Glomerular Diseases

Dear Colleagues,

Glomerular diseases represent a set of renal disorders which are associated with immune-mediated damage to the capillary endothelium, mesangium, or basement membrane. Patients with glomerular diseases present with diverse clinical characteristics ranging from asymptomatic microscopic or gross hematuria and/or proteinuria to massive proteinuria and nephrotic syndrome. Glomerular diseases contribute to the burden of end-stage kidney disease, leading to dialysis and kidney transplantation with tremendous financial and medical problems.

The etiology of most glomerular diseases remains largely undefined, but in many occasions, it is believed to be initiated by environmental insults, particularly infectious processes, that trigger host responses in genetically susceptible individuals, which leads to glomerular injury. Previous mechanistic concepts of these diseases included glomerular trapping of preformed immune complexes while the current view pertains to the idea that most of these diseases are autoimmune in nature mediated by both antibodies and T cells reactive with self-antigens. A typical paradigm of direct immune‐mediated glomerular disease, which comes as a consequence of autoantibodies directed against a constituent renal antigen, is anti‐glomerular basement membrane disease. Yet, indirect immune‐mediated glomerular disease often follows systemic autoimmunity with immune complex formation, or due to unrestrained activation of the complement pathways. Although the range of mechanisms of immune dysregulation leading to glomerular disorders is wide, the pathways leading to damage are similar. Loss of immune homeostasis in the kidney results in perpetual immune cell recruitment and occasionally irreversible renal injury. Uncoordinated attempts at tissue repair, after immune‐mediated disease, result in fibrosis of the glomeruli and the surrounding tissues and eventually to kidney failure. As glomerular disease often manifests clinically only when substantial damage has already occurred, new diagnostic methods are needed for prompt diagnosis and targeted therapies to inhibit progression and promote appropriate tissue repair.

In this Special issue of Life, we aim to present clinical and pathogenetic data and therapeutical advances regarding post-infectious glomerulonephritis, IgA nephropathy, anti-glomerular basement membrane antibody disease, ANCA-associated vasculitis, lupus nephritis, complement-related glomerular diseases as well as minimal change disease, focal segmental glomerulosclerosis, and membranous nephropathy.

Dr. Sophia Lionaki
Dr. Smaragdi Marinaki
Guest Editors

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• glomerular disease
• pathogenesis
• management
• outcome