Protective effects and mechanisms of Baicalin and octreotide on renal injury of rats with severe acute pancreatitis

AIM: To investigate the protective effects and mechanisms of Baicalin and octreotide on renal injury of rats with severe acute pancreatitis (SAP). METHODS: One hundred and eighty SD rats were randomly assigned to the model group, Baicalin-treated group, octreotide-treated group and sham operation group. The mortality, plasma endotoxin level, contents of blood urea nitrogen (BUN), creatinine (CREA), phospholipase A2 (PLA2), nitrogen monoxide (NO), tumor necrosis factor (TNF)-α, IL-6 and endothelin-1 (ET-1) in serum, expression levels of renal Bax and Bcl-2 protein, apoptotic indexes and pathological changes of kidney were observed at 3, 6 and 12 h after operation. RESULTS: The renal pathological changes were milder in treated group than in model group. The survival at 12 h and renal apoptotic indexes at 6 h were significantly (P < 0.05) higher in treated group than in model group [66.67% vs 100%; 0.00 (0.02)% and 0.00 (0.04)% vs 0.00 (0.00)%, respectively]. The serum CREA content was markedly lower in octreotide-treated group than in model group at 3 h and 6 h (P < 0.01, 29.200 ± 5.710 μmol/L vs 38.400 ± 11.344 μmol/L; P < 0.05, 33.533 ± 10.106 μmol/L vs 45.154 ± 17.435 μmol/L, respectively). The expression level of renal Bax protein was not significantly different between model group and treated groups at all time points. The expression level of renal Bcl-2 protein was lower in Baicalin-treated group than in model group at 6 h [P < 0.001, 0.00 (0.00) grade score vs 3.00 (3.00) grade score]. The Bcl-2 expression level was lower in octreotide-treated group than in model group at 6 h and 12 h [P < 0.05, 0.00 (0.00) grade score vs 3.00 (3.00) grade score; 0.00 (0.00) grade score vs 0.00 (1.25) grade score, respectively]. The serum NO contents were lower in treated groups than in model group at 3 h and 12 h [P < 0.05, 57.50 (22.50) and 52.50 (15.00) μmol/L vs 65.00 (7.50) μmol/L; P < 0.01, 57.50 (27.50) and 45.00 (12.50) μmol/L vs 74.10 (26.15) μmol/L, respectively]. The plasma endotoxin content and serum BUN content (at 6 h and 12 h) were lower in treated groups than in model group. The contents of IL-6, ET-1, TNF-α (at 6 h) and PLA2 (at 6 h and 12 h) were lower in treated groups than in model group [P < 0.001, 3.031 (0.870) and 2.646 (1.373) pg/mL vs 5.437 (1.025) pg/mL; 2.882 (1.392) and 3.076 (1.205) pg/mL vs 6.817 (0.810) pg/mL; 2.832 (0.597) and 2.462 (1.353) pg/mL vs 5.356 (0.747) pg/mL; 16.226 (3.174) and 14.855 (5.747) pg/mL vs 25.625 (7.973) pg/mL; 18.625 (5.780) and 15.185 (1.761) pg/mL vs 24.725 (3.759) pg/mL; 65.10 (27.51) and 47.60 (16.50) pg/mL vs 92.15 (23.12) pg/mL; 67.91 ± 20.61 and 66.86 ± 22.10 U/mL, 63.13 ± 26.31 and 53.63 ± 12.28 U/mL vs 101.46 ± 14.67 and 105.33 ± 18.10 U/mL, respectively]. CONCLUSION: Both Baicalin and octreotide can protect the kidney of rats with severe acute pancreatitis. The therapeutic mechanisms of Baicalin and octreotide might be related to their inhibition of inflammatory mediators and induction of apoptosis. Baicalin might be a promising therapeutic tool for severe acute pancreatitis.

Caspase-1 inhibition alleviates acute renal injury in rats with severe acute pancreatitis

AIM: To assess the effect of inhibition of caspase-1 on acute renal injury in rats with severe acute pancreatitis (SAP).

Ligustrazine alleviates acute renal injury in a rat model of acute necrotizing pancreatitis

AIM: To evaluate the effect of ligustrazine, a traditional Chinese medicine, on renal injury in a rat model of acute necrotizing pancreatitis (ANP). METHODS: A total of 192 rats were randomly divided into three groups: control (C group), ANP without treatment (P group), and ANP treated with ligustrazine (T group). Each group was further divided into 0.5, 2, 6, 12 h subgroups. All rats were anesthetized with an intraperitoneal injection of sodium pentobarbital. Sodium taurocholate was infused through the pancreatic membrane to induce ANP. T group was infused sodium taurocholate as above, and 0.6% ligustrazine was then administered via the femoral vein. Serum urea nitrogen (BUN) and creatinine (Cr) concentrations were measured for the evaluation of renal function. The effects of ligustrazine on the severity of renal injury were assessed by renal function, TXA2/PGI2 and histopathological changes. Renal blood flow was determined by the radioactive microsphere technique (RMT).RESULTS: Compared with control group, the renal blood flow in P group was decreased significantly. Serious renal and pancreatic damages were found in P group, the BUN and Cr levels were elevated significantly, and the ratio of TXA2 to PGI2 was increased at 2, 6 and 12 h. Compared with P group, the blood flow of kidney was elevated significantly at 6 and 12 h after induction of ANP, the renal and pancreatic damages were attenuated, and the BUN and Cr levels were decreased significantly, and the ratio of TXA2 to PGI2 was decreased at 6 and 12 h in T group.CONCLUSION: Microcirculatory disorder (MCD) is an important factor for renal injury in ANP. Ligustrazine can ameliorate the condition of MCD and the damage of pancreas and kidney.

Role of Reactive Oxygen Species in Triptolide-induced Apoptosis of Renal Tubular Cells and Renal Injury in Rats

This study investigated the role of reactive oxygen species（ROS） in the pathogenesis of triptolide-induced renal injury in vivo.Rats were randomly divided into 4 groups（n=5 in each）：triptolide group in which the rats were intraperitoneally injected with triptolide solution at a dose of 1 mg/kg of body weight on day 8;control group in which the rats received a single intraperitoneal injection of 0.9% physiological saline on day 8;vitamin C group in which the rats were pretreated with vitamin C by gavage at a dose of 250 mg/kg of body weight per day for 7 days before the same treatment as the control group on day 8;triptolide＋vitamin C group in which the rats were first subjected to an oral administration of vitamin C at a dose of 250 mg/kg of body weight per day for 7 days,and then to the same treatment as the triptolide group on day 8.All the rats were sacrificed on day 10.Blood samples were collected for detection of plasma creatinine（Pcr） and plasma urea nitrogen（PUN） concentrations.Both kidneys were removed.The histological changes were measured by haematoxylin-eosin（HE） staining.The production of ROS was determined by detecting the fluorescent intensity of the oxida-tion-sensitive probe rhodamine 123 in renal tissue.Renal malondialdehyde（MDA） content was meas-ured to evaluate lipid peroxidation level in renal tissue.TUNEL staining was performed to assess apop-tosis of renal tubular cells.Renal expression of apoptosis-related proteins Bcl-2,Bax,Bid,Bad,Fas and FasL,as well as corresponding encoding genes were assessed by Western Blotting and real-time PCR.The results showed that triptolide treatment promoted the generation of a great amount of ROS,up-regulated the expression of Bax,Bid,Bad,Fas and FasL at both protein and mRNA levels,as well as the ratio of Bax to Bcl-2,and caused the apoptosis of renal tubular cells and renal injury.However,pretreatment with an antioxidant,vitamin C,significantly reduced the generation of ROS and effectively inhibited the triptolide-induced apoptosis of renal tubular cells and renal injury.It was concluded that ROS plays a critical role in triptolide-induced apoptosis of renal tubular cells and renal injury.The protective administration of vitamin C may help alleviate triptolide-induced renal injury and nephrotoxicity.

Ligliptin for treatment of type 2 diabetes mellitus with early renal injury: Efficacy and impact on endogenous hydrogen sulfide and endothelial function

BACKGROUND Diabetes is a clinically common chronic disease,and its incidence has been increasing in recent years.Diabetes is believed to accelerate the process of atherosclerosis in patients,and abnormal endothelial function is an important factor leading to diabetic kidney damage.AIM To investigate the efficacy of ligliptin in the treatment of type 2 diabetes mellitus(T2DM)with early renal injury and its effect on serum endogenous hydrogen sulfide(H2S),endothelial cell particles,and endothelial function.METHODS From January 2018 to April 2019,110 patients with T2DM and early kidney injury treated at our hospital were divided into an observation group(receiving ligliptin treatment,n=54)and a control group(receiving gliquidone therapy,n=56).Blood glucose and renal function before and after treatment were compared between the two groups.RESULTS The differences in fasting blood glucose,2 h blood glucose,and glycated hemoglobin were not statistically significant between the two groups after treatment.The urinary albumin excretion rate after treatment in the ligliptin group was 70.32±11.21μg/min,which was significantly lower than that of the gliquidone group(P=0.000).Serum endogenous H2S and endothelial cell microparticles of the ligliptin treatment group were 40.04±8.82 mol/L and 133.40±34.39,respectively,which were significantly lower than those of the gliquidone treatment group(P=0.000 for both);endothelin-dependent diastolic function and nitric oxide after treatment in the ligliptin group were 7.98%±1.22%and 190.78±30.32 mol/L,significantly higher than those of the gliquidone treatment group(P=0.000 for both).CONCLUSION Ligliptin treatment of T2DM with early renal injury has the same glucoselowering effect as gliquidone treatment.Ligliptin treatment has a better effect and it can significantly improve the renal function and vascular endothelial function of patients,and reduce serum endogenous H2S and endothelial cell particle levels.

Safety and efficacy of Endovascular Management of high-grade blunt renal injury

Objectives:To provide data on the safety and efficacy of renal arterial embolization(RAE)in patients with highgrade blunt renal injury.Materials and methods:Fifteen patients with high-grade blunt renal injury(AAST grades IV-V)admitted to our hospital from July 2014 to December 2019 were retrospectively reviewed in this study.Their clinical success rate and complications were investigated accordingly.Results:Fifteen patients with high-grade blunt renal injury,13 men and 2 women with an average age of 41.6 years,including 11 hemodynamically unstable patients and 4 stable patients,were treated with RAE.Among these patients,73.3%(11 of 15)had grade IV,and 26.7%(4 of 15)had grade V injuries,while 53.3%(8 of 15)patients had concomitant injuries.One patient received main RAE and 14 patients received selective RAE.The clinical success rate after the first embolization was 93.3%(14 of 15).RAE was repeated and was successfully performed in one patient with sustained hematuria.No significant difference in creatinine levels was found before and after embolization.During the follow-up period of 2–82 months,two patients required tube drainage due to urine leaks,one patient developed renal failure requiring renal replacement therapy,and one patient developed secondary hypertension.Conclusions:RAE can provide a high success rate of hemostasis for both hemodynamically stable and unstable patients with high-grade blunt renal injury,and only minor complications are observed with this procedure.

Salvianolic acid A alleviates renal injury in systemic lupus erythematosus induced by pristane in BALB/c mice

OBJECTIVE To investigate the effects of salvianolic acid A(SAA)in systemic lupus erythematosus(SLE)induced by pristane in BALB/c mice,this study was performed.METHODS Lupus mice were established by confirming elevated levels of autoantibodies and IL-6 after intraperitoneal injection of pristane.Micewere then treated with daily oral doses of SAA for 5months in parallel with mice treated with prednisone and aspirin as positive controls.The levels of autoantibodies were monitored at monthly intervals and nephritic symptoms observed by hematoxylin and eosin(H&E)and periodic acid-Schiff(PAS)staining.Western blot analysis of renal tissue was also employed.RESULTS SAA treatment caused a significant reduction in the levels of anti-Sm autoantibodies and reduced renal histopathological changes and pathological effects.SAA treatment also significantly inhibited the phosphorylation of IKK,IκB and NFκB in renal tissues of lupus mice.CONCLUSION The results suggest that SAA alleviates renal injury in pristane-induced SLE in BALB/c mice through inhibition of phosphorylation of IKK,IκB and NFκB.

Early renal injury indicators can help evaluate renal injury in patients with chronic hepatitis B with long-term nucleos(t)ide therapy

BACKGROUND Patients with chronic hepatitis B(CHB)with long-term nucleos(t)ide therapy may experience renal insufficiency.Traditional renal function indicators,such as urine protein,serum urea nitrogen(BUN),and serum creatinine,are normal when early mild lesions occur.Therefore,more sensitive renal function indicators are needed.AIM To investigate the significance of early renal injury indicators in evaluating renal injury in patients with CHB with long-term nucleos(t)ide therapy.METHODS We collected the clinical data of 69 outpatients with CHB at Peking University First Hospital from March 2018 to January 2020 who had been treated with longterm nucleos(t)ide therapy and analyzed the results of early renal injury indicators.Continuous normal distribution data were analyzed by the t-test to determine the difference between two groups.Continuous non-normally distributed data were analyzed by the Mann-Whitney U-test between two groups.The Kruskal-Wallis H test was used to determine the differences among multiple groups.Enumeration data were analyzed by the chi-square test.The related factors of early renal injury indicators were analyzed by logistic regression analysis.RESULTS The average treatment duration with nucleos(t)ide analogs of the 69 patients with CHB was 99.7±28.7 mo.The cases of patients with elevated BUN and hypophosphatemia were 6(8.7%)and 13(18.8%),respectively;31(44.9%)patients had abnormal early renal injury indicators,including 9 patients with abnormal urine microalbumin,7 patients with abnormal urine immunoglobulin,6 patients with abnormal urine transferrin,and 19 patients with abnormalα1 microglobulin.There were no significant differences in the mean values of age,sex,BUN,estimated glomerular filtration rate(eGFR),serum uric acid,serum calcium,or serum phosphorus between the two groups of patients with and without early renal injury indicators.However,the mean levels of serum creatinine and urine creatinine,N-acetyl-β-D-glucosidase enzyme,α1 microglobulin,and urine immunoglobulin in the former group of patients were significantly higher than those in the latter group of patients(P<0.05).The incidence of early renal injury in patients with eGFR≥90,60-89,and 30-59 mL/(min·1.73 m2)was 36.4%(8/22),47.6%(20/42),and 60%(3/5),respectively.Logistic regression analysis results showed that gamma-glutamyl transpeptidase[odds ratio(OR)=1.05(1.008-1.093),P=0.020],direct bilirubin[OR=1.548(1.111-2.159),P=0.010],serum creatinine[OR=1.079(1.022-1.139),P=0.006],and age[OR=0.981(0.942-1.022),P=0.357]were independent predictors of early renal injury.CONCLUSION Patients with CHB treated with long-term nucleos(t)ide analog therapy had a high probability of early renal injury,and early renal injury indicators were highly sensitive and could be used to monitor early renal impairment.

CD38 deficiency activates ERK1/2-NF-κB signaling pathway in sepsis-associated renal injury

CD38 is known to play roles in various inflammatory pathways.However,whether it has a protective or detrimental effect during bacterial septicemia remains disputed.Herein,this study aimed to determine the potential effect of CD38 on renal injury in septicemia.Escherichia coli(E.coli)was used to induce sepsis-associated renal injury in mice.WT and CD38-/-mice were stimulated with E.coli.After three hours,the serum was collected to detect renal function.Function mRNA expressions inflammatory cytokines in kidneys were quantified by real-time PCR.Hematoxylin and eosin staining were used to observe the histomorphology of kidney.The expression of TLR4,NF-κB,MAPK and cytokines were detected by Western Blot.Our results demonstrated that 3×10^(8) cfu/mL E.coli is the appropriate dose to induce sepsis mice model.Compared to WT sepsis mice,CD38-/-mice showed aggravated kidney injuries with impaired renal function,increased inflammation and apoptosis after E.coli stimulation.Interestingly,CD38 deficiency also led to elevated expression of TLR4 and increased phosphorylation of NF-κB p65/p105 and ERK1/2.To sum up,our results suggested that CD38 deficiency could aggravate E.coli-induced renal injury through activating ERK1/2-NF-κB signaling pathway.

Advances in oxidative stress and NOD-like/toll-like receptors in acute renal injury

Acute Kidney Injury(AKI)is a clinical syndrome characterized by rapid renal deterioration with high morbidity and mortality.Renal reperfusion(IRI),renal toxicity and sepsis are the main causes of AKI.IRI is one of the main causes of acute kidney injury in clinic,accounting for 75%of all the causes of AKI[1].The fatality rate of AKI caused by IRI is high,and the surviving patients may leave chronic renal impairment with different degrees[2].A number of studies have shown that ischemia-reperfusion injury leading to renal dysfunction is directly related to oxidative stress,and the inhibition of oxidative stress through nod-like/toll-like signaling pathway can reduce acute renal injury.This review summarizes the research progress in regulating oxidative stress and the relationship between innate immune receptors and acute renal injury.

Changes of Apoptosis in Rats of Acute Ischemic Renal Injury under Treatment of Tetrandrine

ObjectiveTo elucidate the effect of tetrandrine on acute ischemic renal injury and its relation with apoptosis. MethodsA model for bilateral post ischemic renal injury in rats was developed by clamping renal pedicles for 45 min. Renal tissular DNA fragmentation analysis and renal tissular HE staining were used. Also quantitative analysis of apoptosis in injured renal tubular epithelium was carried out by using TdT mediated dUTP nick and labeling (TUNEL). ResultsApoptosis of renal tubular epithelium increased in acute ischemic renal injury. Tetrandrine could remarkably decrease the level of apoptosis in injured renal tubule while protecting renal tissue against the ischemic injuries. ConclusionTetrandrine could adjust the level of apoptosis in renal tubular epithelium and alleviate renal tissular injury.

Salvianolic acid A alleviates renal injury in systemic lupus erythematosus induced by pristane in BALB/c mice

The purpose of this study was to investigate the effects of salvianolic acid A (SAA) in systemic lupus erythematosus (SLE) induced by pristane in BALB/c mice. Lupus mice were established by confirming elevated levels of autoantibodies and IL-6 after intraperitoneal injection of pristane. Mice were then treated with daily oral doses of SAA for 5 months in parallel with mice treated with prednisone and aspirin as positive controls. The levels of autoantibodies were monitored at monthly intervals and nephritic symptoms observed by hematoxylin and eosin(H&E) and periodic acid-Schiff (PAS) staining. Western blot analysis of renal tissue was also employed. SAA treatment caused a significant reduction in the levels of anti-Sm autoantibodies and reduced renal histopathological changes and pathological effects. SAA treatment also significantly inhibited the phosphorylation of IKK, I kappa B and NF kappa B in renal tissues of lupus mice. In conclusion, the results suggest that SAA alleviates renal injury in pristane-induced SLE in BALB/c mice through inhibition of phosphorylation of IKK, I kappa B and NF kappa B. (C) 2017 Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. Production and hosting by Elsevier B.V.

Vitamin C Attenuates Hemorrhagic Shock-induced Dendritic Cell-specific Intercellular Adhesion Molecule 3-grabbing Nonintegrin Expression in Tubular Epithelial Cells and Renal Injury in Rats

Background： The expression of dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin （DC-SIGN） in renal tubular epithelial cells has been thought to be highly correlated with the occurrence of several kidney diseases, but whether it takes place in renal tissues during hemorrhagic shock （HS） is unknown. The present study airned to investigate this phenomenon and the inhibitory effect of Vitamin C （VitC）. Methods： A Sprague Dawley rat HS model was established in vivo in this study. The expression level and location of DC-SIGN were observed in kidneys. Also, the degree of histological damage, the concentrations of tumor necrosis factor-or and interleukin-6 in the renal tissues, and the serum concentration of blood urea nitrogen and creatinine at different times （2-24 h） alter HS （six rats in each group）, with or without VitC treatment belbre resuscitation, were evaluated. Results： HS induced DC-SIGN expression in rat tubular epithelial cells. The proinflarnmatory cytokine concentration, histological damage scores, and functional injury of kidneys had increased. All these phenornena induced by HS were relieved when the rats were treated with VitC before resuscitation. Conclusions： The results of the present study illustrated that HS could induce tubular epithelial cells expressing DC-SIGN, and the levels of proinflarnmatory cytokines in the kidney tissues improved correspondingly. The results also indicated that VitC could suppress the DC-SIGN expression in the tubular epithelial cells induced by HS and alleviate the inflammation and functional injury in the kidney.

The p53-mediated Apoptosis in Hypercholesterolemia-induced Renal Injury of Rats

Summary： The apoptosis and the expression of tumor suppressor gene p53 in hypercholesterolemia （HC）-induced renal injury were investigated in rats. A high cholesterol diet （HCD）-induced HC rat model was made and serum lipid, urinary protein excretion （UPE） and N-aceto-β-D-glucosidase （NAG） were measured. The levels of malondialdehyde （MDA）, as an index of lipid peroxidation, in renal cortex and serum were compared between the two diet groups. Apoptosis and p53 expression were determined by TUNEL and immunohistochemistry, respectively. In the HCD-induced HC group, serum total cholesterol （TC）, low density lipoprotein cholesterol （LDL-C） as well as triglyceride （TG） were significantly increased, while the level of high density lipoprotein cholesterol （HDL-C） decreased. Meanwhile, increased excretions of UPE and NAG in urine were observed, which were accompanied with a decrease in urinary creatinine clearance （Ccr） and indicated both glomerular and tubular damages. In addition, apoptotic cell death coexisted in the kidney, as revealed by increased TUNEL positive cells. Finally, an increase in p53 expression was observed in tubuli, but not in glomeruli. Both TUNEL positive cells and p53 expression were found to be correlated to the level of renal cortical MDA （r=0. 817, P〈0.01 and r=0.547, P〈0.01, respectively）. The major manifestation of HCD-induced renal injury is apoptosis. The lipid peroxidation is a critical event to induce DNA damage and p53 is involved in the pathogenesis of lipid-induced renal injury.

Urinary cystatin C:pediatric reference intervals and comparative assessment as a biomarker of renal injury among children in the regions with high burden of CKDu in Sri Lanka

Background Cystatin C(Cys-C)is an emerging biomarker of renal diseases and its clinical use,particularly for screening the communities affected by chronic kidney disease of unknown etiology(CKDu),is hindered due to the lack of reference intervals(RIs)for diverse ethnic and age groups.The present study aimed to define RIs for urinary Cys-C(uCys-C)for a healthy pediatric population in Sri Lanka and in turn compare the renal function of the residential children in CKDu endemic and non-endemic regions in Sri Lanka.Methods A cross-sectional study was conducted with 850 healthy children(10-17 years)from selected locations for reference interval establishment,while a total of 892 children were recruited for the comparative study.Urine samples were collected and analyzed for Cys-C,creatinine(Cr)and albumin.Cr-adjusted uCys-C levels were partitioned by age,and RIs were determined with quantile regression(2.5th,50th and 97.5th quantiles)at 90%confidence interval.Results The range of median RIs for uCys-C in healthy children was 45.94-64.44 ng/mg Cr for boys and 53.58-69.97 ng/mg Cr for girls.The median(interquartile range)uCys-C levels of children in the CKDu endemic and non-endemic regions were 58.18(21.8-141.9)and 58.31(23.9-155.3)ng/mg Cr with no significant difference(P=0.781).A significant variation of uCys-C was noted in the children across age.Conclusions Notably high uCys-C levels were observed in children with elevated proteinuria.Thus,uCys-C could be a potential biomarker in identifying communities at high risk of CKDu susceptibility.

Relationship between hemoglobin A1c and contrast-induced acute renal injury in patients with type 2 diabetes mellitus undergoing cardiac catheterization

Background There were few studies to explore the relationship between hemoglobin Alc （HbAlc）and contrast-induced acute renal injury （CI-AKI）in patients with type 2 diabetes mellitus （T2DM）. Methods Two hundred seventy-nine patients with T2DM undergonging elective cardiac catheterization from Dongguan Kanghua Hospital were recruited. Patients were classified into quartiles based on HbAlc （ 〈 6.30%, 6.30- 6.70%, 6.71-7.70, and 〉 7.70%）. Baseline data, CI-AKI incidence and in-hospital outcomes were compared between the groups. Logistic regression was used to assess the relationship between HbAlc and CI-AKI. Results CI-AKI occurred in 26 （9.3%）patients. CI-AKI incidences of HbAlc quartiles were 4.6 %（3/65）, 2.8%（2/71）, 12.3%（9/73） and 17.1%（12/70） （P = 0.003）, respectively. There were no significant differences in in-hospital death or required renal replacement therapy among the four groups. Univariate logistic analysis showed that HbAlc was related with CI-AKI （OR = 1.319, 95%CI： 1.078-1.615, P = 0.007）. Multivariate analysis found that after adjusting eGFR 〈 60 ml/min/1.73 m2, age 〉 70 years and anemia, I-IbAlc 〉17% was still a significant independent risk factor for CI-AKI in patients with T2DM. Conclusions HbAlc is significantly associated with CI-AKI. HbAlc ≥ 7% may increase the risk of CI-AKI in patients with T2DM undergoing elective cardiac catheterization.

Phellinus igniarius ameliorates renal aging in a rat model of focal and segmental glomerulosclerosis

Objective:To comparatively investigate the ameliorative effect of Phellinus igniarius(P.igniarius)on renal aging in a rat model of focal and segmental glomerulosclerosis(FSGS).Methods:The FSGS model was established in rats by uninephrectomy combined with tail vein injection of doxorubicin.The FSGS rats were randomly divided into the model group,the P.igniarius decoction group,the P.igniarius polysaccharides group,and the P.igniarius polyphenols group.Molecular indicators of cell senescence,renal function indexes,and podocyte injury markers were tested after ten weeks of intragastric administration.Besides,the pathological renal lesions and the ultrastructural changes were observed.Results:FSGS developed in the model group within ten weeks and showed segmental glomerular scarring and renal aging.Following the 10-week intervention,24 h proteinuria,serum creatinine,blood urea nitrogen,P16^(INK4α),thrombospondin-1,and transforming growth factor-β1 were decreased in each treatment group,whereas albumin,erythropoietin,nephrin,and podocin were increased;the pathological renal injury was alleviated,and the number of senescent cells was reduced,especially in rats treated with P.igniarius decoction.Conclusions:P.igniarius ameliorates renal aging and renal injury in the FSGS rat model.Compared with the effective constituents(polysaccharides and polyphenols),P.igniarius decoction has a better curative effect,which is expected to provide a new therapeutic idea for FSGS.

ELABELA protects against diabetic kidney disease by activating high glucose-inhibited renal tubular autophagy

ELABELA(ELA),an endogenous ligand of the apelin receptor(also known as apelin peptide jejunum[APJ]),has been shown to decrease in the plasma of patients with diabetic kidney disease(DKD).In the current study,we explored the potential function as well as the underlying mechanisms of ELA in DKD.We first found that the ELA levels were decreased in the kidneys of DKD mice.Then,we found that ELA administration mitigated renal damage and downregulated the expression of fibronectin,collagenⅣ,and transforming growth factor-β1 in the db/db mice and the high glucose cultured HK-2 cells.Furthermore,the autophagy markers,Beclin-1 and LC3-Ⅱ/LC3-Ⅰratio,were significantly impaired in DKD,but the ELA treatment reversed these alterations.Mechanistically,the inhibitory effects of ELA on the secretion of fibrosis-associated proteins in high glucose conditions were blocked by pretreatment with 3-methyladenine(an autophagy inhibitor).In summary,these in vivo and in vitro results demonstrate that ELA effectively protects against DKD by activating high glucose-inhibited renal tubular autophagy,potentially serving as a novel therapeutic candidate for DKD.

Risk factors of acute renal injury in patients with acute left heart failure

Objective To investigate the risk factors of acute renal injury(acute kidney injury)in patients with acute left heart failure.Methods Clinical data of 188 patients with acute left heart failure who were admitted to our hospital were retrospectively analyzed.Logistic regression analysis was used to assess the risk factors for AKI.

Role of adhesion molecules and dendritic cells in rat hepatic/renal ischemia-reperfusion injury and anti-adhesive intervention with anti-P-selectin lectin-EGF domain monoclonal antibody

AIM: To investigate the role of P-selectin, intercellular adhesion molecule-1 (ICAM-1) and dendritic cells (DCs)in liver/kidney of rats with hepatic/renal ischemiareperfusion injury and the preventive effect of anti-Pselectin lectin-EGF domain monoclonal antibody (anti-PsLEGFmAb) on the injury.METHODS: Rat models of hepatic and renal ischemiareperfusion were established. The rats were then divided into two groups, one group treated with anti-PsL-EGFmAb(n = 20) and control treated with saline (n = 20). Both groups were subdivided into four groups according to reperfusion time (1, 3, 6 and 24 h). The sham-operated group (n = 5) served as a control group. DCs were observed by the microscopic image method, while P-selectin and ICAM-1 were analyzed by immunohistochemistry.RESULTS: P-selectin increased significantly in hepatic sinusoidal endothelial cells and renal tubular epithelial cells 1 h after ischemia-reperfusion, and the expression of ICAM-1 was up-regulated in hepatic sinusoid and renal vessels after 6 h. CD1a+CD80+DCs gradually increased in hepatic sinusoidal endothelium and renal tubules and interstitium 1 h after ischemia-reperfusion, and there was the most number of DCs in 24-h group. The localization of DCs was associated with rat hepatic/renal function.These changes became less significant in rats treated with anti-PsL-EGFmAb.CONCLUSION: DCs play an important role in immune pathogenesis of hepatic/renal ischemia-reperfusion injury.Anti-PsL-EGFmAb may regulate and inhibit local DC immigration and accumulation in liver/kidney.