Endoglin, a transforming growth factor-beta-binding protein, is upregulated in chronic progressive renal disease

Endoglin is a non-signalling receptor for TGF-beta. In view of the importance of transforming growth factor-beta (TGF-beta) in the pathogenesis of renal disease, we have determined the distribution of TGF-beta in human glomerulonephritis. Endoglin was present within the glomerular mesangium and interstitium in normal kidneys. In diseased biopsies, there was a weak but significant correlation between staining for endoglin in the interstitium and the extent of chronic histological damage (r = 0.3343, p = 0.003). This was supported by division of biopsies into those showing mild damage and those with moderate to severe damage, where the latter group had significantly increased interstitial staining for endoglin (p = 0.0035). However, there was no correlation between mesangial staining for endoglin and specific types of glomerular pathology, such as IgA nephropathy, suggesting that the interstitial expression of endoglin is associated with increased renal damage independent of the specific type of glomerular lesion which initiates the process. There was also a positive correlation between mesangial cell staining for endoglin and interstitial endoglin expression (r = 0.3104, p = 0.003), although the former was not independently associated with chronic histological damage. These data suggest that the response of interstitial fibroblasts and mesangial cells may be linked in glomerulonephritis. Both could contribute to renal scarring by increased binding of TGF-beta which would be independent of the type of initial glomerular damage.