Abstract
Systemic lupus erythematosus (SLE) is characterized by a broad spectrum of renal lesions. In lupus glomerulonephritis, histological classifications are based on immune-complex (IC) deposits and hypercellularity lesions (mesangial and/or endocapillary) in the glomeruli. However, there is compelling evidence to suggest that glomerular epithelial cells, and podocytes in particular, are also involved in glomerular injury in patients with SLE. Podocytes now appear to be not only subject to collateral damage due to glomerular capillary lesions secondary to IC and inflammatory processes, but they are also a potential direct target in lupus nephritis. Improvements in our understanding of podocyte injury could improve the classification of lupus glomerulonephritis. Indeed, podocyte injury may be prominent in two major presentations: lupus podocytopathy and glomerular crescent formation, in which glomerular parietal epithelial cells play also a key role. We review here the contribution of podocyte impairment to different presentations of lupus nephritis, focusing on the podocyte signaling pathways involved in these lesions.
Highlights
Systemic lupus erythematosus (SLE) is a chronic immune complex-mediated disease characterized by disseminated inflammation that may affect multiple organs
We found that C-maf-inducing protein (CMIP) was overexpressed in non-proliferative Lupus nephritis (LN), but it was almost undetectable in patients with class III/IV LN
Its expression seems to be related to IC-mediated glomerulonephritis, as observed in LN, and is only very weakly expressed in renal biopsy specimens from patients diagnosed with minimal change disease (MCD), a glomerular disease characterized by the absence of kidney parenchymal inflammation [44,45], suggesting a possible link between ubiquitin C-terminal hydrolase-L1 (UCH-L1) and IC-related mechanisms of injury
Summary
Systemic lupus erythematosus (SLE) is a chronic immune complex-mediated disease characterized by disseminated inflammation that may affect multiple organs. Light microscopy: normal glomeruli/isolated mesangial hypercellularity/focal and segmental glomerulosclerosis (FSGS) Immunofluorescence: no subendothelial or subepithelial deposits, but possible mesangial deposits Electron microscopy: extensive foot process effacement (FPE). Abnormal adaptive and innate immune responses induce the release of inflammatory mediators, such as interferon-α, which amplify glomerular lesions [5,6] These processes take place in glomeruli and may account for the various clinical, biological, and histological features of renal disease. Podocytes are highly differentiated epithelial cells anchored to the basement membrane through foot process extensions, which interact with those of adjacent podocytes to form the slit diaphragm, the ultimate filtration barrier This slit diaphragm is a unique cellular junction formed from podocyte-specific proteins, such as nephrin and podocin, which interact with the actin cytoskeleton [8]. We review here the involvement of podocyte injury in the different classes of LN, highlighting the key role of these cells regardless of the initial immune trigger of disease
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