Abstract
Minimal change disease constitutes a major cause of nephrotic syndrome. It is regarded as a non-immune-complex mediated primary glomerulopathy and pathogenetically is characterised by podocyte injury and effacement of foot processes; therefore, it is also classified as a type of podocytopathy. T cell dysfunction with increased levels of a soluble glomerular permeability factor has been proposed to play a major role in the pathogenesis of minimal change disease. It has been therefore suggested that a dysfunction of regulatory T cells, the orchestrators of immune homeostasis, could be implicated in perpetuating T cell activation in this condition. However, the actual contribution of regulatory T cell dysfunction in the immunopathogenesis of primary minimal change disease is still largely unclear. We here propose a theoretical model based on the available evidence.
Highlights
The glomerulus is the functional unit of the kidney responsible for blood filtration, which is the first step in blood purification and the production of urine
T cell dysfunction along with the presence of a circulating glomerular permeability factor (GPF) is long held to be the main factor implicated in triggering podocyte injury in primary minimal change disease (MCD) [2]
Given the likely involvement of a GPF, a putative cytokine in the pathogenesis of MCD [30, 31], and the many recent studies demonstrating an imbalance between Treg cells and their counterparts, the Th17 cells in MCD patients (Table 1), we believe that Foxp3+ Treg cells could plausibly play a part in the pathogenetic mechanisms of proteinuria in this primary podocytopathy
Summary
The glomerulus is the functional unit of the kidney responsible for blood filtration, which is the first step in blood purification and the production of urine. Normal functioning of the glomerulus requires the integrity of all three major components of the glomerular filtration barrier, that is, endothelial cells, glomerular basement membrane (GBM), and the visceral epithelial cells or podocytes. Many glomerular disease processes cause damage and subsequent disruption to the glomerular filtration barrier, eventually leading to pathological glomerular permeability to proteins. Light microscopy in MCD typically reveals very minor changes such as podocyte enlargement or ectatic capillary loops (Figure 1). Since podocyte injury is the central mechanism in its pathogenesis, MCD has been classified, along with other forms of glomerular disease, as a podocytopathy [1]. T cell dysfunction along with the presence of a circulating glomerular permeability factor (GPF) is long held to be the main factor implicated in triggering podocyte injury in primary MCD [2]. We discuss the potential role of T cells, in particular Treg cells, in the immunopathogenesis of MCD, and propose a pathophysiologic model with Treg cells participating in different stages of the disease process
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