Inflammatory processes in kidney disease
Peritoneal dialysis (PD): Our main line of work is focused on the study of the mechanisms involved in PD-induced damage to the peritoneal membrane. We also studied the influence of various drugs (Paricalcitol, Tamoxifen, Rosiglitazone) on the prevention and repair of peritoneal membrane damage. In the coming years we will try to clarify which mechanisms are responsible for hyalinising vascular disease, the role of activated macrophages alternately in peritoneal damage, and analyse morphological and immunohistochemical findings in peritoneal biopsies of patients treated with conventional or biocompatible liquids.
A project under development is the design of a microchip for the early non-invasive diagnosis of the mesothelial-mesenchymal transition, using peritoneal effluent. Preliminary data have shown that peritoneal dialysis, in mice subjected to cerebral ischaemic damage, is able to decrease brain damage induced by high levels of glutamate. In collaboration with the Department of Neurology we are developing a clinical trial in patients to determine whether peritoneal dialysis can protect against cerebral ischaemic damage in patients in the acute phase of ischaemic stroke.
Nutrition in kidney disease: we have studied the importance of exercise in the proper nutrition and survival of patients with advanced chronic kidney disease and the effect of physical training. To this end, we have analysed the introduction of new indices for the nutritional evaluation of renal patients and we intend to study the balance of myocytokines and their relationship with functionality and muscle strength.
Bone alterations and mineral metabolism in chronic kidney disease (CKD): FGF23 is a molecule involved in phosphorus metabolism but it may be important as a marker of cardiovascular pathology and survival in kidney disease. We have designed a funded clinical trial to analyse the behaviour of FGF23 and PTH fragments in patients with chronic kidney disease treated with cinacalcet within the peritoneal dialysis programme.
José Antonio Sánchez Tomero
Hospital Universitario La Princesa
| Other team members:
Sánchez Tomero, José Antonio. Importance of physical exercise in nutrition and survival of patients with advanced chronic kidney disease. Baxter SA. 2014-2015.
Sánchez Tomero, José Antonio. Tissue repair through repopulation by bone marrow progenitors. Amgen SA and PALEX SA. 2014-2016.
Sánchez Tomero, José Antonio. Development of a programme for the comprehensive approach treating advanced chronic kidney disease. United Surgical Partners Madrid, SL. Hospital Quirón San Camilo. 2013-2015.
Sánchez Tomero, José Antonio. Study of cardiovascular risk markers in kidney disease and prognostic projection. Nipro Europe SA. 2013-2015.
Barril Cuadrado, Guillermina. Balance of myocytokines in haemodialysis. Variations according to the haemodialysis scheme. Sociedad Madrileña de Nefrología. 2013-2015.
Barril Cuadrado, Guillermina. Study of cellulose triacetate dialyser. In vivo behaviour in online haemodiafiltration. Nipro S.A.
Bernis Carro, Carmen. CIFRA: Use of animal and cellular models to characterise acute and multiple organ renal failure. S2010/BMD-2378. CAM. 2012-2015.
Aguilera Peralta, Abelardo Isaac. The abdominal cavity as a source of cardiovascular risk factors and atherosclerosis during peritoneal dialysis: therapeutic alternatives. PI12/01175. ISCIII. 2013-2015.
Aguilera Peralta, Abelardo Isaac. Development of a new, more biocompatible peritoneal dialysis solution based on a mixture of favonoid glucosides as an osmotic agent. PI15/00598. ISCIII. 2016-2018.
Sandoval P, Loureiro J, González-Mateo G, Pérez-Lozano ML, Maldonado-Rodríguez A, Sánchez-Tomero JA, Mendoza L, Santamaría B, Ortiz A, Ruíz-Ortega M, Selgas R, Martín P, Sánchez-Madrid F, Aguilera A, López-Cabrera M. PPAR-gamma agonist rosiglitazone protects peritoneal membrane from dialysis fluid-induced damage. Lab. Invest. 2010. 90: 1517-1532. FI: 4.405(Q1). PMID: 20531289. DOI: 10.1038/labinvest.2010.111.
Conde E, Alegre L, Blanco-Sánchez I, Sáenz-Morales D, Aguado-Fraile E, Ponte B, Ramos E, Sáiz A, Jiménez C, Ordoñez A, López-Cabrera M, del Peso L, de Landázuri MO, Liaño F, Selgas R, Sanchez-Tomero JA, García-Bermejo ML. Hypoxia Inducible Factor 1-Alpha (HIF-1 Alpha) Is Induced during Reperfusion after Renal Ischemia and Is Critical for Proximal Tubule Cell Survival. PLoS One 2012. . FI: 3.730(Q1). PMID: 22432008. DOI: 10.1371/journal.pone.0033258.
Pérez-Lozano ML, Sandoval P, Rynne-Vidal A, Aguilera A, Jiménez-Heffernan JA, Albar-Vizcaíno P, Majano PL, Sánchez-Tomero JA, Selgas R, López-Cabrera M. Functional Relevance of the Switch of VEGF Receptors/Co-Receptors during Peritoneal Dialysis-Induced Mesothelial to Mesenchymal Transition. PLoS One 2013. . FI: 3.534(Q1). PMID: 23585849. DOI: 10.1371/journal.pone.0060776.
Loureiro J, Sandoval P, del Peso G, Gónzalez-Mateo G, Fernández-Millara V, Santamaria B, Bajo MA, Sánchez-Tomero JA, Guerra-Azcona G, Selgas R, López-Cabrera M, Aguilera AI. Tamoxifen Ameliorates Peritoneal Membrane Damage by Blocking Mesothelial to Mesenchymal Transition in Peritoneal Dialysis. PLoS One 2013. FI: 3.534(Q1). PMID: 23637793. DOI: 10.1371/journal.pone.0061165.
Godino Mdel C, Romera VG, Sánchez-Tomero JA, Pacheco J, Canals S, Lerma J, Vivancos J, Moro MA, Torres M, Lizasoain I, Sánchez-Prieto J. Amelioration of ischaemic brain damage by peritoneal dialysis. J. Clin. Invest. 2013. 123: 4359-4363. FI: 13.765(Q1). PMID: 23999426. DOI: 10.1172/JCI67284.