Podocyte and endothelial cell injury develop nephrotic syndrome in proliferative lupus nephritis

Abstract

Aims

Nephrotic syndrome (NS) is a major manifestation of lupus nephritis (LN). The dysregulation of podocyte, glomerular basement membrane (GBM) and endothelial cell (EC) develops proteinuria in glomerular diseases. The aim of our study is to clarify whether the dysregulation of these barriers is associated with NS in proliferative LN and membranous LN.

Methods and results

Fifty six patients with NS including minimal change NS in 15, primary membranous nephropathy (PMN) in 13, Class III/IV LN in 15 and Class V LN in 13 were enrolled in this study. Subjects with idiopathic hematuria were assigned as controls. Glomerular expression of Wilms tumor protein 1 (WT1), nephrin, synaptopodin and podocalyxin was evaluated by immunohistochemistry (IHC) and quantitative RT-PCR. EC injury was evaluated by CD31 immunostaining and electron microscopy (EM). Reduced expression of WT1, nephrin, synaptopodin was found in PMN, Class III/IV and Class V LN by IHC and mRNA analysis compared with controls. Reduced expression of these molecules was not different between Class III/IV LN and Class V LN. Reduced CD31 positive EC was found in Class III/IV LN compared to Class V LN. The EC injury showing subendothelial widening on EM was apparent in Class III/IV LN compared to Class V LN. Foot process effacement was found only along the GBM showing EC injury in Class III/IV LN.

Conclusions

Our study first suggests that coexistence of podocyte and EC injury may lead to NS in proliferative LN. Podocytes damage alone leads to NS in membranous LN.

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