Kidney diseases are among the fastest worldwide growing pathologies. This growth together with their high mortality rate emphasizes the importance of generating vital information about the mechanism involved in their pathophysiology to determine possible therapeutic targets. Recently, mitochondrial damage and their implication in the reactive oxygen spices (ROS) signaling and redox homeostasis have emerged as a hub point in the pathologic mechanism involved in renal pathologies. ROS in low levels are necessary to maintain cell processes as well as the mitochondria homeostasis and its association with other organelles, especially the with the endoplasmic reticulum (ER). However, the information about how redox signaling interacts and interferes with other cellular processes and the mechanism involved has not been fully integrated. Furthermore, in higher concentrations, these ROS promotes pathologic pathways linked to renal disease progression like, mitochondrial biogenesis reduction, ER stress, calcium overload, inflammation, cell death and fibrosis. Therefore, the aim of this review is to describe the molecular mechanisms involved in the redox signaling influence on mitochondrial and ER homeostasis, focusing on lipid metabolism and ß-oxidation, mitochondrial biogenesis, inflammations, ER stress and calcium homeostasis, as well as the effects of these alteration in the genesis and development of renal disease, with emphasis in acute kidney injury (AKI) and chronic kidney disease (CKD).