Localization of Diacylglycerol Kinase ζ in the Kidney of Adult Rats: Its Dominant Expression in Collecting Tubules and its Selective Lack in Proximal Tubules / Localización de Diacilglicerol Quinasa ζ en el Riñón de Ratas Adultas: su Expresión Dominante en Túbulos Colectores y su Carencia Selectiva en Túbulos Proximales

SUMMARY: Diacylglycerol kinase (DGK) exerts balancing the intracellular level between two-second messengers, diacylglycerol and phosphatidic acid, by its phosphorylation activity. DGK ζ is often localized in cell nuclei, suggesting its involvement in the regulation of intranuclear activities, including mitosis and apoptosis. The present immunohistochemical study of rat kidneys first revealed no detection levels of DGK ζ -immunoreactivity in nuclei of most proximal tubule epithelia in contrast to its distinct occurrence in cell nuclei of collecting and distal tubules with the former more dominant. This finding suggests that DGK ζ is a key factor regulating vulnerability to acute kidney injury in various renal tubules: its low expression represents the high vulnerability of proximal tubule cells, and its distinct expression does the resistance of collecting and distal tubule cells. In addition, this isozyme was more or less localized in nuclei of cells forming glomeruli as well as in endothelial nuclei of peritubular capillaries and other intrarenal blood vessels, and epithelial nuclei of glomerular capsules (Bowman's capsules) and renal calyces, including intrarenal interstitial cells.

La diacilglicerol quinasa (DGK) ejerce el equilibrio del nivel intracelular entre dos segundos mensajeros, diacilglicerol y ácido fosfatídico, por su actividad de fosforilación. La DGK ζ a menudo se localiza en los núcleos celulares, lo que sugiere su participación en la regulación de las actividades intranucleares, incluidas la mitosis y la apoptosis. El presente estudio inmunohistoquímico en riñones de rata no reveló niveles de detección de inmunorreactividad de DGK ζ en los núcleos de la mayoría de los epitelios de los túbulos proximales, en contraste a la detección en los núcleos celulares de los túbulos colectores y distales, siendo el primero más dominante. Este hallazgo sugiere que DGK ζ es un factor clave que regula la vulnerabilidad a la lesión renal aguda en varios túbulos renales: su baja expresión representa la alta vulnerabilidad de las células del túbulo proximal, y su expresión distinta hace a la resistencia de las células del túbulo colector y distal. Además, esta isoenzima estaba más o menos localizada en los núcleos de las células que forman los glomérulos, así como en los núcleos endoteliales de los capilares peritubulares y otros vasos sanguíneos intrarrenales, y en los núcleos epiteliales de las cápsulas glomerulares (cápsulas de Bowman) y los cálices renales, incluidas las células intersticiales intrarrenales.

Clinicopathological features analysis of focal segmental glomerulosclerosis after kidney transplantation / 器官移植

Objective To investigate the clinicopathological features of recurrent and de novo focal segmental glomerulosclerosis (FSGS) after kidney transplantation. Methods Thirty-four recipients pathologically diagnosed with FSGS by renal allograft biopsy were enrolled in this clinical trial. According to the detection of primary diseases of renal allografts and circulating permeability factors, 34 recipients were divided into the recurrent FSGS group (n=12) and de novo FSGS group (n=22). The differences of clinical indexes and the degree of pathological injury of renal allografts were compared between two groups. Results There was no significant difference in the mesangial hyperplasia score, glomerulosclerosis rate, renal tubular atrophy score, interstitial fibrosis score and podocyte proliferation rate between two groups (all P > 0.05). In the recurrent FSGS group, segmental glomerulosclerosis rate of the recipients was 0.10 (0.08, 0.27), lower than 0.19 (0.13, 0.33) in the de novo FSGS group (P < 0.05). No significant difference was found in the incidence of antibody-mediated rejection, drug-induced renal tubular injury and BK virus infection between two groups (all P > 0.05). The incidence of T cell-mediated rejection in the recurrent FSGS group was 17%, lower than 55% in the de novo FSGS group (P < 0.05). Immunohistochemical staining showed that the infiltrating inflammatory cells in the renal allografts were mainly T lymphocytes. The positive rates of C4d deposition in peripheral capillaries between the recurrent and de novo FSGS groups were 33% (4/12) and 32% (7/22), with no significant difference (P > 0.05). Immunofluorescence results revealed IgM deposition in the segmental glomerulosclerosis area of renal allografts in most cases. Electron microscopy showed extensive fusion or segmental distribution of podocytes in the glomerulus of renal allografts. Conclusions The degree of renal functional injury and the incidence of T cell-mediated rejection in the recurrent FSGS group are lower than those in the de novo FSGS group. Comprehensive analysis of preoperative and postoperative clinical manifestations, laboratory testing and pathological examination of kidney transplant recipients contribute to early diagnosis and treatment of recurrent and de novo FSGS.

Acetaminophen induces alterations to the renal tubular ultrastructure in a rat model of acute nephrotoxicity protected by resveratrol and quercetin / El acetaminofeno induce alteraciones en la ultraestructura tubular renal en un modelo de rata con nefrotoxicidad aguda protegida por resveratrol y quercetina

Acetaminophen (also called paracetamol, or APAP) induced nephrotoxicity is reported after accidental or intentional ingestion of an overdose of the drug. Renal tubular ultrastructural alterations induced by APAP overdose associated with the induction of biomarkers of kidney injury have not been investigated before. Also, we investigated whether the combined polyphenolic anti-inflammatory and antioxidants agents, resveratrol (RES) and quercetin (QUR) can protect against APAP-induced acute kidney injury. The model group of rats received a single dose of APAP (2 g/kg), whereas the protective group of rats was pre-treated for 7 days with combined doses of RES (30 mg/kg) and QUR (50 mg/kg) before being given a single dose of APAP. All rats were then sacrificed one day post APAP ingestion. Harvested kidney tissues were prepared for transmission electron microscopy (TEM) staining and blood samples were assayed for urea, creatinine, and biomarkers of inflammation and oxidative stress. TEM images and blood chemistry analysis showed that APAP overdose induced kidney damage as demonstrated by substantial alterations to the proximal convoluted tubule ultrastructure, and a significant (p<0.05) increase in urea, creatinine, tumor necrosis factor-alpha (TNF-a), and malondialdehyde (MDA) blood levels, which were protected by RES+QUR. These findings indicate that APAP induces alterations to the renal tubular ultrastructure, which is inhibited by resveratrol plus quercetin, which also decreases blood levels of kidney injury biomarkers.

El objetivo de este trabajo fue estudiar la nefrotoxicidad inducida por acetaminofeno (también llamado paracetamol o APAP) después de la ingestión accidental o intencional de una sobredosis de la droga. Las alteraciones ultraestructurales tubulares renales inducidas por sobredosis de APAP asociadas con la inducción de biomarcadores de daño renal no se han investigado. Además, estudiamos si los agentes combinados antiinflamatorios y antioxidantes polifenólicos, el resveratrol (RES) y la quercetina (QUR) pueden proteger contra la lesión renal aguda inducida por APAP. El grupo modelo de ratas recibió una dosis única de APAP (2 g / kg), mientras que el grupo protector de ratas se trató previamente durante 7 días con dosis combinadas de RES (30 mg / kg) y QUR (50 mg / kg) antes de recibir una dosis única de APAP. Todas las ratas se sacrificaron un día después de la ingestión de APAP. Los tejidos renales fueron preparados para el análisis a través de la microscopía electrónica de transmisión (MET). En las muestras de sangre se determinaron la urea, creatinina y los biomarcadores de inflamación y estrés oxidativo. Las imágenes MET y el análisis químico de la sangre mostraron que la sobredosis de APAP inducía daño renal, como lo demuestran las alteraciones sustanciales en la ultraestructura del túbulo contorneado proximal, y además, de un aumento significativo (p <0,05) de la urea, creatinina, factor de necrosis tumoral alfa y niveles sanguíneos de malondialdehído, protegidos por RES + QUR. Estos hallazgos indican que APAP induce alteraciones en la ultraestructura tubular renal, inhibida por el resveratrol más quercetina, que también disminuye los niveles sanguíneos de biomarcadores de daño renal.

Effect of Fushengong Prescription on Wnt/β-catenin Signaling Pathway in Kidney of Rats with Chronic Renal Failure / 中国实验方剂学杂志

Objective:To observe the effects of Fushengong prescription on secretory glycoprotein （Wnt）/β-serial protein （β-catenin） signaling pathway in kidney of rats with chronic renal failure （CRF），and to further explore its mechanism of releasing the aggregation of extracellular matrix（ECM），inhibiting renal tubule interstitial fibrosis （TIF） and prolonging the progression of CRF. Method:A total of 55 SD male rats were randomly divided into the normal group，the model group，and the low， medium and high dose groups of Fushengong prescription，with 11 rats in each group.The normal group was routinely reared and the other 4 groups of rats were used to establish CRF model with 0.5% adenine fodder， fed them continuously for 21 d. After successful modeling，all model rats were switched to conventional feed. Normal saline （NS） was given the normal group and the model group by 20 mL·kg-1·d-1， the low， middle and high dose groups rats of Fushengong prescription were given intragastric administration Fushengong prescription according to the body weight of 4， 8， 16 g·kg-1，once a day，continuous gavage for 30 d. After the experiment，the pathomorphism change of renal tissues of rats was measured by Masson staining， the expression of Wnt4 and β-catenin mRNA in the kidney tissues were observed by the method of Real-time fluorescence quantitative polymerase chain reaction（Real-time PCR）， the expression of Wnt4，β-catenin and matrix metalloproteinase-7（MMP-7） protein of renal tissues were detected by the methods of Western blot. The expression of Wnt4， β-catenin protein of renal tissues were detected by the methods of immunohistochemistry （IHC）. Result:Compared with normal group，renal tubule interstitial fibrosis of renal tissues increased distinctly and the expression of Wnt4，β-catenin and MMP-7 protein increased significantly in the model group. Wnt4 and β-catenin mRNA also increased significantly in model group（P<0.01）. Compared with model group， the expression of Wnt4， β-catenin and MMP-7 protein in the Fushengong prescription groups decreased obviously （P<0.05）. The expression of Wnt4 and β-catenin mRNA in Fushengong prescription groups also decreased obviously. Conclusion:The mechanism of Fushengong prescription can release the aggregation of ECM，inhibit TIF and delay the progression of CRF，which may be related with the activation of Wnt/β-catenin signal pathway.

Palbociclib induces cell cycle arrest and senescence of human renal tubular epithelial cells / 南方医科大学学报

OBJECTIVE@#To investigate the effect of palbociclib on cell cycle progression and proliferation of human renal tubular epithelial cells.@*METHODS@#Human renal tubular epithelial cell line HK-2 was treated with 1, 5, 10, and 20 μmol/L of palbociclib, and the changes in cell proliferation and viability were examined by cell counting and CCK8 assay. EDU staining was used to assess the proliferation of HK-2 cells following palbiciclib treatment at different concentrations for 5 days. The effect of palbociclib on cell cycle distribution of HK-2 cells was evaluated using flow cytometry. SA-β-Gal staining and C12FDG senescence staining were used to detect senescence phenotypes of HK-2 cells after palbociclib treatment at different concentrations for 5 days. The relative mRNA expression levels of P16, P21, and P53 and the genes associated with senescence-related secretion phenotypes were detected by RT-PCR, and the protein expressions of P16, P21 and P53 were detected by Western blotting.@*RESULTS@#Palbociclib inhibited HK-2 cell proliferation and induced cell cycle arrest in G1 phase. Compared with the control cells, HK-2 cells treated with high-dose (10 μmol/L) palbociclib exhibited significantly suppressed cell proliferation activity, and the inhibitory effect was the most obvious on day 5 (@*CONCLUSIONS@#Palbociclib induces HK-2 cell senescence by causing cell growth arrest and delaying cell cycle progression.

Construction of stable cell lines expressing large conductance Ca2+-activated K+ channel α-subunit and molecular mechanism of potassium excretion in this channel / 上海交通大学学报（医学版）

Objective: To construct stable cell lines expressing the large conductance Ca2+-activated K+ channel (MaxiK or BK) α-subunit and to explore the mechanism of potassium excretion via BKα channel. Methods:The BKα plasmid with Myc tag was constructed and transfected into HEK293 cell lines by lipofectamine 2000. The positive monoclonal cell lines were screened by G418, and the expression of BKα was detected by Western blotting and the location of BKα by immunofluorescence. The stable cell lines expressing BKα protein was cultured on slides to form a single cell layer, which was perfused with different potassium ion concentrations of 5 mmol/L and 100 mmol/L, and the single channel patch clamp recorded the ion flux of BKα. Wild type and mutants (G77R, G130R, C140R and R297C) of the inwardly rectifying potassium channel (Kir4.1) were transfected into HEK293 cells stably transfected with BKα, and then the membrane protein was extracted. The expression of BKα was detected by Western blotting. Results:Stable cell lines expressing BKα channel were selected from HEK293 cells after transfection and cellular immunofluorescence verified the expression of BKα channel and its expression on the cell membrane. The channel open frequency (Npo) of BKα increased rapidly when perfused with 100 mmol/L potassium. After being transfected with wild type or mutants of Kir4.1, the membrane expression of BKα in the stable cell lines showed significant difference among these groups (P<0.05). Conclusion:The HEK293 cell lines stably expressing BKα have been successfully constructed. BKα channel can be activated by high potassium solutions. The function of the BKα subunit can be related to Kir4.1 channel, which may be attributed to the depolarization of the cells transfected by Kir4.1 mutants.

The correlation between oxidized low density lipoprotein receptor CD36 and renal tubular injury in diabetic rats / 中华内分泌代谢杂志

Objective To observe the expressions of oxidized low density lipoprotein ( OxLDL ) receptor CD36 in kidney tissue of diabetic rats and in tubular cells incubated with OxLDL, and to explore the association of CD36 with the tubular injury and renal fibrosis in the process of diabetic nephropathy. Methods Diabetic rat model with hyperlipidemia was established by feeding with high sugar and fat diet and injection of low dose streptozotocin intraperitoneally. The expression of CD36 in kidney tissues was analyzed immunohistochemically. Meanwhile, the tubular sclerosis and fibrosis injury index were estimated and calculated. NRK-52E cells were stimulated with 50 mg/L OxLDL for 5, 10, 24, and 48 h, or 100 and 150 mg/L OxLDLs for 2 and 3 days. The protein expression of CD36 was detected by Western blot. Results The expression of CD36 in the renal tubulointerstitium of diabetic rats was increased comparing to that in control rats, and was localized mainly at tubular region. The renal tubular damage index(STI)ofdiabetesgroupwashigherthanthatincontrolgroup(5.54±1.5vs0.65±0.15,P<0.05). OxLDL stimulated CD36 expression in NRK-52E cells in a dose-and time-dependent manner. Conclusion The expression of CD36 was increased in renal tubular of diabetic rats, in consistent with STI. OxLDL increased CD36 expression in NRK-52E cells. These results suggest that the expression of CD36 is associated with renal tubular damages in experimental rat diabetes.

Expression of AQP-7 in developing renal tubules of mice / 军事医学

Objective To observe the expression of aquaporin-7 (AQP-7)during the development of renal tubules of mice,and investigate the relationships between AQP-7 and renal tubule development.Methods Kidneys were selected from mice at embryonic days(E)12,14,17,and 18 and postnatal days(P)1,3,7,14,24,40 and 70.The expression of AQP-7 was observed by immunohistochemical(IHC)method in renal tubules.The surface area density values of AQP-7 positive expression were measured by stereological method while the content variation of AQP-7 in the renal tissue of mice was examined by Western blot.Results IHC analysis showed that AQP-7 was expressed in developing renal tubules at the proximal tubule at E14 day,localized along the brush border of the proximal straight tubules (S3 segment)where the cortex and outer medullalie after P14 d,but AQP-7 was not observed in the nephrogenic zone or inner medulla.The results of stereology discovered that the surface area density values of AQR-7 had increased gradually in the apical of renal tubule and reached the maximum at P24 d and then remained stable with the growth of mice.Western blot indicated that AQP-7 expression in kidneys had reached the peak at P24 d and remained stable.Conclusion The expressions of AQP-7 in the developing renal tubules of mice show a chronological and spatial sequence,which plays an important role in water and glycerol balance of mouse kidneys at the late stage of development.

Effect of mannitol on oxidative stress of human kidney tubular epithelial cells / 中国药理学与毒理学杂志

OBJECTIVE To observe the effect of mannitol on oxidative stress of human kidney tubular epithelial cells(HK-2). METHODS MTT assay was applied to detect HK-2 cell viability after ex?posure to different concentrations(50,100,150,200,250,300,350 and 400 mmol · L-1)of mannitol for 4,10,24,48 and 72 h. DCFH-DA method was used to determine the level of reactive oxygen species (ROS)after HK-2 cells were exposed to mannitol 100 and 250 mmol · L-1 for 4 h. Furthermore,cell morphology and indexes of oxidative stress such as malondialdehyde(MDA) content,superoxide dismutase(SOD )activity and glutathione(GSH) content were observed at different time points. RESULTS HK-2 cell viability decreased by about 50%after being treated with mannitol 250 mmol · L-1 for 72 h (P<0.05). ROS production in mannitol 250 mmol · L-1 treated group (68.7 ± 3.6) was higher than in solvent control group(50.3 ± 4.6)(P<0.05). HK-2 cells exhibited morphological changes after treatment with mannitol 250 mmol · L-1 for 4-72 h,including cell swelling,vacuoles and fall off. After treatment with mannitol 250 mmol · L-1 for 4,10,24,48 ahd 72 h,the MDA content increased signifi?cantly(P<0.05),while the activity of SOD and the content of GSH decreased significantly compared with solvent control group(P<0.05). CONCLUSION Over-production of ROS in HK-2 cells induced by high concentration(250 mmol·L-1)of mannitol may cause lipid peroxidation and injure the ability of an?tioxidation,which may contribute to mannitol induced cytotoxicity.

The role of renal tubule remodeling in acute kidney injury / 临床儿科杂志

Acute kidney injury (AKI) has emerged as a major public health problem that leads to decreased survival. Renal tubular epithelial cells are mainly damaged cells in AKI. Renal tubular epithelial cell remodeling plays a vital role in AKI. The regulatory mechanism of renal tubule remodeling is not yet clear. This review is written to address the renal tubule remodeling regulation mechanism of AKI.

Role of TLR2 and TLR4 in Mycobacterium bovis Bacillus Calmette-Guérin-induced injury in renal tubule epithelial cells / 中国病理生理杂志

AIM:To explore the effect of Toll-like receptor ( TLR) 2 and TLR4 in Mycobacterium bovis Bacil-lus Calmette-Guérin (BCG)-induced human proximal renal tubule epithelial cell (HK-2) injury.METHODS:HK-2 cells were stimulated by BCG, and the expression of TLR2, TLR4, chemokine (C-X3-C motif) ligand 1 (CX3CL1) and trans-forming growth factor beta 1 ( TGF-β1 ) was detected by quantitative real-time PCR and Western blotting .TLR2 monoclonal antibody and TLR4 inhibitor were used to treat the HK-2 cells 1 h before BCG stimulation.The expression of CX3CL1 and TGF-β1 was evaluated by quantitative real-time PCR and Western blotting .RESULTS: BCG increased the expression of TLR2, TLR4, CX3CL1 and TGF-β1 in the HK-2 cells.Additionally, the expression of CX3CL1 and TGF-β1 was inhibited partly by TLR2 monoclonal antibody or TLR4 inhibitor.CONCLUSION:BCG is able to increase the production of TLR 2, TLR4, CX3CL1 and TGF-β1 in the HK-2 cells.TLR2 and TLR4 signaling pathways play important roles in tubule epitheli-al cell injury induced by BCG .

Construction of Bioartificial Renal Tubule Assist Device In Vitro and Its Function of Transporting Sodium and Glucose / 华中科技大学学报（医学）（英德文版）

e to selectively transport Na+ and glucose.

Renal Recovery from Severe Acute Kidney Injury Requiring Renal Replacement Therapy / 대한신장학회지

PURPOSE: Acute tubular necrosis (ATN) is a serious complication in critically ill patients. This study investigated the renal outcome of severe ATN requiring RRT and prognostic factors for renal recovery. METHODS: Between January 2000 and May 2008, surviving patients with presumed ATN requiring dialysis were analyzed retrospectively. Patients with pre-existing chronic kidney disease and other causes of ARF rather than ATN were excluded. Primary outcomes were complete renal recovery (CR) and dialysis withdrawal. CR was defined as a return to basal serum creatinine level or creatinine <1.5 mg/dL (male) or <1.3 mg/dL (female) without dialysis. RESULTS: Of one hundred twenty two patients, 79 (65%) patients were male. The mean age was 54+/-16 years and 87 patients (71%) received continuous renal replacement therapy. 55% had ischemic ATN, 29% had septic ATN, and 16% had nephrotoxic ATN. Mean duration of dialysis was 12 (6-29) days. Dialysis withdrawal rate at 30 days and at 60 days after initiation of dialysis were 51% and 77 %, respectively. CR at 60 days after initiation was 50%. Multivariate analysis revealed that older age (per year, Hazard ratio (HR)=0.981, 95% Confidence interval (CI) 0.963 to 0.999), ischemic ATN (vs. toxic ATN, HR=0.481, 95% CI 0.238 to 0.974),and longer duration of oliguria (per day, HR=0.979, 95 % CI 0.962 to 0.996) were independent prognostic factors of renal recovery. CONCLUSION: Young age and short duration of oliguria were favorable factors for renal recovery from ATN requiring dialysis. The cause of ATN might be also an independent prognostic factor.

Association of rOAT1 with Caveolin-1 in Rat Kidney / 대한신장학회지

PURPOSE: A family of organic anion transporters (OAT) has been identified, and several isoforms have been reported. The regulatory mechanisms of OATs functions, however, still remain to be elucidated. The rat OAT1 contributes to move a number of negatively-charged organic compounds between cells and their extracellular milieu. Caveolin (Cav) also plays a role in membrane transport. To address this issue, we investigated the protein-protein interaction between rOAT1 and Cav-1. METHODS: The expressions of rOAT1 and Cav-1 (mRNA and protein) were evaluated using RT-PCR and Western blot analysis. The localization of rOAT1 and Cav-1 was determined in the caveolae-rich membrane fraction isolated by sucrose density gradient ultra-centrifugation. For the direct binding between the rOAT1 and Cav-1 proteins, the immuno-precipitation method and confocal microscopy were employed. To perform functional analysis, a Xenopus oocytes expression system with the antisense oligonucleotides (ODN) technique was used. RESULTS: The expressions of rOAT1 and Cav-1 were detected in the kidney. The caveolae-rich membranous fractions from the kidney contained both rOAT1 and Cav-1 in the same fractions. The immuno-precipitation experiments showed the formation of a complex between the rOAT1 and Cav-1. The confocal microscopy using primary cultured renal proximal epithelial cells also supported the co-localization of rOAT1 and Cav-1 at the plasma membrane. The uptake function of rOAT1, as assessed by using a Xenopus oocytes expression system, was inhibited by the Xenopus Cav-1 antisense ODN. CONCLUSION: rOAT1 co-localizes with caveolin-1 in the caveolae, and caveolin-1 plays an important role in regulating the function of rOAT1.

Influence of albumin-activated renal proximal tubular epithelial cells on peritubular capillaries and its potential mechanism / 中华肾脏病杂志

Objective To explore the influence of albumin-activated renal tubular epithelial cells (RTECs)on peritubular capillaries in co-culture system and its potential mechanism. Methods Endocytosis of TRITC labeled bovine scrum albumin (TRITC-BSA) by HKC was detected by laser scanning confocal fluorescence microscope. HKC or HKC transfected with cubilin (endocytic receptor of albumin) siRNA or pre-treated with rotenone was incubated with albumin(20 g/L) for 24 h respectively. Fluorescence probe technique and spectrometry were applied for determination of intracellular superoxide anion O2-and H2O2 in supematant. Then, the albumin-aetivated-HKC, pretreated-HKC with cubilin siRNA or rotenone, was cultured with HUVEC for 24 h in co-culture system respectively. HUVEC proliferation was determined by MTT and cellular apoptosis was analyzed by flow cytometry. Tabular morphogenesis of endothelial cells was examinedby microscopy. Results TRITC-BSA uptake was obviously lower in HKC transfected with cubilin siRNA. Intracellular generation of O2-and H2O2 in culture supernatant was increased in dose-and time-dependent manner after stimulating with albumin. The levels of O2-and H2O2 were suppressed by cubilin siRNA and rotenone. In co-culture system, albumin-activated-HKC induced endothelial cells apoptosis and inhibited their capillary tubular morphogenesis. Pretreatment of HKC with cubilin siRNA or rotenone could suppress endothelial cells apoptosis and promote capillary tubular morphogenesis. Conclusions There may be a crosstalk between RTECs and peritubular microvascular endothelial cells in renal proteinurie diseases. The generation of ROS by albumin-activated RTECs may play an important role in this process.

Experimental study on apoptosis of renal tubule epithelium after cardiopulmonary resuscitation in rats / 中华急诊医学杂志

Objective To investigate the apoptosis of renal tubule epithelium after cardiopulmonary resuscitation(CPR)in rats and its possible mechanism.Methods Cardiac arrest was induced by asphyxiation(succinylcholine)and ice-cold 0.5 mol/l KCL in rats,and resuscitation started at 5 minutes after arrest.Forty-eight male SD rats were randomly divided into 6 groups:sham(control group);after cardiopulmonary resuscitation rats were allowed to reperfuse spontaneously for 3 hours,6 hours,12 hours,24 hours and 48 hours(n=8,per group).The apoptosis of renal tubule epithelium was assessed by TUNEL.Fas and Bcl-2 protein expression were observed using immunocytochemistry in every group.Results The apoptosis of renal tubule epithelium was singnificantly increased at 3 hours after resuscitation and peaked at 24 hours(P

Expression of Tubular Intercellular Adhesion Molecule-1 (ICAM-1) as a Marker of Renal Injury in Children with IgA Nephropathy

PURPOSE: In order to evaluate the value of the renal expression of ICAM-1 as a marker of renal injury, we analyzed the relationship between abnormal tubular expression of ICAM-1 and histopathological features and clinical manifestations in children with IgA nephropathy (IgAN). METHODS: The clinical data from 43 patients with IgAN were analyzed retrospectively and compared to the histopathologic subclassification proposed by Haas. ICAM-1 in tubular epithelium was assessed using the LSAB(Labeled streptavidine biotin) kit on the renal biopsy specimens. RESULTS: In 43 patients with primary IgAN, 28 males and 15 females aged 12.2+/-2.2 years were studied. There were no differences of renal tubular expression of ICAM-1 between patients with gross hematuria and without gross hematuria. But renal tubular expression of ICAM-1 in patients with proteinuria was significantly higher than that of in patients without proteinuria(78.72+/-14.19% vs. 55.80+/-32.20%, P0.05; F=0.31, P>0.05; F=0.21, P>0.05). CONCLUSION: Renal tubular expression of ICAM-1 can be a useful marker of renal injury in children with IgAN.

A Case of Renal Hypouricemia and Hypercalciuria / 대한신장학회잡지

We encountered a case of renal hypouricemia and absorptive hypercalciuria. Although renal hypouricemia is asymptomatic as usual, it is rarely complicated with acute renal failure and urolithiasis. A 43-year-old man had hypouricemia (serum uric acid, 0.6-1.0mg/dl) with an increased renal uric acid clearance (69.4ml/min), hypercalciuria (367.2mg/day). In present case, there was no response of uric acid excretion to either pyrazinamide or probenecid and hypercalciuria disappeared after calcium restriction diet. These results suggest that the present case had the defect of both pre-and postsecretory reabsorption of uric acid and absorptive hypercalciuria.

Effect of connective tissue growth factor on transdifferentiation of human renal tubular epithelial cell / 中华肾脏病杂志

Objective To investigate the role of connective tissue growth factor (CTGF) in transdifferentiation of human renal tubular epithelial cells (HKC).Methods Cultured HKC were divided into 3 groups: (1) negative control; (2) low dose CTGF treated (rhCTGF 2. 5 ng/ml); (3) high dose CTGF treated (rhCTGF,5. 0 ng/ml). Expression of ?-smooth muscle actin (?-SMA) and fibronectin(FN) mRNA were measured by RT-PCR. Indirect immunofluorescence and flow cytometry methods were used to assess the level of intracellular ?-SMA protein. Concentration of FN secreted into the media was determined by ELBA. Results Upon the stimulations of different concentrations of rhCTGF,expression of ?-SMA and FN mRNA increased markedly(P

Study of renal tubular epithelial cells transformations in rat tubulointerstitial fibrosis / 中华肾脏病杂志

Objective To observe the phenotypic changes between renal tubular epithelial cells and mesenchymal cells in rat tubulointerstitial fibrosis(TIF) .Methods The renal tubulointerstitial fibrosis models of Wistar rats were established by gavage with excessive adenine. The morphological changes of model kidney were observed by light microscopy, electron microscopy, polarizing microscopy. The?-smooth muscle actin(a-SMA), vimentin, and keratin were examined by immunohistochemistry staining. While the proliferating cell nuclear antigen (PCNA) was also assessed. Results There were many 2, 8-dioxyadenine crystals derived from the metabolite of adenine to deposit in the renal tubules, which induced the injury. Tubular epithelial cells degeneration and regeneration, loss of renal tubules, mononuclear cells infiltration in renal interstitium and the accumulation of extracellular matrix protein were observed. Both ?-SMA and vimentin were positive in some of renal tubules. And consecutive sections of immunohistochemical staining showed that the area of distribution of a-SMA positive cells was almost the same area as that of vimentin positive cells. Polarizing microscopy results showed that there was a mass of interstitial collagen ( Ⅲ and Ⅰ) accumulation. And electron microscopy examination proved that epithelial cells invaded into the renal interstitium. Conclusion There is tubular epithelial cells-myofibroblasts transdifferentiation in the process of TIF, and which plays a key role in the accumulation of extracellular matrix.