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P0054ACQUIRED DIFFERENTIAL EXPRESSION IN ACUTE KIDNEY INJURY OF GENES RESPONSIBLE FOR HEREDITARY NEPHROPATHIES


 
 
 Gene sequencing is becoming an important diagnostic tool in a great number of medical specialties. Despite its interpretation is still a challenge, allows the identification of genes related to hereditary diseases and bild a base for the study of acquired nephropathies. We hypothesize that those genes responsible for hereditary nehpropathies could contribute to the pathogenesis of acquired nephropathies.
 
 
 
 In a murine model of acute kidney disease induced by folic acid, we analyzed the kidney transcriptomic after 24 hours of damage. In this database we evaluated if 625 genes described as responsible for hereditary nephropathies were expressed significantly. Later, we evaluated the correlation between diferentially expressed genes and glomerular filtration, using transcriptomic databases of human nephropathies (Nephroseq), so that, we could identify those relevant in acquired human nephropathies and in experimental settings. A functional enrichment analysis was done using the software Gorilla, and some of the genes were validated in our laboratory using RT-PCR.
 
 
 
 In acute kidney disease, the renal expression of 3906/25051 (15.59%) genes increased and the expression of 3537 (14.11%) decreased significantly (p<0.05). The percentage of genes expressed diferentially was higher when analysing the 625 genes responsible of familiar nephropathies. We identified 615 of those in the murine model and 105/615 (17.07%) increased it expression, and 155 (25.20%), decreased it (p<0.05 when compared with the database with 25051 genes). 241 of those 260 diferentially expressed genes (92.69%) where associated significantly with glomerular filtration rate in human nephropathies. The most enriched GO process were “complement activation", "protein activation cascade", "activation of immune response" and "RNA processing”. We have validated the expression of 7 of the genes in acute kidney injury (SLC34A1, SLC34A3, Klotho, MAGED2, NLRP3, FN1, COL4A1), which supports the relevance of the transcriptomic results.
 
 
 
 Genes involved in familiar nephropathies are overexpressed between genes diferentially expressed in acquired nephropathies, suggesting that they could play a role in the pathogenesis of the last, throught the regulation of the RNA processing, protein activation or immune response and complement regulation. The analysis of the functioning of genes responsible for familiar nephropathies in acquired nephropaties could identify new therapeutic targets in kidney damage.
