Abstract
Diseases affecting the glomerulus are the most common cause of end-stage kidney disease in developed countries (1). These disorders are characterized by significant proteinuria, and the level of proteinuria is an independent risk factor for disease progression (2). Podocytes are thought to play a key role in the pathogenesis of glomerular diseases (3, 4). The importance of podocytes in glomerular diseases is highlighted by genetic studies, which have identified mutant podocyte proteins that cause familial forms of nephrosis (5). Because podocytes are terminally differentiated cells with little capacity for replication, their ability to compensate for podocyte loss is limited (3). A component of current therapy is, therefore, focused on reducing podocyte injury by decreasing systemic blood pressure (BP) and inhibition of the renin–angiotensin system (2, 6).
Highlights
Diseases affecting the glomerulus are the most common cause of end-stage kidney disease in developed countries [1]
The immune system was thought to play a significant role in non-genetic forms of nephrosis including acquired diseases such as minimalchange disease (MCD) and focal segmental glomerulosclerosis (FSGS) [7]
A seminal observation was that the actin-associated protein synaptopodin (SYN) was phosphorylated by either protein kinase A (PKA) or calcium/calmodulin-dependent protein kinase II (CaMKII)
Summary
Diseases affecting the glomerulus are the most common cause of end-stage kidney disease in developed countries [1]. The importance of podocytes in glomerular diseases is highlighted by genetic studies, which have identified mutant podocyte proteins that cause familial forms of nephrosis [5]. We acknowledge that these reports have significant limitations, the data support the concept that that steroids and/or CNIs may have beneficial effects unrelated to their immunosuppressive actions.
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