Dear Colleagues,

This Special Issue, “Cellular and Molecular Mechanisms in Glomerulonephritis 2.0”, will collect a selection of recent research topics and current review articles related to the role of “Cellular and Molecular Mechanisms in Primary and Secondary Glomerulonephritis” in order to update the current knowledge in this field. Original papers, up-to-date review articles, and commentaries are all welcome.

Extensive progress has been made in the understanding of the mechanisms underpinning renal diseases, and advances in this field will open the road to new therapeutic targets and better diagnostic and treatment approaches.

Glomerulonephritis (GN) refers to a group of heterogeneous diseases arising from inflammatory processes or metabolic diseases that affect the kidney. As a consequence, they are initiated mostly by local glomerular abnormalities, including genetic disease, with frequent involvement of renal tubulo-interstitium.

To date, GN remains a leading cause of end-stage renal disease (ESRD) and accounts for about 20% of chronic kidney disease (CKD) cases in most countries in the world. However, this percentage underestimates the real incidence of GN because of the commonly asymptomatic GN phenotype, incidentally diagnosed by abnormal urinary findings. In fact, GN is considered a public health issue, and during the past three decades, the incidence and prevalence of ESRD have risen progressively. In terms of numbers, by 2030, it is expected that the annual number of people with new onset of ESRD will exceed 450,000, and those receiving dialysis or who have had kidney transplants will exceed 2 million. Thus, more effort in research is needed to understand the causes and pathophysiology of GN in order to ameliorate the diagnosis and identify new therapeutic approaches.

Prof. Dr. Elena Ranieri
Dr. Giuseppe Stefano Netti
Guest Editors

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