Chronic kidney disease (CKD), independently of its etiology, is a major public health problem. This disease is characterized by a persistent inflammation, leading to fibrosis and loss of renal function. During renal inflammation, resident cells can produce a large array of inflammatory mediators, such as cytokines and adhesion molecules and also induce the activation of the complement system to contribute to the recruitment of leukocytes into the kidney. The activation of these responses occurs through a wide and complex axis of signalling pathways inducing the infiltration of inflammatory cells and the differentiation/proliferation of myofibroblasts. These processes contribute to the chronification of the inflammatory process and, ultimately, to fibrosis.

Nowadays, the therapeutic protocols applied for CKD treatment have limited effectiveness underscoring the importance of the development of new molecular diagnostic approaches and therapeutic targets to either prevent or delay the progression of the renal diseases. We invite the original research as well as review articles that will help to understand the inflammatory and profibrotic mechanisms that regulate key processes in the renal pathology and new therapeutic strategies for the treatment and prevention of CKD.

Potential topics include but are not limited to the following:

• Immune response associated to Inflammation in renal pathology
• Inflammatory and profibrotic regulators as potential therapeutic targets
• Inflammation and fibrotic process and downstream signalling during the CKD and acute kidney disease
• The tipping point between inflammation and fibrosis in CKD
• In vitro and in vivo models to study the inflammatory and fibrotic mechanisms of Kidney diseases
• Breakthrough advancements in the current understanding of the role of inflammation and fibrosis in renal diseases