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2. Cardiac dysfunction and remodeling regulated by anti-angiogenic environment in patients with preeclampsia : the ANGIOCOR prospective cohort study protocol

Author

Ullmo, Johana, Cruz-Lemini, Monica, Sánchez-García, O., Bos-Real, L., Fernandez-Llama, Patricia, Calero, F., Domínguez-Gallardo, Carla, Garrido-Giménez, Carmen, Trilla, Cristina, Carreras Costa, Francesc, Sionis, Alessandro, Mora, J., García Osuna, Álvaro, Ordoñez Llanos, Jorge, Llurba, E., and Universitat Autònoma de Barcelona

Subjects
Adult, Heart Diseases, Pregnancy Trimester, Third, Neovascularization, Physiologic, sFlt-1, Cohort Studies, Study Protocol, Pre-Eclampsia, Pregnancy, Humans, Prospective Studies, Placenta Growth Factor, Cardiac remodeling, Sflt-1, Vascular Endothelial Growth Factor Receptor-1, Angiogenic factors, Obstetrics and Gynecology, Gynecology and obstetrics, Preeclampsia, Cardiovascular risk, Pregnancy Complications, Pregnancy Trimester, First, Cardiac biomarkers, PlGF, Echocardiography, Heart Disease Risk Factors, Spain, Case-Control Studies, RG1-991, Cardiac dysfunction, Female, Biomarkers
Abstract

Background Cardiovascular diseases (CVD) are cause of increased morbidity and mortality in spite of advances for diagnosis and treatment. Changes during pregnancy affect importantly the maternal CV system. Pregnant women that develop preeclampsia (PE) have higher risk (up to 4 times) of clinical CVD in the short- and long-term. Predominance of an anti-angiogenic environment during pregnancy is known as main cause of PE, but its relationship with CV complications is still under research. We hypothesize that angiogenic factors are associated to maternal cardiac dysfunction/remodeling and that these may be detected by new cardiac biomarkers and maternal echocardiography. Methods Prospective cohort study of pregnant women with high-risk of PE in first trimester screening, established diagnosis of PE during gestation, and healthy pregnant women (total intended sample size n = 440). Placental biochemical and biophysical cardiovascular markers will be assessed in the first and third trimesters of pregnancy, along with maternal echocardiographic parameters. Fetal cardiac function at third trimester of pregnancy will be also evaluated and correlated with maternal variables. Maternal cardiac function assessment will be determined 12 months after delivery, and correlation with CV and PE risk variables obtained during pregnancy will be evaluated. Discussion The study will contribute to characterize the relationship between anti-angiogenic environment and maternal CV dysfunction/remodeling, during and after pregnancy, as well as its impact on future CVD risk in patients with PE. The ultimate goal is to improve CV health of women with high-risk or previous PE, and thus, reduce the burden of the disease. Trial registration NCT04162236

Published
2021

4. Urinary Proteome Analysis Identified Neprilysin and VCAM as Proteins Involved in Diabetic Nephropathy

Author

Guillén-Gómez, Elena, Bardají de Quixano, Beatriz, Ferrer, Sílvia, Brotons, Carlos, Knepper, Mark A., Carrascal Pérez, Montserrat, Abian, Joaquin, Mas, José M., Calero, Francesca, Ballarín Castan, José Aurelio, Fernandez-Llama, Patricia, Universitat Autònoma de Barcelona, Ministerio de Sanidad, Servicios Sociales e Igualdad (España), Instituto de Salud Carlos III, European Commission, Red Española de Investigación Renal, Consejo Superior de Investigaciones Científicas (España), Universidad Autónoma de Barcelona, Guillén-Gómez, Elena [0000-0002-8498-2579], Abián, Joaquín [0000-0003-2823-5429], Fernández-Llama,Patricia [0000-0002-7472-2124], Guillén-Gómez, Elena, Abián, Joaquín, and Fernández-Llama,Patricia

Subjects
Male, Proteomics, 0301 basic medicine, medicine.medical_specialty, Proteome, Article Subject, Urinalysis, Endocrinology, Diabetes and Metabolism, Urinary system, Vascular Cell Adhesion Molecule-1, lcsh:Diseases of the endocrine glands. Clinical endocrinology, Diabetic nephropathy, 03 medical and health sciences, Endocrinology, Internal medicine, medicine, Albuminuria, Humans, Diabetic Nephropathies, Neprilysin, Aged, lcsh:RC648-665, medicine.diagnostic_test, business.industry, Middle Aged, medicine.disease, 030104 developmental biology, Losartan, Diabetes Mellitus, Type 2, Female, Microalbuminuria, Sample collection, medicine.symptom, business, Biomarkers, Research Article, medicine.drug
Abstract

Urinary proteome was analyzed and quantified by tandem mass tag (TMT) labeling followed by bioinformatics analysis to study diabetic nephropathy (DN) pathophysiology and to identify biomarkers of a clinical outcome. We included type 2 diabetic normotensive non-obese males with () and without () incipient DN (microalbuminuria). Sample collection included blood and urine at baseline (control and DN basal) and, in DN patients, after 3 months of losartan treatment (DN treated). Urinary proteome analysis identified 166 differentially abundant proteins between controls and DN patients, 27 comparing DN-treated and DN-basal patients, and 182 between DN-treated patients and controls. The mathematical modeling analysis predicted 80 key proteins involved in DN pathophysiology and 15 in losartan effect, a total of 95 proteins. Out of these 95, 7 are involved in both processes. VCAM-1 and neprilysin stand out of these 7 for being differentially expressed in the urinary proteome. We observed an increase of VCAM-1 urine levels in DN-basal patients compared to diabetic controls and an increase of urinary neprilysin in DN-treated patients with persistent albuminuria; the latter was confirmed by ELISA. Our results point to neprilysin and VCAM-1 as potential candidates in DN pathology and treatment., Funding was granted by Fondo de Investigación Sanitaria, Ministerio de Sanidad (PI10/01261) to Patricia Fernández-Llama) and ISCIII RETIC REDINREN FEDER Funds (RD12/0021/0033). The proteomics laboratory CSIC/UAB is a member of Proteored, PRB2-ISCIII and is supported by grant PT13/0001, of the PE I+D+i 2013-2016, funded by ISCIII and FEDER.

Published
2018
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5. Cyclooxygenase inhibitors increase Na-K-2Cl cotransporter abundance in thick ascending limb of Henle's loop

Author

Fernandez-Llama, Patricia, Ecelbarger, Carolyn A., Ware, Joseph A., Andrews, Peter, Lee, Alanna J., Turner, Rachel, Nielsen, Soren, and Knepper, Mark A.

Subjects
Diclofenac -- Physiological aspects, Indomethacin -- Physiological aspects, Oxidases -- Physiological aspects, Prostaglandins -- Physiological aspects, Biological sciences
Abstract

Rats were treated with the cyclooxygenase inhibitors indomethacin and diclofenac to test the hypothesis that long-term inhibition of prostaglandin synthesis increases the expression level of the Na-K-2Cl cotransporter in the thick ascending limb of Henle's loop. The effects of the two cyclooxygenase inhibitors were determined using semiquantitative immunoblotting. Results provide evidence to support the hypothesis.

Published
1999

7. Ultramicrodetermination of vasopressin-regulated urea transporter protein in microdissected renal tubules

Author

Kishore, B.K., Terris, James, and Fernandez-Llama, Patricia

Subjects
Urea -- Physiological aspects, Renal tubular transport -- Physiological aspects, Carrier proteins -- Physiological aspects, Enzyme-linked immunosorbent assay -- Research, Vasopressin -- Physiological aspects, Biological sciences
Abstract

Fluorescence-based enzyme-linked immunoabsorbent assay (ELISA) was utilized to determine the mechanisms that mediate the regulatory role of vasopressin regulated urea transporter (VRUT) in microdissected renal tubules. ELISA analysis of VRUT activity in inner medullary collecting duct (IMCD) cells indicated the role of postranslationally modified-VRT in increasing urea transport. Furthermore, the increase in urea transport in IMCD cells was also mediated by increased paracellular permeability.

Published
1997

9. Cystatin C estimated glomerular filtration rate to assess renal function in early stages of autosomal dominant polycystic kidney disease

Author

Sans, Laia, Radosevic, Aleksandar, Quintian, Claudia, Montañés, Rosario, Gràcia, Silvia, Vilaplana, Carles, Mojal, Sergi, Ballarín Castan, José Aurelio, Fernandez-Llama, Patricia, Torra Balcells, Roser, Pascual, Julio, Universitat Autònoma de Barcelona, Sans, Laia, Radosevic, Aleksandar, Quintian, Claudia, Montañés, Rosario, Gràcia, Silvia, Vilaplana, Carles, Mojal, Sergi, Ballarín Castan, José Aurelio, Fernandez-Llama, Patricia, Torra Balcells, Roser, Pascual, Julio, and Universitat Autònoma de Barcelona

Abstract

Height-adjusted total kidney volume (htTKV) is the best marker of disease progression in early autosomal dominant polycystic kidney disease (ADPKD) when renal function still remains normal. The usefulness of cystatin-C as a biomarker to assess renal function according to renal volume has not been studied in ADPKD patients. Observational and cross-sectional study of 62 ADPKD patients. htTKV, creatinine and cystatin-C estimated glomerular filtration rate (eGFR) were determined. Correlations between htTKV and eGFR were studied. A control group was used to determine the association between renal function differences and htTKV. htTKV significantly correlated with cystatin-C-eGFR (r = -0.384, p = 0.002) but not with creatinine-eGFR (r = -0.225, p = 0.078). With htTKV stratified into tertiles, a significant difference of cystatin-C-eGFR but not in creatinine-eGFR was detected in the third tertile when compared with the first tertile group (110.0±22.2 vs 121.3±7.2; p = 0.023 and 101.8±17.2 vs 106.9±15.1; p = 0.327 respectively). When cystatin-C-eGFR of the controls was used as the reference, htTKV above 605 ml/m identified with a 75% sensitivity and 84.9% specificity those patients with a significant worse kidney function. However, this cut-off value could not be identified using creatinine-eGFR. Cystatin-C-eGFR but not creatinine-eGFR correlated with htTKV in ADPKD patients in early stages of the disease. Differences in cystatin-C-eGFR but not in creatinine-eGFR have been identified through htTKV tertiles. A htTKV above 605 ml/m is associated with a worse renal function only if cystatin-C-eGFR is used. Cystatin-C-eGFR should be studied in prospective studies of early stages of ADPKD to determine its usefulness as an early marker of disease progression.

Published
2017

10. Colaboradores

Author

Abalovich, Marcos S., Adamo, Bárbara, García-Navarro, Alvar Agustí, García-Navarro, Carlos Agustí, Alcalá Hernández, Luis, Alcaraz Asensio, Antonio, Alcázar Arroyo, Roberto, Alegre de Miquel, Víctor, Almirante Gragera, Benito, Alonso Fernández, Pedro Luis, Alonso Pérez, Manuel, Alonso Tarrés, Carles, Alsina Gibert, Mercè, Alsina Manrique de Lara, Laia, José Álvarez Martínez, Miriam, Luis Álvarez-Sala Walther, José, Álvarez Twose, Iván, Ambrosioni Czyrko, Juan, Ancochea Bermúdez, Julio, Andrade Bellido, Raúl J., Antón López, Jordi, Antón Nieto, Esperanza, Aran Perramon, Josep Maria, Arance Fernández, Ana, Arboleya Rodríguez, Luis, Arias Gómez, Manuel, Ariza Cardenal, Xavier, Armengol Dulcet, Lluís, Aróstegui Gorospe, Juan Ignacio, Arranz Amo, José Antonio, Arrese, Marco, Arribas López, José Ramón, Audí Parera, Laura, Aulinas Masó, Anna, Azpiroz Vidaur, Fernando, Ramon Badia Jobal, Joan, Badimon Maestro, Lina, Baena Caparrós, Jacinto, Martínez de Irujo, Jaume Baldirà, Barbé Illa, Ferran, Barberà Mir, Joan Albert, Barberán López, José, Barile Fabrís, Leonor, Bartra Tomás, Joan, Bassas Arnau, Lluís, Bassat, Quique, Bataller Alberola, Luis, Bataller Alberola, Ramon, Bayés Colomer, Mónica, Berdasco Menéndez, María, Bernabeu Morón, Ignacio, Bernardo Arroyo, Miquel, Berraondo López, Pedro, Berzigotti, Annalisa, Bielsa Marsol, Isabel, Bladé Creixenti, Joan, Blanco Arévalo, José Luis, Blanco García, Francisco Javier, Blanco Vich, Isabel, Blasco Pelicano, Miquel, Blesa González, Rafael, Bodegas Cañas, Andrés Ignacio, Bodro Marimont, Marta, Boronat Guerrero, Susana, Borràs Andrés, Josep Maria, Borrego Rabasco, Francisco, Bosch Genover, Xavier, Bosch Mestres, Jordi, Botey Puig, Albert, Bouza Santiago, Emilio, Brugada Terradellas, Josep, Brugada Terradellas, Ramon, Bruix Tudó, Jordi, Bruna Escuer, Jordi, Buján Rivas, Segundo, Fernández de Piérola, Luis Bujanda, Burgos Rincón, Felip, Buti Ferret, María, Caballería Rovira, Joan, Cabellos Mínguez, Carmen, Cahn, Pedro, Calvet Calvo, Xavier, Campins Martí, Magda, Campistol Plana, Josep M.ª, Campo Güerri, Elías, Campuzano Larrea, Óscar, Campuzano Uceda, Victoria, Cardellach López, Francesc, Carmena Rodríguez, Rafael, Carmona Herrera, Francisco, Carracedo Álvarez, Ángel, Carracedo Pérez, Arkaitz, Carreres Molas, Anna, Casabona i Barbarà, Jordi, Casademont Pou, Jordi, Casanueva Freijo, Felipe F., Cases Amenós, Aleix, Castells Garangou, Antoni, Castelo-Branco, Camil, Castón Osorio, Juan José, Castro Fornieles, Josefina, Castro Rebollo, Pedro, Catalán Eraso, Beatriz, Caylà Buqueras, Joan A., Cervantes Requena, Francisco, Cervera Álvarez, Carlos, Cervera Segura, Ricard, Chamorro Sánchez, Ángel, Cid Xutglà, María Cinta, Cinca Cuscullola, Juan María, Coll Daroca, Joaquim, José Coll Rosell, M.ª, Colmenero Arroyo, Jordi, Compta Hirnyi, Yaroslau, Conesa Bertrán, Gerardo, Corell Almuzara, Alfredo, Crespo Casal, Manuel, Crespo Conde, Gonzalo, Crespo García, Javier, Cristòfol Allué, Ramon, Cigudosa García, Juan Cruz, Cubiella Fernández, Joaquín, Cuenca Estrella, Manuel, Cuevas Esteban, Jorge, Dalmau Obrador, Josep, Davant Llauradó, Ester, Iserte, Alejandro de la Sierra, Pascual, Enrique de Madaria, Rabassó, Joan de Pablo, Galván, Eduardo de Teresa, Casanelles, Miguel del Campo, Bueno, Ana del Río, Delgado González, Julio, Diekmann, Fritz, Domínguez Benítez, José Antonio, Domínguez García, Ángela, Domínguez Luengo, Carmen, Ángeles Domínguez Luzón, M.ª, Jesús Domínguez Tordable, M.ª, Dopazo Blázquez, Joaquín, Dueñas Laita, Antonio, Durán Rebolledo, Carlos Eduardo, Duró Pujol, Joan Carles, Echevarría Mayo, Juan Emilio, Eiros Bouza, José M.ª, Ignaci Elizalde Frez, J., Embid López, Cristina, Engel Rocamora, Pablo, de Salamanca Lorente, Rafael Enríquez, Escorsell Mañosa, Àngels, España Alonso, Agustín, Esteban Mur, Rafael, Esteller Badosa, Manel, Esteve Comas, María, Esteve Pardo, María, Esteve Reyner, Jordi, Estruch Riba, Ramón, Fainboim, Leonardo, Feliu Frasnedo, Evarist, Fernández Bañares, Fernando, Fernández Fernández, Óscar, Fernández Gómez, Javier, Fernández Llama, Patricia, Ferrándiz Foraster, Carlos, Ferrer Monreal, Miguel, Figuerola Pino, Daniel, Fillat Fonts, Cristina, Fonollosa Pla, Vicent, Fontanellas Romá, Antonio, Forcada Vega, Carme, Forner González, Alejandro, Forns Bernhardt, Xavier, Fortuny Guasch, Claudia, Franco de Castro, Agustín, Fresno Escudero, Manuel, Fullana Rivas, Miquel A., Gaba García, Lydia, Gaig Ventura, Carles, Galarza Delgado, Dionicio Ángel, Galicia Paredes, Miguel, Gállego Culleré, Montserrat, García de Vinuesa, Pastora Gallego, Garcia-Esteve, Lluïsa, García Lareo, Manuel, García-Moncó, Juan Carlos, García Nieto, Víctor, García-Pagán, Juan Carlos, García Sánchez, José Elías, Garrido Marín, Eduardo, Gascón Brustenga, Joaquim, Gatell Artigas, Josep M.ª, Gaztambide Sáenz, Sonia, Genescà Ferrer, Joan, Giavina-Bianchi, Pedro, Gil de Extremera, Blas, Giménez Pérez, Montserrat, Giné Soca, Eva, Ginès Gibert, Pere, Goday Arnó, Albert, Gómez-Batiste Alentorn, Xavier, Gómez Dantés, Héctor, Gómez Gil, Esther, Gomollón García, Fernando, Xavier González Argenté, F., González Juanatey, José Ramón, González Macías, Jesús, González Martín, Julià, González Tugas, Matías, Gracia Guillén, Diego, Grande i Fullana, Iria, Grau de Castro, Juan José, Grau Junyent, Josep M.ª, García-Milà, Isabel Graupera, Graus Ribas, Francesc, Gual Solé, Antoni, Guañabens Gay, Nuria, Gurguí Ferrer, Mercè, Ponce de León, Fernando Gutiérrez, Halperin Rabinovich, Irene, Alexandra Hanzu, Felicia, Hawkins Carranza, Federico G., Hernández García, Miguel Teodoro, Hernández Gea, Virginia, Hernández Rodríguez, José, Herrero Santos, José Ignacio, Ibáñez Toda, Lourdes, Illa Sendra, Isabel, Iranzo de Riquer, Alejandro, Pérez de Guzmán, Dolores Jaraquemada, Jiménez Castro, David, Juan Otero, Manuel, Juanola Roura, Xavier, Kalil, Jorge, Khamashta, Munther A., Labarca Labarca, Jaime, Laborde, Amalia, Lanas Arbeloa, Ángel, Landete Rodríguez, Pedro, Larrosa Escartín, Nieves, Lens García, Sabela, Carlota Londoño, Maria, Bernaldo de Quirós, Juan Carlos López, López de Sá, Esteban, López Guillermo, Armando, López-Sendón, José, López-Vélez Pérez, Rogelio, Lozano Sánchez, Francisco S., Lozano Soto, Francisco, Lumbreras Bermejo, Carlos, Mallolas Masferrer, Josep, Manzanera López, Rafael, Mañá Rey, Juan, Marco Reverté, Francesc, Ángeles Marcos Maeso, M.ª, Marimón Ortiz de Zarate, José María, Mariño Méndez, Zoe, Maroñas Amigo, Olalla, Marrades Sicart, Ramon M.ª, Marrugat de la Iglesia, Jaume, Martí Domènech, María Josep, Martí Mestre, Francesc Xavier, Martí Ripoll, Mercè, Cristina Martín Sierra, M.ª, Martínez Díaz-Guerra, Guillermo, Martínez-Lavín, Manuel, Martínez Martínez, José Antonio, Martínez Valle, Fernando, Martínez Vea, Alberto, Martínez Yoldi, Miguel Julián, Martorell Pons, Jaume, Mas Capó, Jordi, Masana Marín, Lluís, Masana Montejo, Guillem, Mascaró Galy, José Manuel, Matas Andreu, Lurdes, Maurel Santasusana, Joan, Melero Bermejo, Ignacio, Melero Maseda, Marcelo José, Mellado González, Begoña, Mensa Pueyo, José, Mercé Klein, Jorge, Mestres Alomar, Gaspar, Milà Recasens, Montserrat, Milone, Jorge H., Miralles Basseda, Ramón, Miralles Hernández, Manuel, Miró Meda, José María, Mòdol Deltell, Josep M.ª, Molero Richard, Xavier, Molina Infante, Javier, Molina Molina, María, Molins López-Rodó, Laureano, Mont Girbau, Lluís, Montoro Huguet, Miguel Ángel, Montserrat Canal, Josep Maria, Mora Casterá, Elvira, Mora Porta, Mireia, Morales-Olivas, Francisco, Morales Romero, Blai, Morán Chorro, Indalecio, Morata Ruiz, Laura, Asunción Moreno Camacho, M.ª, Moreno Carriles, Rosa María, Muga Bustamante, Roberto, Muñoz Almagro, Carmen, Muñoz Bermúdez, Rosana, Muñoz García, José Esteban, García-Paredes, Patricia Muñoz, Muñoz Gutiérrez, José, Muñoz Mateu, Montserrat, Muñoz Villegas, Álvaro, África Muxí Pradas, María, Navarro Acebes, Xavier, Navasa Anadón, Miquel, Nicolás Arfelis, José María, Nolla Solé, Joan Miquel, Norman, Francesca F., Obach Baurier, Víctor, Obrador Vera, Gregorio Tomás, Oliva Dámaso, Elena, Olivé Marqués, Alejandro, Oriola Ambròs, Josep, Ortiz Arduan, Alberto, de Lejarazu Leonardo, Raúl Ortiz, Oteo Revuelta, José Antonio, Palau Martínez, Francesc, Pallarés Giner, Román, Palou Rivera, Eduardo, Panés Díaz, Julián, Parés Darnaculleta, Albert, Pascal Capdevila, Mariona, Pascual Gómez, Eliseo, Pascual Gómez, Julio, Pascual Mateos, Juan Carlos, Pedro-Botet Montoya, Juan, Luisa Pedro-Botet Montoya, M.ª, Pereira Saavedra, Arturo, Pérez Gisbert, Javier, Pérez-Jurado, Luis Alberto, Pérez Sáenz, José Luis, Picado de Puig, Albert, Picado Valles, César, Picó Alfonso, Antonio, Pigrau Serrallach, Carlos, Jesús Pinazo Delgado, M.ª, Pintado García, Vicente, Pintos Morell, Guillem, Piñeiro Ibáñez, Daniel José, Piqueras Carrasco, Josep, López de Briñas, Esteban Poch, Pons-Estel, Bernardo A., Pons-Estel, Guillermo J., Pons Lladó, Guillem, Porcel Pérez, José Manuel, Portela Hernández, Margarita, Praga Terente, Manuel, Prat Aparicio, Aleix, Puig Domingo, Manuel, Pujol-Borrell, Ricardo, Pulido Mestre, Marta, Pumarola Suñé, Tomàs, Puras Mallagray, Enrique, Quintana Porras, Luis F., Quintero Carrión, Enrique, Adrián Rabinovich, Gabriel, Rabionet Janssen, Raquel, Ramos Casals, Manuel, Raya Sánchez, José María, Rego Castro, Maria José, Reguart Aransay, Noemí, Reverter Calatayud, Joan Carles, Reverter Calatayud, Jorge Luis, Reyes Moreno, José, Riambau Alonso, Vicente, Ribera Casado, José Manuel, Ribera Santasusana, Josep M.ª, Ribes Rubió, Antonia, Robert Boter, Neus, Roca Lecumberri, Alba, Roca Torrent, Josep, Roche Rebollo, Enric, Gonzalo de Liria, Carlos Rodrigo, Rodríguez Baño, Jesús, Rodríguez de Castro, Felipe, Rodríguez Panadero, Francisco, Rodríguez Pérez, José Carlos, Rodríguez-Roisin, Roberto, Rodríguez Valero, Natalia, Roig Minguell, Eulàlia, Rojas García, Ricardo, Roman Broto, Antonio, Romero Gómez, Manuel, Ros Cerro, Cristina, Rovira Cañellas, Àlex, Rozman, Ciril, Rozman Jurado, María, Ruiz-Argüelles, Guillermo José, Ruiz Granell, Ricardo, Ruiz Manzano, Juan, Ruiz Moreno, Javier, Sabaté Tenas, Manel, Saiz Hinajeros, Albert, Sala Sanjaume, Joan, Salgado García, Emilio, Salinas Vert, Isabel, San Miguel Izquierdo, Jesús F., Sánchez del Valle Díaz, Raquel, Sánchez González, Marcelo, Sánchez Rodríguez, Ángel, Sanmartí Sala, Raimon, Ángel Sanz Alonso, Miguel, Sanz Santillana, Guillermo F., Saperas Franch, Esteban, Saurí Nadal, Tamara, Schwarzstein, Diego, Segura Egea, Antònia, Segura Porta, Ferrán, Sellarés Torres, Jacobo, Selva O’Callaghan, Albert, Serra Majem, Lluís, Serrano Gimaré, Mercedes, Sibila Vidal, Oriol, Sierra Gil, Jorge, Sierra Romero, Gustavo Adolfo, Sitges Carreño, Marta, Solà Vergés, Elsa, Solana Lara, Rafael, Solans Laqué, Roser, Gloria Soldevila Melgarejo, M.ª, Soler Porcar, Néstor, Sopena Galindo, Nieves, Soriano Viladomiu, Álex, Soy Muner, Dolors, Suárez Fernández, Ricardo, Suela Rubio, Javier, Targarona Soler, Eduardo M.ª, Tejedor Jorge, Alberto, Tolosa Sarró, Eduardo, Tornero Molina, Jesús, Tornos Mas, Pilar, Torra Balcells, Roser, Torregrosa Prats, José Vicente, Torres Hortal, Montserrat, Torres Martí, Antoni, Torres Ramírez, Armando, Torrico, Faustino, Trilla García, Antoni, Tuca Rodríguez, Albert, Tudela Hita, Pere, Urbano Ispizua, Álvaro, Urrutia de Diego, Agustín, Valero Santiago, Antonio Luis, Valle Velasco, Laura, Eugenia Valls Lolla, M.ª, Valls Solé, Josep, Vaquero Raya, Eva C., Varsavsky, Mariela, Vázquez Martínez, Clotilde, San Miguel, Federico Vázquez, Vázquez Zaragoza, Miguel Ángel, Vicente García, Vicente, Vidal Bermúdez, José Ernesto, Vidal Losada, Maria, Vidal-Puig, Antonio, Vieta Pascual, Eduard, Vila Estapé, Jordi, Vilardell Tarrés, Miquel, Vilaseca González, Isabel, Vilella i Morató, Anna, Villà i Freixa, Salvador, Villabona Artero, Carles, Villamor Casas, Neus, Vinuesa Aumedes, Teresa, Viñolas Segarra, Nuria, Vives Corrons, Joan Lluís, Volberg Vincent, Veronica Inés, Vollmer Torrubiano, Ivan, Webb Youdale, Susan M., Yagüe Ribes, Jordi, Yugueros Castellnou, Xavier, and Zarranz Imirizaldu, Juan José

Published
2020
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11. Renal volume and cardiovascular risk assessment in normotensive autosomal dominant polycystic kidney disease patients

Author

Sans, Laia, Pascual, Julio, Radosevic, Aleksandar, Quintian, Claudia, Ble, Mireia, Molina, Lluís, Mojal, Sergi, Ballarín Castan, José Aurelio, Torra Balcells, Roser, Fernandez-Llama, Patricia, and Universitat Autònoma de Barcelona

Subjects
Male, Sistema cardiovascular -- Malalties, 030232 urology & nephrology, Blood Pressure, 030204 cardiovascular system & hematology, Kidney, urologic and male genital diseases, Severity of Illness Index, 0302 clinical medicine, Reference Values, Pulse wave velocity, education.field_of_study, autosomal dominant polycystic kidney disease, Age Factors, Organ Size, General Medicine, Middle Aged, Polycystic Kidney, Autosomal Dominant, Prognosis, medicine.anatomical_structure, Cardiovascular Diseases, Hypertension, Disease Progression, Cardiology, Female, medicine.symptom, Research Article, cardiovascular risk, Adult, medicine.medical_specialty, Ronyons -- Malalties, Population, Autosomal dominant polycystic kidney disease, Observational Study, Risk Assessment, Asymptomatic, Statistics, Nonparametric, 03 medical and health sciences, Sex Factors, Internal medicine, medicine, Humans, education, Analysis of Variance, business.industry, renal volume, medicine.disease, Cardiovascular risk, Cross-Sectional Studies, Blood pressure, ROC Curve, Intima-media thickness, Multivariate Analysis, Microalbuminuria, business, Renal volume
Abstract

Cardiovascular disease, closely related to an early appearance of hypertension, is the most common mortality cause among autosomal dominant polycystic kidney disease patients (ADPKD). The development of hypertension is related to an increase in renal volume. Whether the increasing in the renal volume before the onset of hypertension leads to a major cardiovascular risk in ADPKD patients remains unknown. Observational and cross-sectional study of 62 normotensive ADPKD patients with normal renal function and a group of 28 healthy controls. Renal volume, blood pressure, and renal (urinary albumin excretion), blood vessels (carotid intima media thickness and carotid-femoral pulse wave velocity), and cardiac (left ventricular mass index and diastolic dysfunction parameters) asymptomatic organ damage were determined and were considered as continuous variables. Correlations between renal volume and the other parameters were studied in the ADPKD population, and results were compared with the control group. Blood pressure values and asymptomatic organ damage were used to assess the cardiovascular risk according to renal volume tertiles. Even though in the normotensive range, ADPKD patients show higher blood pressure and major asymptomatic organ damage than healthy controls. Asymptomatic organ damage is not only related to blood pressure level but also to renal volume. Multivariate regression analysis shows that microalbuminuria is only associated with height adjusted renal volume (htTKV). An htTKV above 480 mL/m represents a 10 times higher prevalence of microalbuminuria (4.8% vs 50%, P 336 mL/m) show higher urinary albumin excretion, but the 3rd tertile htTKV (htTKV > 469 mL/m) group shows the worst cardiovascular risk profile. Normotensive ADPKD patients show in the early stages of the disease with slight increase in renal volume, higher cardiovascular risk than healthy controls. An htTKV above 468 mL/m is associated with the greatest increase in cardiovascular risk of normotensive ADPKD patients with normal renal function. Early strategies to slow the progression of the cardiovascular risk of these patients might be beneficial in their long-term cardiovascular survival.

Published
2016

13. Abstract P358: Central BP Variability is Increased in Hypertensive-related Target Organ Damage

Author

De La Sierra, Alejandro, primary, Pareja, Julia, additional, Yun, Sergi, additional, Acosta, Eva, additional, Aiello, Francesco, additional, Oliveras, Anna, additional, Vazquez, Susana, additional, Armario, Pedro, additional, Blanch, Pere, additional, Sierra, Cristina, additional, Calero, Francesca, additional, and Fernandez LLama, Patricia, additional

Published
2017
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14. Long-term regulation of renal Na-dependent cotransporters and ENaC: response to altered acid-base intake

Author

KIM, GHEUN-HO, MARTIN, STEPHEN W., FERNANDEZ-LLAMA, PATRICIA, MASILAMANI, SHYAMA, PACKER, RANDALL K., and KNEPPER, MARK A.

Subjects
Renal tubular transport -- Physiological aspects, Ion channels -- Analysis, Metabolic regulation -- Research, Amiloride -- Physiological aspects, Biological sciences
Abstract

Long-term regulation of renal Na-dependent cotransporters and ENaC: response to altered acid-base intake. Am J Physiol Renal Physiol 279: F459-F467, 2000.--Increased systemic acid intake is associated with an increase in apical Na/H exchange in the renal proximal tubule mediated by the type 3 Na/H exchanger (NHE3). Because NHE3 mediates both proton secretion and Na absorption, increased NHE3 activity could inappropriately perturb Na balance unless there are compensatory changes in Na handling. In this study, we use semiquantitative immunoblotting of rat kidneys to investigate whether acid loading is associated with compensatory decreases in the abundance of renal tubule Na transporters other than NHE3. Long-term (i.e., 7-day) acid loading with [NH.sub.4]Cl produced large decreases in the abundances of the thiazide-sensitive Na-C1 cotransporter (TSC/NCC) of the distal convoluted tubule and both the [Beta] and [Gamma]-subunits of the amiloride-sensitive epithelial Na channel (ENaC) of the collecting duct. In addition, the renal cortical abundance of the proximal type 2 Na-dependent phosphate transporter (NaPi-2) was markedly decreased. In contrast, abundances of the bumetanide-sensitive Na-K-2C1 cotransporter of the thick ascending limb and the [Alpha]-subunit of ENaC were unchanged. A similar profile of changes was seen with short-term (16-h) acid loading. Long-term (7-day) base loading with NaH[CO.sub.3] resulted in the opposite pattern of response with marked increases in the abundances of the [Beta]- and [Gamma]-subunits of ENaC and NaPi-2. These adaptations may play critical roles in the maintenance in Na balance when changes in acid-base balance occur. sodium-proton exchange; sodium-potassium-2 chloride cotransport; distal convoluted tubule; collecting duct; amiloride-sensitive epithelial sodium channel

Published
2000

16. Reduced abundance of aquaporins in rats with bilateral ischemia-induced acute renal failure: prevention by [Alpha]-MSH

Author

KWON, TAE-HWAN, FROKIAER, JORGEN, FERNANDEZ-LLAMA, PATRICIA, KNEPPER, MARK A., and NIELSEN, SOREN

Subjects
Necrosis -- Research, Intermedin -- Research, Acute renal failure -- Research, Urination -- Analysis, Biological sciences
Abstract

Kwon, Tae-Hwan, Jorgen Frokiaer, Patricia Fernandez-Llama, Mark A. Knepper, and Soren Nielsen. Reduced abundance of aquaporins in rats with bilateral ischemia-induced acute renal failure: prevention by [Alpha]-MSH. Am. J. Physiol. 277 (Renal Physiol. 46): F413-F427, 1999.--We examined the effect of temporary renal ischemia (30 min or 60 min) and reperfusion (1 day or 5 days) on the expression of renal aquaporins (AQPs) and urinary concentration in rats with bilateral ischemia-induced acute renal failure (ARF). Next, we tested whether reducing ischemia/reperfusion (I/R) injury by treatment with [Alpha]-melanocyte stimulating hormone ([Alpha]-MSH) affects the expression of AQPs and urine output. Rats with ARF showed significant renal insufficiency, and urinary concentration was markedly impaired. In rats with mild ischemic injury (30 min), urine output increased significantly to a maximum at 48 h, and then nearly normalized within 5 days. Consistent with this, semiquantitative immunoblotting revealed that kidney AQP1 and AQP2 abundance was significantly decreased after 24 h to 30 [+ or -] 5% and 40 [+ or -] 11% (n = 8) of controls (n = 9), respectively (P [is less than] 0.05). Five days after ischemia, AQP2 abundance was not significantly decreased and urine output was normalized. In contrast, severe ischemic injury (60 min) resulted in a marked reduction in urine output at 24 h, despite a significant decrease in urine osmolality and solute-free water reabsorption, [T.sup.c][H.sub.2]O. AQP1 and AQP2 abundance was markedly decreased to 51 [+ or -] 5% and 31 [+ or -] 9% (n = 10) of controls (n = 8) at 24 h (P [is less than] 0.05). After 5 days, the rats developed gradually severe polyuria and had very low AQP2 and AQP1 levels [11 [+ or -] 4% and 6 [+ or -] 2% (n = 5) of controls (n = 8), respectively; P [is less than] 0.05]. A similar reduction was observed for AQP3. The reduction in AQP expression in the proximal tubule and inner medullary collecting duct was confirmed by immunocytochemistry. Next, we found that intravenous [Alpha]-MSH treatment of rats with ARF significantly reduced the ischemia-induced downregulation of renal AQPs and reduced the polyuria. In conclusion, the I/R injury is associated with markedly reduced expression of the collecting duct and proximal tubule AQPs, in association with an impairment of urinary concentration. Moreover, [Alpha]-MSH treatment significantly prevented the reduction in expression of AQPs and renal functional defects. Thus decreased AQP expression is likely to contribute to the impairment in urinary concentration in the postischemic period. acute tubular necrosis; [Alpha]-melanocyte stimulating hormone; collecting duct; proximal tubule; urinary concentration mechanism

Published
1999

18. Hypertension in autosomal-dominant polycystic kidney disease (ADPKD)

Author

Sans-Atxer, Laia, Torra Balcells, Roser, Fernandez-Llama, Patricia, and Universitat Autònoma de Barcelona

Subjects
cardiovascular risk, medicine.medical_specialty, Ambulatory blood pressure, Original Contributions, Population, Autosomal dominant polycystic kidney disease, Renal size, blood pressure profile, urologic and male genital diseases, in-Depth Review, Polycystic kidney disease, renal size, Internal medicine, medicine, education, Cause of death, Transplantation, education.field_of_study, Kidney, polycystic kidney disease, business.industry, Blood pressure profile, medicine.disease, Cardiovascular risk, ambulatory blood pressure monitoring, Endocrinology, medicine.anatomical_structure, Blood pressure, Nephrology, Cardiology, Microalbuminuria, Ambulatory blood pressure monitoring, business
Abstract

Altres ajuts: FISPI10-01261 Altres ajuts: FISPI12-01523 Cardiovascular (CV) complications are the major cause of death in autosomal-dominant polycystic kidney disease (ADPKD) patients. Hypertension is common in these patients even before the onset of renal insufficiency. Blood pressure (BP) elevation is a key factor in patient outcome, mainly owing to the high prevalence of target organ damage together with a poor renal prognosis when BP is increased. Many factors have been implicated in the pathogenesis of hypertension, including the renin-angiotensin-aldosterone system (RAAS) stimulation. Polycystin deficiency may also contribute to hypertension because of its potential role in regulating the vascular tone. Early diagnosis and treatment of hypertension improve the CV and renal complications of this population. Ambulatory BP monitoring is recommended for prompt diagnosis of hypertension. CV risk assessment is mandatory. Even though a nonpharmacological approach should not be neglected, RAAS inhibitors are the cornerstone of hypertension treatment. Calcium channel blockers (CCBs) should be avoided unless resistant hypertension is present. The BP should be

Published
2013

19. Recommendations for Biomarker Identification and Qualification in Clinical Proteomics

Author

Mischak, Harald, primary, Allmaier, Günter, additional, Apweiler, Rolf, additional, Attwood, Teresa, additional, Baumann, Marc, additional, Benigni, Ariela, additional, Bennett, Samuel E., additional, Bischoff, Rainer, additional, Bongcam-Rudloff, Erik, additional, Capasso, Giovambattista, additional, Coon, Joshua J., additional, D’Haese, Patrick, additional, Dominiczak, Anna F., additional, Dakna, Mohammed, additional, Dihazi, Hassan, additional, Ehrich, Jochen H., additional, Fernandez-Llama, Patricia, additional, Fliser, Danilo, additional, Frokiaer, Jorgen, additional, Garin, Jerome, additional, Girolami, Mark, additional, Hancock, William S., additional, Haubitz, Marion, additional, Hochstrasser, Denis, additional, Holman, Rury R., additional, Ioannidis, John P. A., additional, Jankowski, Joachim, additional, Julian, Bruce A., additional, Klein, Jon B., additional, Kolch, Walter, additional, Luider, Theo, additional, Massy, Ziad, additional, Mattes, William B., additional, Molina, Franck, additional, Monsarrat, Bernard, additional, Novak, Jan, additional, Peter, Karlheinz, additional, Rossing, Peter, additional, Sánchez-Carbayo, Marta, additional, Schanstra, Joost P., additional, Semmes, O. John, additional, Spasovski, Goce, additional, Theodorescu, Dan, additional, Thongboonkerd, Visith, additional, Vanholder, Raymond, additional, Veenstra, Timothy D., additional, Weissinger, Eva, additional, Yamamoto, Tadashi, additional, and Vlahou, Antonia, additional

Published
2010
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20. Sodium retention in cirrhotic rats is associated with increased renal abundance of sodium transporter proteins

Author

Fernandez-Llama, Patricia, primary, Ageloff, Shana, additional, Fernandez-Varo, Guillermo, additional, Ros, Josefa, additional, Wang, Xiaoyan, additional, Garra, Nuria, additional, Esteva-Font, Cristina, additional, Ballarin, Jose, additional, Barcelo, Pere, additional, Arroyo, Vicente, additional, Stokes, John B., additional, Knepper, Mark A., additional, and Jimenez, Wladimiro, additional

Published
2005
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21. Altered expression of Na transporters NHE-3, NaPi-II, Na-K-ATPase, BSC-1, and TSC in CRF rat kidneys

Author

Kwon, Tae-Hwan, Frokiaer, Jorgen, Fernandez-Llama, Patricia, Maunsbach, Arvid B., Knepper, Mark A., and Nielsen, Soren

Subjects
Chronic kidney failure -- Physiological aspects, Kidneys -- Physiological aspects, Rats -- Physiological aspects, Sodium in the body -- Physiological aspects, Biological sciences
Abstract

Semiquantitative immunoblotting and immunochemistry were performed on rats with chronic renal failure induced by 5/6 nephrectomy to look for changes in total kidney levels per nephron of major proximal and major distal tubule sodium transporters and to determine whether these changes are related with changes in the urinary sodium excretion. Increased fractional sodium excretion was found to be associated with altered expression of the Na transporters NHE-3, NaPi-II and Na-K-AtPase. Compensatory increases in BSC-1 and TSC expression per nephron were also found in distal segments.

Published
1999

23. Recombinant PTH associated with hypercalcaemia and renal failure.

Author

Ayasreh, Nadia, Fernandez-Llama, Patricia, Lloret, MJ, Da Silva, Iara, Ballarín, Jose, and Bover, Jordi

Subjects
*CHRONIC kidney failure, *KIDNEY diseases, *NONSTEROIDAL anti-inflammatory agents, *HYPERCALCEMIA
Abstract

The article presents a case study of a 77-year-old male with acute impairment of renal function. The patient has history of frequent use of nonsteroidal anti-inflammatory agents as well as drugs potentially causing hypercalcaemia. The article also discusses some basic aspects of the diagnosis and current treatment of osteoporosis in patients with renal impairment. It suggests the need to contraindicate teriparatide when chronic kidney disease and secondary hyperparathyroidism are present.

Published
2013

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