IgA Nephropathy In Patients With Renal Tissue And Urine Expression And Significance In CTGF

Background: IgA nephropathy is the world's most common glomerulonephritis in primary glomerulonephritis in China accounted for 20% -30%, the most typical pathological changes are focal or diffuse mesangium mesangial cells and mesangial matrix increase in tubulointerstitial lesions with focal tubular atrophy, inflammatory cell infiltration and interstitial fibrosis seen thus against renal fibrosis in the protection of renal function has become the focus of treatment [1]. Renal interstitial fibrosis is characterized by normal renal tubular structure and has been gathering a large number of extracellular matrix replaced by the tissue repair mechanism that is the dark side. A large number of studies have shown that renal interstitial fibrosis and renal function of the degree of correlation than the glomerular sclerosis and renal function is more closely related. Now widely recognized that TGF-βin the pathogenesis of renal fibrosis plays an important role in blocking TGF-βif the system is the prevention and treatment of renal fibrosis in the most effective way of hope. However, because TGF-βeffects in addition to promoting fibrosis, there are anti-inflammatory, anti-tumor and immune suppression, such as biological effects, it completely blocked the long-term may lead to out-of-control cell growth, immune disorders, inflammation and other serious side effects [2] . CTGF is the TGF-βactivity in the lower reaches of Desmoplastic media signal can be mediated by TGF-β-induced stimulation of cell proliferation and extracellular matrix (exctracellular matrix, ECM) formation, in the kidney plays an important role in fibrosis, and biological effects than a single, became the current Prevention of renal fibrosis research a new hot spot, but also for the treatment of IgA nephropathy will provide new ideas, and this paper used for the first time urinary CTGF detection to determine the IgA nephropathy in the tubulointerstitial disease situation, a certain degree of innovation.Objective: To CTGF in the urine of patients with IgA nephropathy and renal tissue distribution of clinical treatment for IgA nephropathy to provide a scientific basis.Methods: January 2008 to July, our patient collected 56 cases of primary IgA nephropathy urine specimens, urine specimens remission in urinary protein negative (2 weeks, 3 times the normal urine) collected. Detection of CTGF in urine by enzyme-linked immunosorbent assay (ELISA) and renal biopsy of renal collecting tissue samples, using immunohistochemical method of detection of renal expression of CTGFResults: The patient group compared with the control group, urine levels of CTGF expression in the control group (P <0.01), after treatment in patients with urine levels of CTGF expression significantly decreased (P <0.05). 2, a different degree of tubulointerstitial lesions comparison group, I -class, II grade, III level in urine of patients with renal CTGF expression in patients with an average of more than 0, the difference was significant (P <0.01), 0 level , I -class, II grade, III grade comparison group were 22 differences (P <0.05), 3, Spearman correlation analysis showed that, IgA nephropathy in patients with the expression level of CTGF in renal tissue and urine levels of CTGF expression in renal tubulointerstitial lesions with increase the level of increase. 4. 3 months hormone therapy is not in complete remission in patients with urinary levels of CTGF expression to reduce to a lesser extent.Conclusion: CTGF in IgA nephropathy in patients with tubulointerstitial disease mechanisms play an important role, testing the urine of renal tissue and urine levels of CTGF expression in patients with IgA nephropathy, treatment response, prognosis and pathological diagnosis, Detection of urinary CTGF for IgA nephropathy Clinical pathology reference classification.