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Hector Rios Duro

Institutions of which they are part

Research technician
Kidney Physiopathology
Vall Hebron Institut de Recerca

Hector Rios Duro

Institutions of which they are part

Research technician
Kidney Physiopathology
Vall Hebron Institut de Recerca

Projects

Biomarcadores, dianas y soluciones terapéuticas para mejorar el cuidado de pacientes afectados de Hipomagnesemia Familiar con Hipercalciuria y Nefrocalcinosis (HFHNC).

IP: Gema Ariceta Iraola
Collaborators: Hector Rios Duro, Mónica Durán Fernández, Gloria Mª Fraga Rodriguez, Julieta Torchia, Julieta Torchia
Funding agency: Instituto de Salud Carlos III
Funding: 202070
Reference: PI22/01946
Duration: 01/01/2023 - 31/12/2025

Papel del ClC-5 en la fibrosis renal. Identificación de posibles biomarcadores y dianas terapéuticas para la progresión de la enfermedad de Dent 1

IP: Gerard Cantero Recasens
Collaborators: Papel del ClC-5 en la fibrosis renal. Identificación de posibles biomarcadores y dianas terapéuticas para la progresión de la e, Hector Rios Duro, Mónica Durán Fernández, Gloria Mª Fraga Rodriguez, Julieta Torchia, Julieta Torchia, Andrea Casal Pardo
Funding agency: Instituto de Salud Carlos III
Funding: 123420
Reference: PI22/00741
Duration: 01/01/2023 - 31/12/2025

Patologia Cel·lular

IP: Patologia Cel·lular
Collaborators: Gema Ariceta Iraola, Alejandro Cruz Gual, Gerard Cantero Recasens, David Lorente García, Marina Muñoz López, Mercedes López González, Hector Rios Duro, Mónica Durán Fernández, Luis Augusto Castro Sáder, Gloria Mª Fraga Rodriguez, Julieta Torchia
Funding agency: Agència Gestió Ajuts Universitaris i de Recerca
Funding: 40000
Reference: 2021 SGR 01600
Duration: 01/01/2022 - 30/06/2025

Related news

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.

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