About the VHIR
Here at the Vall d'Hebron Research Institute (VHIR) we promote biomedical research, innovation and teaching. Over 1,800 people are seeking to understand diseases today so the treatment can be improved tomorrow.
Research
We are working to understand diseases, to find out how they operate and to create better treatments for patients. Get to know about our groups and their lines of research.
People
People are the centre of the Vall d'Hebron Research Institute (VHIR). This is why we are bound by the principles of freedom of research, gender equality and professional attitudes that HRS4R promotes.
Clinical trials
Our work is not just basic or translational; we are leaders in clinical research. Enter and find about the clinical trials we are conducting and why we are a world reference in this field.
Progress
Our aim is to make the research carried out at the Vall d’Hebron Research Institute (VHIR) a driving force for transformation. How? By identifying new channels and solutions for the promotion of people's health and well-being.
Core facilities
We offer specialist support for researchers, internal and external alike, ranging from specific services to preparing complete projects. All this, from a perspective of quality and speed of response.
News
We offer you a gateway for staying up to date on everything going on at the Vall d’Hebron Research Institute (VHIR), from the latest news to future solidarity activities and initiatives that we are organising.
Our main scientific interest is to understand, from a multidisciplinary and translational approach, the molecular and cellular processes leading to renal dysfunction in several kidney pathologies. Specifically, our research lines are
We are experts on the following areas:
To sum up, our research main objective is to combine –omic data from cellular and animal models with patients’ data to identify novel biomarkers and possible treatments for several renal diseases.
PMID: 35795075 Journal: European Urology Open Science Year: 2022 Reference: Eur Urol Open Sci. 2022 Jul 1;42:40-41. doi: 10.1016/j.euros.2022.06.002. eCollection 2022 Aug. Impact factor: 0 Publication type: Letter whit IF Authors: Trilla, Enrique; Esteban, Luis M; Triquell, Marina; Morote, Juan; Borque-Fernando, Angel et al. DOI: 10.1016/j.euros.2022.06.002
PMID: 35810139 Journal: Journal of Pediatric Urology Year: 2022 Reference: J Pediatr Urol. 2022 Jun 25. pii: S1477-5131(22)00288-1. doi: 10.1016/j.jpurol.2022.06.019. Impact factor: 1.83 Publication type: Paper in international publication Authors: Gander, Romy; Asensio, Marino; Andres Molino, Jose; Fatou Royo, Gloria; Lopez-Gonzalez, Mercedes; Perez, Victor; Lopez, Manuel; Ariceta, Gema et al. DOI: 10.1016/j.jpurol.2022.06.019
PMID: 35810826 Journal: AMERICAN JOURNAL OF KIDNEY DISEASES Year: 2022 Reference: Am J Kidney Dis. 2022 Jul 7. pii: S0272-6386(22)00772-7. doi: 10.1053/j.ajkd.2022.05.013. Impact factor: 8.86 Publication type: Letter or abstract Authors: Forero-Delgadillo, Jessica, Sanchez-Kazi, Cheryl, Principi, Iliana, Pecoraro, Carmine, Parolin, Mattia, Nastausheva, Tatiana, Muller, Rebekka, Moczulska, Anna, Maxted, Andrew, Marks, Stephen et al. DOI: 10.1053/j.ajkd.2022.05.013
PMID: 35552824 Journal: PEDIATRIC NEPHROLOGY Year: 2022 Reference: Pediatr Nephrol. 2022 May 12. pii: 10.1007/s00467-022-05591-5. doi: 10.1007/s00467-022-05591-5. Impact factor: 3.714 Publication type: Paper in international publication Authors: Ariceta, Gema, Collard, Laure, Abroug, Saoussen, Moochhala, Shabbir H, Gould, Edward, Boussetta, Abir, Ben Hmida, Mohamed, Hunley, Tracy E, Jarraya, Faical, Fraga, Gloria et al. DOI: 10.1007/s00467-022-05591-5
Funding has been obtained for 43 projects under the calls for Health R&D&I Projects, Health Technology Development, and Independent Clinical Research
The aim of the project is to establish kidney organoids derived from patients with familial hypomagnesaemia with hypercalciuria and nephrocalcinosis, which will be essential tools for studying the disease and testing new treatments.
The work identifies variants in genes such as NFU1 that, combined with the disease-causing mutation, can accelerate kidney deterioration.
