Abstract
Background Podocyte injury probably plays important roles in the pathogenesis of IgA nephropathy (IgAN). We studied intra-renal and urinary messenger RNA (mRNA) expression of podocyte-associated molecules in patients with IgAN. Methods We studied 43 consecutive patients with biopsy-proven IgAN. Intra-renal and urinary expression of mRNAs was determined and compared to that of 20 patients with nephrectomy for kidney cancer and 12 normal subjects. Results Intra-renal mRNA expression levels of nephrin, podocin and synaptopodin were significantly lower in patients with IgAN than that of controls. In contrast, their urinary mRNA expression levels were similar. Intra-renal gene expression of nephrin inversely correlated with proteinuria (r = –0.620, P < 0.001), GFR (r = 0.538, P < 0.001), and the degree of tubulointerstitial scarring (r = –0.423, P = 0.013). After followed for an average of 33.4 ? 12.6 months, intra-renal nephrin expression significantly correlated with the rate of GFR decline (r = 0.324, P = 0.041). Conclusions Intra-renal mRNA expression of podocyte associated molecules was down-regulated in patients with IgAN, and the degree of down- regulation of nephrin correlated with disease severity and the rate of progression. Our result supports the hypothesis that podocyte injury is an important component in the pathophysiology of IgAN.
Highlights
Immunoglobulin A nephropathy (IgAN) is the most common form of primary glomerulonephritis throughout the world, and a good portion of patients with biopsy-provenIgA nephropathy (IgAN) progresses to ESRD in 10 to 20 years [1,2,3]
Intra-renal messenger RNA (mRNA) expression of podocyte associated molecules was down-regulated in patients with IgAN, and the degree of downregulation of nephrin correlated with disease severity and the rate of progression
Our result supports the hypothesis that podocyte injury is an important component in the pathophysiology of IgAN
Summary
Immunoglobulin A nephropathy (IgAN) is the most common form of primary glomerulonephritis throughout the world, and a good portion of patients with biopsy-proven. The most prominent pathological changes of IgAN are deposition of pathogenic polymeric IgA1 in the mesangium, proliferation of mesangial cells, excessive synthesis of extracellular matrix (ECM), and infiltration of inflammatory cells. Podocyte injury might provide additional prognostic information in patients with IgAN [5]. It has been shown that Bcl-2 expression by podocytes exerts modulatory effects on cellular processes that contribute to progressive glomerular injury of IgAN [6], while humoral factors released from mesangial cells may alter glomerular permeability by reducing the expression of podocyte markers [7]. We explore the intra-renal and urinary messenger RNA (mRNA) expression of podocyte-associated molecules in patients with IgA nephropathy
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