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.
Our group is focused in research in primary or inherited tubular renal diseases, such as Dent’s Disease, Bartter syndrome, Tubular Acidosis, Familial Hypomagnesemia with Hypercalciuria and Nephrocalcinosis, among others. Currently we are collaborating with other groups in Spain, within a research project named Renaltube the main purpose of which is to build a database while facilitating access to genotyping in order to improve the clinical and molecular knowledge of primary tubulopathies. Renaltube has a web-based approach with multilateral collaboration scheme that enhances the recruitment of data and promotes the understanding of underlying mechanisms of rare inherited diseases, defines more accurate diagnostic and follow-up criteria, develops new molecular techniques and will improve the overall care of the patients. Currently we are offering the analysis of 22 genes corresponding to 23 primary tubulopathies. After two years of activity Renaltube has collected data from 222 patients, the mayority from Spain and Latin America (85.3%). The most common tubulopathies are distal renal tubular acidosis (22.5%), and classical Bartter syndrome (19.3%) followed by familial hypomagesemia with hipercalciuria and nephrocalcinosis (15.7%), and Gitelman syndrome (15%).
IP: Gema Ariceta Iraola, Anna Meseguer Navarro
Among the genes identified in our laboratory that are kidney-specific and regulated by androgens at the transcriptional level we are particularly focused on the one that codes for the kidney androgen-regulated protein (KAP). Besides characterization of the functional promoter elements that enable KAP expression in proximal tubule epithelial cells, we have generated a transgenic (Tg) mouse model that overexpresses KAP in proximal tubule cells under the presence of androgens, in order to mimick the endogenous KAP expression pattern. KAP Tg mice show altered lipid metabolism, glycosuria, proteinuria and hypertension, as well as focal segmental glomerulosclerosis mediated by increased oxidative stress. We are currently working in this Tg model and also preparing conditional knock-out mice to further caharacterize the role of KAP in renal pathophysiology. Moreover, we are also studying the role of KAP in the metabolic syndrome. Besides KAP, we are studying the role of KAP-interacting immunophilins in inflammation and kidney fibrosis.
IP: Anna Meseguer Navarro
IP: Gema Ariceta Iraola Collaborators: Cristina Martínez Martínez, Julieta Torchia Pruzzo Funding agency: AIRG - ESPAÑA Funding: 10000 Reference: CGE/ARICETA/2023 Duration: 01/01/2024 - 01/01/2025
IP: Mercedes López González Collaborators: Gema Ariceta Iraola, Laura Donadeu Casassas, Delphine Kervella Funding agency: Sociedad Española de Trasplantes Funding: 20000 Reference: SET/AYUDAS.PROYECTOS/2023/LOPEZ Duration: 01/01/2024 - 31/12/2025
IP: Francesc Moreso Mateos Collaborators: Gema Ariceta Iraola, Joan López Hellin Funding agency: Instituto de Salud Carlos III Funding: 42900 Reference: PMP22/00119 Duration: 01/01/2023 - 31/12/2025
IP: La variabilidad fenotípica en pacientes afectados de Hipomagnesemia Familiar con Hipercalciuria y Nefrocalcinosis (HFHNC) como o Collaborators: Gema Ariceta Iraola, Gerard Cantero Recasens Funding agency: Sociedad Española de Nefrología (S.E.N.) Funding: 24000 Reference: SENEFRO/PROJECTES/2023/MESEGUER Duration: 27/11/2023 - 26/11/2025
The team has discovered that a protein called SEC22B acts as a phenotype modifier and could be used as a potential urinary marker of the disease.
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.
