Enfermedad renal crónica en pediatría y nuevos marcadores moleculares

chronic renal failure (crf) is associated in the mid and long-term to severe complications. new therapies have been introduced in the last decades, however some disturbances as growth failure, mineral metabolism, and anemia, among others, still remain unresolved, and long-term cardiovascular morbimortality remains unacceptable high. in recent years, new molecular markers have been introduced as promising tools in the prevention and management of uremic disturbances. fibroblast growth factor23 (fgf23), klotho, hepcidin and growth hormone (gh) intracellular signaling are discussed in this article. fgf23, acting through klotho protein, increases the rate of urinary excretion of phosphate and inhibits renal production of 1,25-dihydroxy-vitamin d, as an important regulator of mineral metabolism. hepcidin inhibits intestinal iron absorption and iron release from macrophages and hepatocytes; its production is increased by inflammation and high hepcidin plasma levels limit iron availability for erythropoiesis, playing a major role in the anemia and rhepo resistance in these patients. in the field of growth, phosphorylation of jak2 and the downstream gh signaling molecules stat5, stat3 and stat 1 are impaired, leading to decreased igf-1 dna gene transduction. suppressed gh signaling cause up-regulation of socs2 and socs3 expression and increased tyrosine phosphatase activity contributing to enhance dephosporylation and deactivation of the signaling proteins. the knowledge of the role of these factors in normal physiology will be a central key in the management of uremic patients in the future.