Chronic kidney disease is a major public health problem affecting more than 10% of the population in Western countries, with a continuous increase in its incidence that also entails higher cardiovascular morbidity and mortality of our patients. Identification of more sensitive and specific biomarkers is urgently needed for early diagnosis and evaluation of the nature, severity, and rate of progression of kidney disease. Also, a better understanding of the pathophysiological pathways involved is essential to help us in a better therapeutic approach.
The pathophysiology associated with kidney damage is complex and different factors are involved, such as genetic factors, but especially post-transcriptional mechanisms that lead to protein modifications, regardless of the genetic influences.
Within kidney damage, there are common pathways associated with inflammation, oxidation, or senescence processes and specific pathways for each renal disease. As numerous pathways are simultaneous and synergistically involved, a holistic multifaceted approach is needed. High-performance technologies have helped us to open new hypotheses about the pathophysiological pathways related to kidney damage. In addition, in recent years, the therapeutic options for the management of our patients have evolved, such as the sodium-glucose co-transporter 2 inhibitors or the Glucagon-like peptide-1 receptor agonists, which have drastically modified the prognostic of the renal disease and the cardiovascular risk of both patients with diabetic kidney disease and in patients without diabetes. However, we still do not know the precise mechanisms by which these and other treatments may be modifying the evolution of kidney disease.
With this Research Topic, we want to appeal to the scientific community interested in the study of the pathophysiological mechanisms underlying renal damage. We encourage studies that use cutting-edge omic to generate new hypotheses about renal pathogenesis and enlighten aspects evolving the kidney physiopathology.
With this aim, we welcome studies carried out both in experimental animals or in vitro, focused on the analysis of the pathophysiological pathways associated with kidney damage, as well as clinical studies address to elucidate alternative mechanisms of kidney damage in any of its stages, from the initial changes of systemic diseases such as diabetes or autoimmune diseases, as well as, aspects related to a patient undergoing renal replacement treatment such as kidney transplantation. Both, original articles and reviews will be considered, preferring systematic reviews.
Chronic kidney disease is a major public health problem affecting more than 10% of the population in Western countries, with a continuous increase in its incidence that also entails higher cardiovascular morbidity and mortality of our patients. Identification of more sensitive and specific biomarkers is urgently needed for early diagnosis and evaluation of the nature, severity, and rate of progression of kidney disease. Also, a better understanding of the pathophysiological pathways involved is essential to help us in a better therapeutic approach.
The pathophysiology associated with kidney damage is complex and different factors are involved, such as genetic factors, but especially post-transcriptional mechanisms that lead to protein modifications, regardless of the genetic influences.
Within kidney damage, there are common pathways associated with inflammation, oxidation, or senescence processes and specific pathways for each renal disease. As numerous pathways are simultaneous and synergistically involved, a holistic multifaceted approach is needed. High-performance technologies have helped us to open new hypotheses about the pathophysiological pathways related to kidney damage. In addition, in recent years, the therapeutic options for the management of our patients have evolved, such as the sodium-glucose co-transporter 2 inhibitors or the Glucagon-like peptide-1 receptor agonists, which have drastically modified the prognostic of the renal disease and the cardiovascular risk of both patients with diabetic kidney disease and in patients without diabetes. However, we still do not know the precise mechanisms by which these and other treatments may be modifying the evolution of kidney disease.
With this Research Topic, we want to appeal to the scientific community interested in the study of the pathophysiological mechanisms underlying renal damage. We encourage studies that use cutting-edge omic to generate new hypotheses about renal pathogenesis and enlighten aspects evolving the kidney physiopathology.
With this aim, we welcome studies carried out both in experimental animals or in vitro, focused on the analysis of the pathophysiological pathways associated with kidney damage, as well as clinical studies address to elucidate alternative mechanisms of kidney damage in any of its stages, from the initial changes of systemic diseases such as diabetes or autoimmune diseases, as well as, aspects related to a patient undergoing renal replacement treatment such as kidney transplantation. Both, original articles and reviews will be considered, preferring systematic reviews.
