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Updated: Jul 11, 2025

Isolation of Glomeruli and In Vivo Labeling of Glomerular Cell Surface Proteins
Published on: January 18, 2019
Drug-induced glomerular diseases
Anne-Sophie Garnier1, Hélène Laubacher2, Marie Briet3
1Service de néphrologie-dialyse-transplantation, CHU d'Angers, 49000 Angers, France; UFR Santé, université d'Angers, 49000 Angers, France; Université d'Angers, UMR CNRS 6015, Inserm U1083, unité MitoVasc, Team Carme, SFR ICAT, 49000 Angers, France; Laboratoire MitoVasc, UMR Inserm 1083 CNRS 6215, 49000 Angers, France.
Abstract:
Drug-induced kidney diseases represent a wide range of diseases that are responsible for a significant proportion of all acute kidney injuries and chronic kidney diseases. In the present review, we focused on drug-induced glomerular diseases, more precisely podocytopathies - minimal change diseases (MCD), focal segmental glomerulosclerosis (FSGS) - and membranous nephropathies (MN), from a physiological and a pharmacological point of view. The glomerular filtration barrier is composed of podocytes that form foot processes tightly connected and directly in contact with the basal membrane and surrounding capillaries. The common clinical feature of these diseases is represented by the loss of the ability of the filtration barrier to retain large proteins, leading to massive proteinuria and nephrotic syndrome. Drugs such as non-steroidal anti-inflammatory drugs (NSAIDs), D-penicillamine, tiopronin, trace elements, bisphosphonate, and interferons have been historically associated with the occurrence of MCD, FSGS, and MN. In the last ten years, the development of new anti-cancer agents, including tyrosine kinase inhibitors and immune checkpoint inhibitors, and research into their renal adverse effects highlighted these issues and have improved our comprehension of these diseases.
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