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Objective:To investigate the correlation between Piwi-interacting RNA (piRNA) and diabetic nephropathy (DN).Methods:The differential expression profiles of piRNAs in renal tissues of patients with DN (experimental group) and renal tissues adjacent to tumors of patients with renal tumors (control group) were detected by high-throughput sequencing. The biological function of differentially expressed piRNAs was described by gene ontology and Kyoto encyclopedia of genes and genomes enrichment analysis. Real-time fluorescence quantitative PCR was used to detect the serum expression level of target piRNAs in patients with DN. Spearman correlation analysis was used to analyze the correlation between serum target piRNAs and clinical indexes of patients with DN.Results:The results of high throughput sequencing showed that there were 127 differentially expressed piRNAs between DN group and control group, with screening condition of |log 2(fold changes)|≥2 and P<0.05. Among them, there were 99 up-regulated piRNAs and 28 down-regulated piRNAs. The top 5 up-regulated piRNAs were piRNA-hsa-161686, piRNA-hsa-349255, piRNA-hsa-355720, piRNA-hsa-151229 and piRNA-hsa-154959, respectively. The top 5 down-regulated piRNAs were piRNA-hsa-1929960, piRNA-hsa-174194, piRNA-hsa- 148658, piRNA-hsa-172594 and piRNA-hsa-172421, respectively. The PCR verification results of 3 up-regulated genes and 3 down-regulated genes with low P values and high expression levels showed that serum expression level of piRNA-hsa-77976 was significantly down-regulated in patients with DN ( P=0.028), which was consistent with that of sequencing, while the expression levels of other genes were inconsistent with the sequencing results or had no statistical significance. Bioinformatics analysis results predicted that significantly differentially expressed piRNAs might participate in the regulation of DN through Rap1, Ras, PI3K-Akt and axon guiding pathways. The results of correlation analysis showed that the expression level of piRNA-hsa-77976 was negatively correlated with blood urea nitrogen ( r=-0.584, P=0.028), serum creatinine ( r=-0.637, P=0.014), cystatin C ( r=-0.738, P=0.003) and β2 microglobulin ( r=-0.822, P<0.001), and positively correlated with estimated glomerular filtration rate ( r=0.661, P=0.010). Conclusion:The differential expression of piRNA is closely related to DN, and may be used as a new biomarker for the diagnosis and prognosis of DN.
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Objective@#To investigate the risk factors of clinically diagnosed acute kidney injury (AKI) patients progressing to acute kidney disease (AKD).@*Methods@#The clinical data of AKI patients admitted to the First Affiliated Hospital of Zhengzhou University from January 1, 2018 to December 31, 2018 were retrospectively analyzed. According to the outcome of the patients, AKI patients were divided into non-acute kidney disease (NAKD) group and AKD group. Clinical characteristics and laboratory data of two groups were compared. The risk factors of AKD in patients with AKI were analyzed by logistic regression, and then the receiver operating characteristic curve (ROC) was drawn to evaluate the predictive value of these risk factors.@*Results@#A total of 254 patients with AKI were enrolled, and 186 patients developed AKD with an incidence of 73.2%. The incidences of AKD in stage 1, stage 2 and stage 3 of AKI were 20.0%, 46.7% and 83.5% respectively. Multivariate logistic regression analysis showed increased peak serum creatinine (within 7 days after AKI diagnosis) (OR=2.561, 95% CI 1.584-4.140, P<0.001), proteinuria (OR=2.952, 95% CI 1.162-7.500, P=0.023) and increased intact parathyroid hormone (OR=1.757, 95%CI 1.104-2.797, P=0.017) were independent risk factors for progression to AKD in patients with AKI. The ROC showed that increased peak serum creatinine (within 7 days after AKI diagnosis) was an important predictor of AKD in patients with AKI (AUC=0.798, P<0.001).@*Conclusion@#Increased peak serum creatinine (within 7 days after AKI diagnosis), proteinuria and increased intact parathyroid hormone are independent risk factors for progression to AKD in patients with AKI, providing new evidences and ideas for clinical preventions and treatments of AKD.
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Objective To investigate the risk factors of clinically diagnosed acute kidney injury (AKI) patients progressing to acute kidney disease (AKD). Methods The clinical data of AKI patients admitted to the First Affiliated Hospital of Zhengzhou University from January 1, 2018 to December 31, 2018 were retrospectively analyzed. According to the outcome of the patients, AKI patients were divided into non - acute kidney disease (NAKD) group and AKD group. Clinical characteristics and laboratory data of two groups were compared. The risk factors of AKD in patients with AKI were analyzed by logistic regression, and then the receiver operating characteristic curve (ROC) was drawn to evaluate the predictive value of these risk factors. Results A total of 254 patients with AKI were enrolled, and 186 patients developed AKD with an incidence of 73.2％. Theincidences of AKD in stage 1, stage 2 and stage 3 of AKI were 20.0％, 46.7％and 83.5％respectively. Multivariate logistic regression analysis showed increased peak serum creatinine (within 7 days after AKI diagnosis) (OR=2.561, 95％ CI 1.584-4.140, P<0.001), proteinuria (OR=2.952, 95％ CI 1.162-7.500, P=0.023) and increased intact parathyroid hormone (OR=1.757, 95％CI 1.104-2.797, P=0.017) were independent risk factors for progression to AKD in patients with AKI. The ROC showed that increased peak serum creatinine (within 7 days after AKI diagnosis) was an important predictor of AKD in patients with AKI (AUC=0.798, P<0.001). Conclusion Increased peak serum creatinine (within 7 days after AKI diagnosis), proteinuria and increased intact parathyroid hormone are independent risk factors for progression to AKD in patients with AKI, providing new evidences and ideas for clinical preventions and treatments of AKD.
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Objective To explore the effects of BSA on hypoxia inducible factor/hypoxia response element (HIF/HRE) transcription activity in rat tubular epithelial cells (NRK-52E) with HRE-Luc reporter plasmid.Methods Luciferin activity of NRK-52E cells incubated by a medium contained BSA in varying concentration (0,5,10,20 mg/ml) and stimulus duration (24,48,72 h) was detected by dual luciferase detecting system based on HRE-Luc reporter plasmid and HIF-1 α expression was detected by Western blotting.Results HIF/HRE transcription activity of NRK-52E cells was increased in BSA incubation group (10 mg/ml,48 h) compared with blank control (BSA 0 mg/ml,48 h) [(2.59±0.35)vs (1.03±0.09),P=0.000].HIF-1α expression of NRK-52E cells was increased in BSA incubation group (20 mg/ml,48 h) compared with blank control (BSA 0 mg/ml,24 h) [(0.052±0.010) vs (0.014±0.003),P=0.000].Conclusion Albumin can increase HIF/HRE transcription activity of TEC.
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Objective To study the pathogenesis of anemia in chronic aristolochic acid nephmpathy(CAAN) rats. Methods The hemoglobin(Hb)values of sixty-two male SD rats were assayed to determine its normal range.Among them,24 rats with normal Hb value were randomly divided into 2 groups:model group (MG)in which rats received the extract of Aristololochia manshuriensis Kom (AmK) by gavage,and control group (CG) received tap water only by gavage.Body weisht(BW),Hb,24 h urinary protein excretion(UP)and creatinine clearance (Ccr)of 6 rats in each group were measured before administration and at the end of the 8th week, respeetively.then these rats were sacrificed.The relative area of renal interstitial fibrosis was measured by microscopy.The mRNA expression of erythropoietin (EPO)in kidney tissue Was determined by real-time RT-PCR;protein expression of type I collagen(Coll),aminopeptidase P (APP),hypoxia indHeible factor let and 2α(HIF-1α and HIF-2α)in kidney tissue Was examined by immunohistochemistry staining. Results Hb values of normal rats presented normal distribution. The normal Hb was (155.9±16.5) g/L. Rat anemia was diagnosed when Hb was below 123.6 g/L. There was no difference in all the examination results between CG and MG before administration (P>0.05). Compared with CG, the Hb and Cer in MG were significantly decreased [(121.66±15.68) g/L vs (169.00±12.89) g/L, (0.63±0.13) ml/min vs (1.27±0.18) ml/min, P< 0.01], and the UP in MG was significantly increased at the end of the 8th week [(27.04±9.40) mg/d vs (6.11±0.84) mg/d, P<0.01]; the relative areas of fibrosis and Col l in renal interstitium of MG were significantly enlarged [(12.89±2.33)% vs (0.55±0.10)%, (13.92±2.92)% vs (1.32±0.84)%, P<0.01]; the protein expression of APP and the mRNA expression of EPO in the kidney tissue of MG were significantly down-regulated [(0.55±0.23)% vs (3.77±1.06)%, 0.005±0.001 vs 0.032±0.013, P<0.01]; the protein expression of HIF-lα and HIF-2α in the kidney tissue of MG was significantly up-regulated (2.55±0.16 vs 1.12±0.46, 2.33±0.33 vs 1.15±0.27, P<0.01), at the end of the 8th week. Conclusions The pathogenesis of anemia in CAAN may be due to the decreased production of EPO caused by the destruction of peritubular capillary. The compensatory up-regulation of HIF-lα and HIF-2α expression can not prevent the anemia development.