IP: Dr. Guillermo Gervasini Rodríguez

Resumen del proyecto: The nephropathy of vascular origin is, together with diabetic nephropathy, the major contributor to the progression of chronic renal patients to the terminal state. The high prevalence of the disease leads to the occurrence of many cases in which kidney failure worsens cardiovascular risk and this in turn increases the progression of the disease. However, there are no diagnostic methods to detect which patients are going to show a poor evolution, nor are there specific therapies that improve the current preventive renal and cardioprotective treatments. Although the etiopathogenic mechanisms of the disease are not exactly known, it is known that prostaglandins play an important role. Of these, PGE2, generated by the cyclooxygenase pathway of the arachidonic acid, is the main route at the renal level, being a major actor in both renal homeostasis and pathological mechanisms in the kidney. There is evidence that genetic variants in the pathway leading to PGE2 and its receptors may have renal and cardiovascular repercussions. In this project we will determine the genetic variability in the cycloxygenase pathway of PGE2 (10 genes) through two complementary approaches: (i) genotyping of tagSNPs already identified by a previous analysis and (ii) genotyping of SNPs in the pathway with reported implications in the cardiorenal function; totalizing 215 SNPs. We will thus create a genetic profile in 600 patients with vascular nephropathy and 600 controls. Through the retrospective review of clinical histories and the association with the resulting genotypes, we will elaborate models that, integrating clinical, demographic and genetic variables, will help to identify patients with a putative worse evolution.

Entidad financiadora: Instituto de Salud Carlos III