Diabetes mellitus (DM) is a major metabolic disease endangering global health, with diabetic nephropathy (DN) as a primary complication lacking curative therapy. Sporoderm-broken spores of Ganoderma lucidum (GLP), an herbal medicine, has been used for the treatment of metabolic disorders. In this study, DN was induced in Sprague-Dawley rats using streptozotocin (STZ) and a high-fat diet (HFD), and the protective mechanisms of GLP were investigated through transcriptomic, metabolomic, and network pharmacology (NP) analyses. Our results demonstrated that GLP intervention ameliorated renal damage and inflammation levels in DN rats. Integrative metabolomic and transcriptomic analysis revealed that GLP treatment modulated glucose and cellular energy metabolisms by regulating relevant genes. GLP significantly suppressed the inflammations by impacting glucose and energy metabolism-related gene expression (Igfbp1 and Angptl4) and enhanced metabolic biomarkers of 4-Aminocatechol. In addition, NP analysis further indicated that GLP may efficiently alleviate DN via immune-related pathways. In conclusion, this study provides supportive evidence of the anti-inflammatory effects of GLP supplements, highlighting their potential for promising clinical applications in treating DN.

Objective:To investigate the effects of hyperuricemia on the prognosis of IgA nephropathy (IgAN) using propensity score matching (PSM) method.Methods:IgAN patients proven by biopsy were included. PSM was used to match patients. Kaplan-Meier method was used for survival analysis, and Cox regression analysis was used to analyze the effects of hyperuricemia on IgAN prognosis. Primary outcome events were defined as death, or end-stage renal disease (dialysis, transplantation), or a decrease in estimated glomerular filtration rate (eGFR) greater than 40%. Renal outcome was defined as end-stage renal disease (dialysis, transplantation), or a decrease in eGFR greater than 40%.Results:A total of 1 454 IgAN patients were included in this study, including 850 females and 604 males. Uric acid level was (368.26±92.87) μmol/L in the males, and (277.23±92.71) μmol/L in the females. The median follow-up time was 85.00(56.10, 106.33) months. During the follow-up period, a total of 134 patients reached the primary outcome events, including 5 deaths, 24 dialysis patients, 5 kidney transplant patients, and 100 patients with eGFR decreased by more than 40%. After 1∶1 matching, 131 males and 159 females in the hyperuricemia group were successfully matched with 131 males and 159 females in the normal uric acid group, and there was no significant statistical difference in each parameter in baseline between the hyperuricemia group and normal uric acid group after matching. Kaplan-Meier survival analysis showed that either before or after matching, the incidence of primary outcome events in male or female patients with hyperuricemia was higher than those with normal uric acid, but there was no statistically significant difference in incidence of primary outcome events between female hyperuricemia group and female normal uric acid group after matching (Log-rank test, χ2=3.586, P=0.058). Cox proportional hazard regression model showed that, in the pre-match fully adjusted model, the hazard ratio ( HR) of entering primary outcome events was 2.29-fold (95% CI 1.27-4.11, P=0.006) for men with hyperuricemia and 1.85-fold (95% CI 1.01-3.37, P=0.045) for women with hyperuricemia compared with those with normal uric acid. In the post-match fully adjusted model, the HR of entering primary outcome events was 2.41-fold (95% CI 1.18-4.93, P=0.016) for men with hyperuricemia and 1.83-fold (95% CI 0.91-3.67, P=0.091) for women with hyperuricemia compared with those with normal uric acid. In the pre-match fully adjusted model, the HR of entering renal outcome events was 2.68-fold (95% CI 1.47-4.88, P=0.001) for men with hyperuricemia and 1.81-fold (95% CI 0.99-3.33, P=0.056) for women with hyperuricemia compared with those with normal uric acid. In the post-match fully adjusted model, the HR of entering renal outcome events was 2.89-fold (95% CI 1.36-6.15, P=0.006) for men with hyperuricemia and 1.81-fold (95% CI 0.88-3.72, P=0.106) for women with hyperuricemia compared with those with normal uric acid. Conclusion:Hyperuricemia may be associated with IgAN progression, and it has a more significant effect on male IgAN patients.

Objective: To analyze the risk factors for large renal hematoma caused by percutaneous renal biopsy (PRB) in order to provide evidence for early clinical prevention and Effective nursing. Methods: The data of 707 patients who underwent PRB in nephrology department in Hangzhou Hospital of Traditional Chinese Medicine from January 2016 to January 2017 were retrospectively identified. Demographic and clinical data were collected, including general status (gender, age, body mass index, histological diagnosis, associated diseases), laboratory indexes and related examination during PRB (serum creatinine, estimated glomerular filtration rate, creatinineclearance rate, serumuricacid, serumalbumin, hemoglobin, platelet count, prothrombin time, activated partial thromboplastin time, kidney size), blood pressure(history of hypertension, systolic blood pressure, diastolic blood pressure and mean arterial blood pressure before PRB). Univariable logistic regression analysis, linear diagnosis, factor analysis, multivariable logistic regression analysis and receiver operating characteristic curve (ROC curve) were used to assess risk factors. Results: Over the period, 707 native kidney biopsies were performed. Hematoma occurred in 609 biopsies (86.1%), including 558 minorhematomacases (78.9%), 51 largehematoma cases (7.2%), no severe complications were observed. Univariable logistic regression analysis of risk factors in 51 patients with large hematoma after PRB found that there were significant differences in renal tubulointerstitial fibrosis, crescents > 25%, serum creatinine, history of hypertension, systolic blood pressure, diastolic blood pressure and mean arterial pressure before PRB (P< 0.05). Compared with the non-hematoma/minor-hematoma group, the blood pressure before PRB increased significantly in large hematoma group (OR=1.414, 95%CI=1.007-1.985, P=0.045) . More patients with a history of hypertension in large hematoma group (OR=1.997, 95% CI=0.995-4.009, P=0.052) .The area under the ROC curve for predicting large hematoma after PRB was 0.634 for blood pressure before PRB and history of hypertension, the Youden index was 0.27. The blood pressure before PRB and hypertension history were used to predict the formation of large hematoma separately, and the Youden index was 0.28 vs. 0.22 (P> 0. 05). Conclusions History of hypertension and blood pressure before PRB were independent risk factors for large renal hematoma after PRB.Patients with history of hypertension were more likely to develop large hematoma than those with no history of hypertension, and those with higher blood pressure before PRB were more likely to develop large hematoma. The history of hypertension and the blood pressure before PRB have certain effect in predicting the formation of large hematoma after PRB. Each of them have a certain predictive effect on the formation of largehematoma after PRB, and the prediction effect trend of blood pressure before PRB is slightly better than that of history of hypertension.

Aim To investigate the relationship be-tween the cardioprotection of apigenin ( Api ) from an-oxia/reoxygenation ( A/R) injury and Bcl-2 pathway. Methods H9 c2 cardiomyocytes were cultured and di-vided into normal control group, A/R group, Api pre-treatment group ( Api ) , Api + Bcl-2 inhibitor group ( Api + ABT-737 ) . Expression of Bcl-2 was deter-mined by Western blot,and cell viability was measured by MTT method. LDH, SOD, GSH-Px, MDA activity were determined by chromometry. ROS generation, mi-tochondrial membrane potential and apoptosis were de-termined by flow cytometry. Results 25h after apige-nin precondition,the expression of Bcl-2 was upregulat-ed in cardiomyocytes ( P <0. 01 ) . In the group pre-treated with 40 μmol · L-1 apigenin before A/R, the activity of LDH in culture medium decreased; the ac-tivity of intracellular SOD, GSH-Px increased; the content of MDA and ROS generation decreased; cell viability increased; mitochondrial membrane potential could be more stable and cell apoptosis decreased ( P<0. 01 ) . However, all these protective effects were attenuated significantly in the group pretreated with apigenin and Bcl-2 inhibitor ABT-737 . Conclusion The effect of apigenin against A/R injury in cardiomyo-cytes involves Bcl-2 pathway, and at least partly de-pends on its effect on upregulating the expression of Bcl-2 .

Objective To study the CT manifestations of delayed traumatic hematomas of the brain and evaluate their diagnostic significance in predicting the delayed traumatic brain hematoma. Methods The manifestations of initial CT studies and follow-up CT examinations of 31 delayed traumatic brain hematomas were analyzed. Another 50 CT studies of head trauma without delayed brain hematomas were included randomly as control. Results The abnormal findings of CT studies of the 31 delayed traumatic brain hematomas included: (1)Decreased density of the local brain parenchyma and disappeared difference between gray and white matter of the same area in 18 cases; (2)Local subarachnoid space hemorrhage in 24 cases; (3)Slight mass effect of local brain parenchyma in 16 cases. (4)Subdural hematoma in 9 cases. The locations of the abnormalities were roughly the same with the delayed hematoma except one local subarachnoid space hemorrhage, which was in the opposite of the delayed hematoma. The appearing rate of those abnormal findings in the control group was low and the difference was statistically significant. Conclusion The decrease of density of local brain parenchyma, the disappeared difference between the gray and white matter, local subarachnoid space hemorrhage, and local swollen of brain presented in the initial CT study of the patient with head trauma should be taken as indicators of delayed hemorrhage of the same area of brain, and it is necessary to do follow-up CT studies to exclude it.