Objective To analyze clinical and pathological data of IgA nephrology patients with microalbuminuria and investigate risk factors of its prognosis.Methods Clinical and pathological data of IgA nephrology patients with microalbuminuria were confirmed with renal biopsy and follow-up time with ＞ 6 months of trace was reviewed retrospectively;24-hour urine protein quantification ＞ 1 g, normal serum creatinine level when renal biopsy turned into abnormal level, or doubled serum creatinine level was defined as end point of follow-up.Renal survival was calculated with Kaplan-Meier survival analysis, and risk factors of progression were analyzed with univariate and multivariate Cox regression models.Results A total of 96 patients was followed up successfully, with an average follow-up time of (35.6 ± 22.7) months, and 34 cases (35.42％) entered the endpoint.The 12-, 24-, 36-, 48-, 60-, and 72-month renal survival rate was 97.92％, 92.71％, 86.45％ , 81.25％ , 71.88％, and 64.58％, respectively.Urine proteins, abnormal serum creatinine, Lee's Ⅲ～ V, renal interstitial fibrosis, glomerular sclerosis, and crescentic body were independent risk factors to affect prognosis of IgA nephropathy with microalbuminuria.Conclusions Early and active control of urinary microalbumin, and acute kidney injury caused by treatment of crescentic formation could slow the progress of IgA nephropathy.

Objective To analyze the clinical and pathological data and prognosis of microalbuminuria IgA nephrology patients with decreased serum C3 level, and investigate the significance of decreased serum C3 level in microalbuminuria IgA nephrology patients. Methods Clinical and pathological data of microalbuminuria IgA nephrology patients confirmed by renal biopsy and followed up more than 6 months were reviewed. The patients were divided into decreased serum C3 level group (34 cases, 25.19%) and normal serum C3 level group (101 cases, 74.81%) according to the serum C3 level. Twenty-four hours urine protein quantitative > 1 g, or normal serum creatinine level turning into abnormal level at renal biopsy, or doubling of serum creatinine level was defined as the end point of follow-up. Renal survival was calculated by Kaplan-Meier survival analysis and risk factors of progression were analyzed by Cox regression models. Results Total of 135 microalbuminuria IgA nephrology patients were followed up successfully, with an average follow-up time (53.4 ± 21.9) months. There were 27 cases (79.41%) and 32 cases (31.68%) in the decreased serum C3 level group and the normal serum C3 level group respectively at the endpoint. Kaplan-Meier survival analysis showed that the median survival time was significantly shorter in decreased serum C3 level group compared with that in normal C3 level group: (46.7 ± 9.1) months vs. (68.4 ± 9.9) months, P =0.014. Cox regression analysis showed that abnormal serum creatinine (RR = 1.147, 95% CI: 1.129-1.395, P = 0.008), decreased serum C3 level (RR=1.028, 95%CI:0.672-1.495, P=0.039), urine protein quantitative>1 g/24 h (RR=2.066, 95%CI:1.242-3.838, P=0.006) and renal biopsy pathological indicators Lee classⅢ-Ⅴ(RR=2.820, 95%CI:1.249-5.638, P=0.041), glomerular sclerosis or adhesions (RR=1.232, 95%CI: 1.065-1.520, P = 0.040), renal interstitial atrophy or interstitial fibrosis (RR = 2.604, 95% CI:1.748- 4.104, P = 0.037), endocapillary cell proliferation (RR = 0.872, 95% CI: 0.491- 1.275, P =0.042), crescentic (RR = 1.528, 95% CI: 1.073- 2.385, P = 0.009) affected prognosis of microalbuminuria IgA nephropathy as the independent risk factors. Conclusions The clinical and pathological features in patients of microalbuminuria IgA nephropathy with decreased serum C3 level is more severe, and the prognosis is poor. The patients should be followed up closely and early intervention treatment and early active control of microalbuminuria should be done at the same time.

Objective:To investigate the changes of serum micro ribonucleic acid-155 (miR-155) and suppressor of cytokine signaling-1 (SOCS-1) levels in patients with IgA nephropathy and their relationship with renal interstitial fibrosis.Methods:A total of 365 patients with primary IgA nephropathy admitted to Jining First People′s Hospital from January 2009 to June 2018 were selected as the research objects. According to the degree of renal interstitial fibrosis, the patients were divided into T0 group (139 cases), T1 group (124 cases) and T2 group (102 cases). In addition, 361 healthy subjects who had physical examination in our hospital in the same period were selected as the healthy control group. Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression level of miR-155 in serum of all the subjects; the levels of serum SOCS-1, transforming growth factor-β1 (TGF-β1) and monocyte chemoattractant protein-1 (MCP-1) were detected by enzyme-linked immunosorbent assay (ELISA). Logistic regression model was used to analyze the influencing factors of renal interstitial fibrosis in patients with IgA nephropathy; Pearson method was used to analyze the correlation between serum miR-155, SOCS-1 levels and influencing factors of renal interstitial fibrosis, TGF-β1 and MCP-1; receiver operating characteristic (ROC) curve was used to analyze the predictive value of serum miR-155 and SOCS-1 levels in patients with IgA nephropathy.Results:The levels of systolic blood pressure (SBP), diastolic blood pressure (DBP), 24 h urine protein, serum creatinine, serum uric acid, miR-155, TGF-β1, MCP-1, urinary retinol binding protein (RBP) and acetyl β D-glucosaminidase (NAG) in healthy control group, T0 group, T1 group and T2 group were significantly increased in turn, while the levels of hemoglobin, estimated glomerular filtration rate (eGFR), urinary osmotic pressure and serum SOCS-1 were significantly decreased in turn (all P<0.05). High SBP, high DBP, low hemoglobin, high serum creatinine, high uric acid, high 24-hour urine protein and low eGFR level were independent risk factors of renal interstitial fibrosis in patients with IgA nephropathy (all P<0.05). The serum miR-155 level was positively correlated with TGF-β1, MCP-1, SBP, DBP, serum creatinine, serum uric acid levels and 24 h urine protein, but negatively correlated with SOCS-1, hemoglobin and eGFR levels (all P<0.05). The serum SOCS-1 level was negatively correlated with TGF-β1, MCP-1, SBP, DBP, serum creatinine, uric acid levels and 24 h urine protein, but positively correlated with hemoglobin and eGFR levels (all P<0.05). The area under the curve of predicting the occurrence of renal interstitial fibrosis in patients with IgA nephropathy by serum miR-155 and SOCS-1 combined detection was 0.882, which was significantly larger than that by serum miR-155 and SOCS-1 alone ( P<0.05). Conclusions:The expression of miR-155 is up-regulated and SOCS-1 is down-regulated in IgA nephropathy patients, they may be used as predictors to evaluate the occurrence of renal interstitial fibrosis.