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.
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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.
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: Androgen activity in renal pathophysiology: Identification of androgen-regulated kidney-specific genes and functional characteri
Idiopathic nonfamilial focal segmental glomerulosclerosis (FSG) is a disease with no treatment, whose usual outcome is end-stage renal disease frequently recidivating after transplantation. In close cooperation with the Nephrology and Paediatric Nephrology services of Vall d'Hebron hospital together with hospitals throughout the country that provide a significant number of patients, we intend to identify the hypothetical blood factor that causes the proteinuria observed in this disease. Identification of such plasma factor, by means of differential proteomic analysis, would allow the definition of therapeutic targets for the disease, which currently lacks an effective treatment. Our second objective is to find biomarkers that enable us to foresee a potential recidivation and the consequent loss of the graft following renal transplantation to FSG patients.
IP: Joan López Hellin
Pediatric patients with chronic kidney disease (CKD) constitude a high risk group for cardiovascular disease (CVD) related to traditional and non-traditional risk factors. We are interested in studying the relationship between traditional CVD risk factors (obesity, overweight, anemia, dyslipemia, malnutrition, hypertension, and non-traditional CVD risk factors (homocysteine, asymmetric dymethylarginine (ADMA), FGF23, ultraselective protein C (PCR) and carotid intima-media thickness (cIMT) in children and adolescents with CKD, based on its severity and duration. Further, we are also interested in finding a biomarker to identify early in the disease, those patients with increased CVD risk and poor outcome.
IP: Gema Ariceta Iraola
Chronic allograft nephropathy (CAN) is one of the major causes of graft loss in kidney-transplanted patients. The pathogenetic mechanisms of CAN are probably multifactorial, including early noxious agents as a consequence of ischemia/ reperfusion of the graft or high loading doses of anticalcineurinics (aCN), and also chronic damage following aCN therapy, rejection or other reasons. We want to determine the proteomic and genomic changes occurring in tubular cells after different noxious agents (cyclosporin, tacrolimus, other renal toxicants, hypoxia), and also the effects caused by immunophilin silencing (anticalcineurin receptors) in the renal proximal tubule cells. Our objective is to identify specific markers of kidney injury that would be useful to anticipate toxicity or injury in early starges. Those putative markers will be clinically validated in collaboration with the Nephrology and the Pathology services of Vall d’Hebron Hospital.
IP: -
IP: - Collaborators: - Funding agency: Fundació Institut de Recerca HUVH Funding: 180000 Reference: MESEGUER/RISE/2024 Duration: 15/11/2024 - 14/11/2028
IP: Cristina Martínez Martínez Collaborators: Julieta Torchia Funding agency: Instituto de Salud Carlos III Funding: 146250 Reference: PI24/00547 Duration: 01/01/2025 - 31/12/2027
IP: Enric Miret Alomar Collaborators: Enric Trilla Herrera, David Lorente García, Aroa Gomez Brey, Maria Eugenia Semidey Raven, Delphine Kervella Funding agency: Instituto de Salud Carlos III Funding: 52500 Reference: PI24/00895 Duration: 01/01/2025 - 31/12/2027
IP: Cristina Martínez Martínez Collaborators: Alejandro Cruz Gual, Alvaro Domingo Madrid Aris, Ana Maria Gonzalez Castro Funding agency: Instituto de Salud Carlos III Funding: 38585.07 Reference: PI21/00757 Duration: 01/01/2022 - 30/06/2026
PhD student: Gerard Cantero Recasens Director/s: Anna Meseguer Navarro University: Universitat Pompeu Fabra Year: 2021
PhD student: Mónica Vall Palomar Director/s: Gema Ariceta Iraola, Anna Meseguer Navarro University: Universidad Autònoma de Barcelona Year: 2020
PhD student: Stephane Nemours , Stephane Nemours Director/s: Anna Meseguer Navarro University: Universidad Autònoma de Barcelona Year: 2020
PhD student: Mónica Durán Fernández Director/s: Anna Meseguer Navarro, Gema Ariceta Iraola University: Universidad Autònoma de Barcelona Year: 2020
PhD student: Jazmine Paola Arevalo Bautista Director/s: Anna Meseguer Navarro University: Universidad Autònoma de Barcelona Year: 2019
PhD student: Irene Campoy Moncayo Director/s: Antonio Gil Moreno, Jaume Reventós Puigjaner, Eva Colas Ortega University: Universidad Autònoma de Barcelona Year: 2017
PhD student: Maria Eugenia Semidey Raven, Maria Eugenia Semidey Raven Director/s: Jordi Giralt López de Sagred, Santiago Ramon y Cajal Agüeras, Margarita Alberola Ferranti, Margarita Alberola Ferranti University: Universidad Autònoma de Barcelona Year: 2016
PhD student: Eduard Sarro Tauler Director/s: University: Universidad Autònoma de Barcelona Year: 2008
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.
