Molecular Advances in Glomerular Diseases, 2nd Edition

Dear Colleagues,

This Special Issue is a continuation of our previous Special Issue, “Molecular Advances in Glomerular Diseases”.

Glomerular diseases are a heterogeneous group of inflammatory diseases that represent an important cause of chronic morbidity and may potentially progress to renal failure. Pathological features, specific mechanisms causing glomerular damage, and association with extra-renal conditions form the basis of a general classification that has clear clinical implications. Renal pathology ranges from minimal lesions to diffuse glomerular proliferation, thickening of the basement membrane, and alteration of the microvasculature. Circulating autoantibodies against intrinsic or implanted antigens are often involved as initiating mechanisms, and deposition of components of the complement cascade may represent a pathogenetic feature. Variable degrees of proteinuria, including nephrotic syndrome and hematuria, are the classical hallmarks that aggregate different conditions.

Recent advances in the pathogenesis of glomerular diseases are substantial and include the identification of new autoantibodies causative of primary and secondary forms (e.g., membranous nephropathy, lupus nephritis), the involvement of regulatory cells in inflammation, and additional mechanisms of direct damage. However, therapeutic approaches have not mirrored these advances and, for many years, have relied on the same drugs (steroids, CNI, mycophenolate mofetyl, anti-CD20).

Recognizing molecular factors will help identify potential therapeutic targets, which is of particular interest in an era when many new drugs targeting specific actors of inflammation—such as T/B cells, interleukins, and intracellular factors—have been developed and are already used successfully in other inflammatory conditions.

Dr. Gian Marco Ghiggeri
Guest Editor

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