Objective To explore the effect of serum uric acid (SUA) on the clinicopathological manifestation and prognosis of IgA nephropathy(IgAN)patients. Methods A total of 348 patients with renal biopsy-proven IgAN in our hospital were enrolled in this study.The data were retrospectively analyzed to examine the association of SUA level with clinicopathological manifestation and prognosis of IgA nephropathy(IgAN)patients. Results There were no significant differences of 24 hour proteinuria,BUN and Scr between patients of high SUA level with various GFR and those of normal SUA level.While differences of glomerular sclerosis,tubulointerstitial scores and vascular injury between these two groups were significant (P＜0.05).At the end of follow-up,prevalence of GFR decline and ESRD was significantly higher in patients with high SUA as compared to those with normal SUA(40.82%vs 15.70%,64.71% vs 35.00%,respectively,P＜0.05). Conclusions Patients with different SUA levels have similar clinical manifestations,but different pathological findings and prognosis.It is important to pay attention to the follow-up of SUA level in IgAN patients.

Objective To investigate the effects of rosiglitazone on the expression of peroxisome proliferator-activated receptor-γ (PPARγ) and matrix metalloproteinase-9 (MMP-9) in renal interstitial fibroblasts induced by cyclosporine A, and discuss renal protective effect of rosiglitazone on renal toxicity of cyclosporine A. Methods Construction, screening and amplification of the target siRNA vector for PPARγ were carried out.The inhibitory effect of siRNA on the expression of PPARγ in normal rat kidney (NRK) cells was evaluated.NRK cells were cultured in the routine way.Experimental groups: (1)control group:single NRK cells without treatment; (2)RGZ group:NRK cells with RGZ (10 μmol/L); (3)CsA group:NRK cells with CsA (1.0 mg/L); (4)CsA+RGZ group:NRK cells with CsA (1.0 mg/L) plus RGZ (10 μ mol/L); (5)CsA+RGZ+siRNA group:pRNAT-U6.2/Lenti-PPARγ-236 plasmid transfected into NRK cells,then CsA (1.0 mg/L) plus RGZ (10 μmol/L).The mRNA expression of PPARγ was detected by real-time RCR.The mRNA expressions of MMP-9 and TIMP-1 were detected by RT-RCR.The protein expression of FN was detected by Western blotting. Results CsA up-regulated the mRNA level of PPARγ,MMP-9 and TIMP-1 (P＜0.05),and the up-regulation was inhibited by RGZ significantly (P＜0.05).The application of PPARγ siRNA resulted in the decreasing of PPARγ mRNA (P＜0.05),and partly reversed the inhibition effect of RGZ on MMP-9 and TIMP-1 mRNA (all P＜0.05).CsA up-regulated the protein level of FN (P＜0.05),and this effect was significantly inhibited by RGZ (P＜0.05).The application of PPARγ siRNA could reverse the inhibition effect of RGZ on FN protein expression (P＜0.05). Conclusion RGZ can inhibit the expressions of FN,MMP-9 and TIMP-1 induced by CsA which may be the mechanism of the protective effect of RGZ on renal interstitial fibrosis induced by CsA.

Objective To investigate the protective effects of fluvastatin(Flu) on rat renal fibroblasts proliferation and cytokines expression induced by cyclosperine A (CsA). Methods The fibroblasts were cultured with CsA or with CsA plus fluvastatin. The cellular proliferation was determined by MTT colorimetry. The mRNA expression of transforming growth factor β1(TGF-[β1), connetive tissue growth factor (CTGF) and c-fos was detected by BT-RCB. The protein level of flbronecfin (FN) was measured by Western blotting. Results CsA inhibited the proliferation of fibroblasts in dose- and time-dependent manner (P＜0.05). Treatment with Flu accelerated the suppression of fibroblasts resulted from CsA (P＜0.O1). CsA stimulated the expression of TGF-β1, CTGF, c-fos and FN compared with control group(P＜0.05), which could be down-regulated by Flu (P＜0.05). Conclusion Fluvastatin may relieve CsA-induced nephrotoxicity in rat fibroblasts.

Objective To investigate the effect of rosiglitazone on renal interstitial fibrosis in chronic cyclosporine nephropathy (CCN) rats.Methods Twenty-eight rats were randomly assigned to control group,rosiglitazone (RGZ,5 mg·kg-1·d-1) group,cyclosporine A(CsA,15 mg·kg-1·d-1) group,rosiglitazone (5 mg·kg-1·d-1) +CsA group.Real-time PCR and RT-PCR methods were used to investigate the expressions of OPN,RANTES on the 14th day and MMP-9,TIMP-1 on the 35th day in kidney of CCN respectively.Results In comparison with control group,the expressions of OPN,RANTES,MMP-9,TIMP-1 in CsA and RGZ+CsA groups were increased (P＜0.05).In comparison with the CsA group,the expressions of OPN,RANTES,MMP-9,TIMP-1 in CsA+RGZ group significantly decreased (P＜0.05).Conclusion Rosiglitazone may protect renal tissue after CCN by decreasing expressions of OPN,RANTES,MMP-9,TIPM-1.

Objective To investigate the effect of rosiglitazone on the expr es sion of PPAR?,TGF-a1 and PCNA and its mechanism on renal interstitial fibrosi s following unilateral ureteral obstruction(UUO) in rat kidney. Methods Thirty r ats were randomly assigned to shame operation group(sham group),UUO group, rosig litazone(5 mg穔g-1?d-1) treatment group after UUO. Immunohistochemistry,RT-PCR,Western blotting were performed to investigate renal pathological changes an d examine the expression of PPAR?,TGF-a1,PCNA on the 7th and 14th day in the kidney. Results In comparison with the shame group,the expression of PPAR?,TGF-a1,PCNA of UUO and treatment groups increased significantly(P

Objective To investigate the protective effects of rosiglitazone (RSG) on normal rat kidney cells (NRK) damaged by cyclosporine A(CsA). Methods The NRK cells were cultured with CsA or with CsA plus rosiglitazone. The cellular proliferation was determined by MTT colorimetry. The mRNA expression of TGF-?1 and PPAR? was detected by RT-RCR. Protein levels of PPAR?, p-ERK,FN and AT1R were examined by Western blotting. The level of TGF-?1 in the supernatants was measured by enzyme-linked immunosorbant assay (ELISA). Results CsA inhibited the proliferation of NRK cells in dose and time dependent manner (P

Diabetic nephropathy is a complication of diabete and its incidence is increasing obviously these years. The pathogenic mechanisms of DN are complex, with multiple factors involved such as the glycometabolism disorders , hemodynamic changes, aldose reductase pathway activation, alterations in cytokines, oxidative stress, protein kinase C activation, lipid metabolism disorders and genetic susceptibility etc, which are not completely clear yet. Thus, the research progress of DN pathogenesis is to be reviewed.

Objective To investigate the mechanism of renal protective effect of rosiglitazone on diabetic rat kidney. Methods Eighteen rats were assigned to normal control(C) group,diabetic rat(DM) group, rosiglitazone(5 mg?kg-1?d-1)treatment(R) group.Immunohistochemistry,RT PCR,Western blot were used to examine the pathological change of kidney and expression of PPAR?、TGF ?1 after 8 weeks in the kidney of rats. Results In comparison with normal group, the expression of PPAR?and TGF ?1 in diabetic rat and treatment groups was markedly increased(P

Objective To investigate the efficacy and feasibility of combination of leflunomide and clopi-dogrel in the treatment of IgA nephropathy. Methods 84 patients with primary IgA nephropathy were randomly divided into four groups: Control group (group 1) received valsartan; test group (group 2) received valsartan +clopidogrel; group 3 received valsartan + leflunomide; group 4 received valsartan + clopidogrel + leflunomide. The level of 24 h urinary protein,serum creatinine, glomerular filtration rate and therapeutic efficacy, adverse reactions were detected and recorded during the 48 weeks follow-up. Results The 24 h urinary protein of 84 patients showed a downward trend during the course of treatment , but there were statistical differences between groups since 8 weeks after treatment (P < 0.05). The level of urine protein in group 3 and group 4 decreased significantly to 61.48% and 67.23% respectively in 48 weeks after treatment. At the end of the follow up , the serum creatinine levels in group 1 and group 2 significantly increased while the glomerular filtration rate de-creased obviously (P < 0.05). Conclusion The combination of leflunomide with clopidogrel could reduce the level of urinary proteins and slow renal function deterioration in the treatment of IgA nephropathy with less ad-verse reactions. This study provides a new idea for treatment of IgA nephropathy.