vasculitis in Spain.

Author

Draibe, Juliana, Rodó, Xavier, Fulladosa, Xavier, Martínez-Valenzuela, Laura, Diaz-Encarnación, Montserrat, Santos, Lara, Marco, Helena, Quintana, Luis, Rodriguez, Eva, and Barros, Xoana

Abstract

Background The closure of long-standing gaps in our knowledge of aetiological factors behind anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a major challenge. Descriptive and analytical epidemiological studies can improve our understanding of environmental influences. Reported seasonal variations in AAV, mainly related to Wegener's disease, have shown an increasing number of cases in the winter months, which could be related to an extrinsic factor underlying infection. The objective of this paper was to study seasonal variations in AAV with respect to renal affectation diagnosed in Catalonia, Spain. Methods Two hundred and thirty-four patients diagnosed for renal AAV between 2001 and 2014 in eight hospitals in Catalonia were included in the study. We used medical records to retrospectively analyse the date of the first symptoms attributed to the AAV, ANCA subtypes, the degree of renal impairment and renal histology. Results Of the 234 patients studied, 49.2% were male and 50.8% female. For ANCA status, 8.5% were positive, 15.9% were proteinase-3-positive and 75.6% were myeloperoxidase-positive. In relation to histological classification, 17.8% were sclerotic, 11.7% focal, 38.8% crescentic and 31.7% mixed. Regarding seasonal distribution, we observed a clear seasonal periodicity with a significantly higher incidence of cases in the winter. Applying an Eigen decomposition, we observed a periodic fluctuation of frequencies around the annual cycle with peaks every 10–12 months, and higher incidence of AAV cases in February. Conclusions Our results confirm, in Catalonia, the seasonal periodicity of AAV with a higher incidence in the winter, as formerly described in the literature for other regions. An environmental factor, likely one that is infectious, may explain this finding. [ABSTRACT FROM AUTHOR]

Published
2018
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41. Tratamiento eficaz de la arteriolopatía urémica calcificante con bifosfonatos

Author

Torregrosa,José V., Durán,Carlos E., Barros,Xoana, Blasco,Miquel, Arias,Marta, Cases,Aleix, and Campistol,Josep M.

Subjects
Hiperparatiroidismo secundario, Arteriolopatía urémica calcificante, Calcifilaxis, Trasplante renal, Bifosfonatos, Enfermedad renal crónica
Abstract

Antecedentes y objetivos: La arteriolopatía urémica calcificante (CUA) o calcifilaxis es una enfermedad rara pero potencialmente mortal que afecta casi exclusivamente a pacientes con enfermedad renal crónica. Para su tratamiento se han empleado diferentes alternativas con resultados irregulares, siendo los bifosfonatos una de ellas. Desde 2002 iniciamos en nuestra Unidad el tratamiento con bifosfonatos en todos los pacientes con diagnóstico de CUA. Material y métodos: Se recogieron prospectivamente, entre 2002 y 2010, ocho pacientes (cuatro hombres, cinco en diálisis y tres con trasplante renal funcionante) con CUA tratados con bifosfonatos. El diagnóstico se realizó por sospecha clínica y biopsia de confirmación. Cinco pacientes con antecedentes de producto calcio-fósforo elevado, seis con antecedentes de hormona paratiroidea elevada (> 800 pg/ml), cuatro paratiroidectomizados, cinco con elevada dosis acumulada de esteroides y seis recibiendo dicumarínicos. Ningún paciente presentaba obesidad ni diabetes mellitus. Resultados: En todos los casos se constató disminución de sintomatología (dolor) a los pocos días y regresión de las lesiones entre 2 a 4 semanas tras iniciar los bifosfonatos, sin cambios en los valores séricos de calcio y fósforo. La mejoría fue más rápida en los que recibieron ibandronato intravenoso. Todos se mantuvieron en tratamiento con bifosfonatos durante al menos 6 meses, hasta que las heridas se curaron completamente. No se han observado recurrencias tras un seguimiento de entre 1 y 9 años. La función renal se mantuvo estable en los pacientes trasplantados. El tratamiento fue bien tolerado y no se observaron efectos adversos. Conclusiones: Los bifosfonatos podrían constituir una alternativa nueva y atractiva para el tratamiento de la CUA.

Published
2012

43. Epicardial adipose tissue in long-term hemodialysis patients: its association with vascular calcification and long-term development

Author

Barros, Xoana, primary, Dirrichs, Timm, additional, Koos, Ralf, additional, Reinartz, Sebastian, additional, Kaesler, Nadine, additional, Kramann, Rafael, additional, Gladziwa, Ulrich, additional, Ketteler, Markus, additional, Floege, Jürgen, additional, Marx, Nikolaus, additional, Torregrosa, José V., additional, Keszei, András, additional, and Brandenburg, Vincent M., additional

Published
2015
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44. DXA Variations and Fractures After Simultaneous Pancreas-Renal Transplantation

Author

Torregrosa, José-Vicente, primary, Sánchez-Escuredo, Ana, additional, Fuster, David, additional, Barros, Xoana, additional, Campos, Francisco, additional, Muxí, África, additional, Perlaza, Pilar, additional, Marzola, Maria Cristina, additional, Chondrogiannis, Sotirios, additional, Colletti, Patrick M., additional, Rubello, Domenico, additional, and Ricart, María José, additional

Published
2015
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49. What Infusion Flow Should Be Used for Mid-Dilution Hemodiafiltration?

Author

Maduell, Francisco, primary, Arias, Marta, additional, Fontseré, Néstor, additional, Vera, Manel, additional, Masso, Elisabeth, additional, Garro, Julia, additional, Barros, Xoana, additional, Martina, Maria N., additional, Elena, Montserrat, additional, Bergadá, Eduardo, additional, Cases, Aleix, additional, Bedini, Jose Luis, additional, and Campistol, Josep M., additional

Published
2010
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50. Mid-Dilution Hemodiafiltration: A Comparison with Pre- and Postdilution Modes Using the Same Polyphenylene Membrane

Author

Maduell, Francisco, primary, Arias, Marta, additional, Vera, Manel, additional, Fontseré, Néstor, additional, Blasco, Miquel, additional, Barros, Xoana, additional, Garro, Julia, additional, Elena, Montserrat, additional, Bergadá, Eduardo, additional, Cases, Aleix, additional, Bedini, Jose Luis, additional, and Campistol, Josep M., additional

Published
2009
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