Progress in the Mechanism of IgA Nephropathy Renal Injury

Si-Qi ZHANG, Rui-Si XU, Jian YIN


IgA nephropathy is the most common primary glomerular disease in the world,
accounting for about 25% ~50% of primary glomerular diseases [1]. Clinical IgA nephropathy occurs in young and middle-aged adults, and about 30-40% of patients enter the end-stage renal failure (ESRD) in 10-20 years[2], which brings a heavy burden to the country and society. IgA nephropathy pathogenesis is not clear at present, has long been a mesangial cells is considered to be major cell types of the disease, IgA nephropathy and recent study found that IgA nephropathy mesangial cells and sertoli cell and the interaction between the tubular epithelial cells, the common cause of kidney damage of IgA nephropathy [3-5]. 2009 international IgA nephropathy group proposed IgA nephropathy Oxford disease classification, it included four
indicators of clinical outcomes with independent predictive value, namely, mesangial matrix (M), segmental sclerosis (S), endothelial cell hyperplasia (E) and tubular atrophy and interstitial fibrosis (T) [6]. Has rainbow multicenter IgA nephropathy as verification of Oxford's pathological classification in China, M, S, T three pathological indexes closely related to long-term renal outcomes for patients with IgAN, but E no obvious correlation with long-term prognosis. Therefore, mesangial cells, foot cells and tubule epithelial cells play an important role in the development of IgA nephropathy. In this paper, combined with domestic and foreign literature on mesangial cells, sertoli cell and tubular epithelial cells of IgA nephropathy renal injury mechanism, to clarify to the pathogenesis of IgA nephropathy[7], and clinical diagnosis and treatment to provide new inspiration point and basis.


Si-Qi ZHANG1,a, Rui-Si XU2,b, Jian YIN3


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