33 Smad3 plays an essential

role in TGF-β1-induced EMT.34 Evidence of renal EMT has been obtained by numerous independent studies in different animal models of chronic renal disease and also in human kidney biopsies.35–38 The inverse correlation between increasing numbers of tubular epithelial cells undergoing EMT and decline of excretory renal function suggests a pathological role of EMT in the progression of renal fibrosis.39,40 The observation that reversal of EMT improved renal function and decreased mortality in a mouse model with nephrotoxic serum nephritis further confirmed the importance of EMT in the progression of chronic renal disease.34 Advanced glycation end-product (AGE)-induced EMT has been implicated in the pathogenesis of DN.41 TGF-β1, AGE, high glucose,42 angiotensin II43 and oxidative stress44 are also key EMT inducers, shown to be involved in the development and progression of diabetic renal see more fibrosis. Endothelium is a simple squamous epithelium, a specialized type of epithelial tissue. www.selleckchem.com/products/bmn-673.html Thus, EndoMT can be considered to be a specific form of EMT. EndoMT is an essential mechanism in cardiac development.45 During heart valve formation, a subset of EC overlying the future valve site delaminate, differentiate into mesenchymal cells and migrate into the cardiac jelly to form cardiac cushions, a process

referred to as endothelial-mesenchymal transition.46 Disruption of Notch signalling results in failure of EndoMT, revealing an essential role for notch in the control of endocardial cushion EndoMT.47,48 Evidence that wnt/β-catenin signalling was restricted to a subset of mesenchymal cells in endocardial cushions in the developing mouse heart49 and that antagonism of wnt/β-catenin signalling in zebrafish embryos inhibited cardiac cushion EndoMT suggested wnt/β-catenin signalling may activate expression of genes crucial for EndoMT.49β-catenin also acts as a structural link between actin and Vascular Endothelial Cadherin

(VE-cadherin) to form the cell–cell adherens junction necessary for polarity of EC.50 Bone morphogenetic proteins 2 and 4 (BMP-2 and 4), TGF-β2 and TGF-β3 are required for initiation 5-Fluoracil and completion of EndoMT.46 The role of TGF-β and BMP signalling pathways in endocardial cushion EndoMT has been thoroughly studied.51,52 Recent studies have demonstrated that EndoMT contributes to the development of tissue fibrosis. Zeisberg et al.53 used Tie1Cre; R26RstoplacZ mice to track cells of endothelial origin, and placed aortic bands on the hearts of mice to induce cardiac fibrosis. They showed that EC undergo EndoMT during cardiac fibrosis and contribute to the total pool of cardiac fibroblasts. In addition, they showed that TGF-β1 induced EndoMT, whereas BMP7 abrogated EndoMT, preserved the endothelial phenotype and reversed or prevented TGF-β1-induced EndoMT and cardiac fibrosis.

Therefore,

we used flow cytometry-based mixed lymphocyte culture (MLC), the so-called multi-parameter MLC–5-,6-carboxyfluorescein diacetate succinimidyl ester (CFSE)-assay, which can measure simultaneously MS-275 ic50 the precursor frequency of both CD4+ and CD8+ alloreactive T cells, in combination with qualitative T cell properties [22]. We questioned whether this assay would detect differences between patients with various post-transplant outcomes. In this study we show that patients with a high precursor frequency of alloreactive T cells and low percentage of interleukin (IL)-7Rα expressing alloreactive CD8+ T cells before transplantation have an increased risk of acute rejection after transplantation. This study was approved by the Medical Ethics Committee of the Academic Medical Center, Amsterdam (METC 06/157) and informed consent was given by all participants. The study population consisted of 46

renal allograft recipients. Rejectors were selected based on the availability of both patient cells collected before transplantation and donor cells. The non-rejectors were matched for type of donor (i.e. post mortem and living related), age and sex (Table 1). Blood samples were obtained from healthy individuals mTOR inhibitor and from renal transplant recipients on the day of transplantation before start of immunosuppressive treatment and before transplant surgery. Donor cells were derived from peripheral blood of living related donors and from spleen cells of post-mortem donors. As third-party cells, fully human leucocyte antigen (HLA)-A/B/DR mismatched spleen cells were used for post-mortem donor MLC and fully mismatched PBMC were used for living related donor MLC. PBMC were isolated check details from heparinized whole blood by Ficoll density centrifugation (Pharmacia Biotech AB, Uppsala, Sweden). All cells were frozen and stored in liquid nitrogen until the day of analysis. All patients received induction therapy with anti-CD25 monoclonal

antibody (mAb) in combination with maintenance treatment, consisting of prednisolone, mycophenolate and cyclosporin. Twenty-two patients with an uncomplicated post-transplantation course and 24 patients who developed an episode of acute rejection during the first 3 months after transplantation were included. Diagnosis of acute rejection was based on clinical and laboratory criteria, and was followed by a core biopsy in all patients. Biopsies were scored blindly and independently by two pathologists, according to the Banff criteria [23] (Table 2). All rejection episodes, except for the one that was classified as type III, were treated with corticosteroids. The type III T cell-mediated rejection was treated successfully with anti-thymoglobulin (ATG) and plasmapheresis. Response to therapy was evaluated based on the change in plasma creatinine concentration.

The dose of MSC administered to the mice was approximately 1–2 × 106 Flk-1+ MSCs per mouse; compared to 108 or more splenocytes in each mouse, the stimulatory effect of Flk-1+ MSCs might play a dominant role on B cells in CIA animals.

Consistently, MSC-treated mice showed a mild increase in serum IgG compared to untreated CIA mice. Alternatively, the enhancement of splenocyte proliferation and IgG secretion in Flk-1+ MSC-treated mice might be caused by the specific in vivo environment of CIA, rather than a dose-dependent effect of Flk-1+ MSCs observed in in vitro culture. It is known that in vitro suppression in a mixed lymphocyte Alectinib reaction (MLR) does not always correlate with in vivo immune modulation. To address this question, we

should increase the dose given to mice and examine the dose-dependency in vivo. However, we failed to increase the dose of MSC infusion to 1–2 × 107 because of pulmonary embolism and the subsequent death of the animals. The mechanism of the differential regulation of B cell proliferation by MSC in vitro is still unknown. Rasmusson et al. have reported previously that similar differential regulation of human B cells by MSCs might be associated with the intensity of stimulation [23]. The dose effect of MSC and the dose effect of stimulation might share some common mechanisms. IL-6 is a cytokine that enhances see more B cell function. The co-existence of increased production of

IL-6 (Fig. 4) and decreased proliferation of B cells (Fig. 5), while MSCs were co-cultured with splenocytes at ratio of 1:10, indicates that two independent pathways co-exist – one promotes B cells, and the other suppresses B cells. The subtle balance between them may explain the differential regulation of B cell proliferation by MSCs in our and other studies [23]. Flk-1+ MSCs exacerbated CIA only in the day 21 Montelukast Sodium infusion group and not in the day 0 group. The difference in the in vivo physiological environment of the animal between days 0 and 21 might account for this issue. The onset of arthritis begins after the second injection of CII on day 21. Therefore, the physiological condition of the animal on day 21 is closer to that of the animal suffering from arthritis, while the physiological condition of the animal on day 0 is closer to that of the healthy animals. The results of day 0 mice indicated that Flk-1+ MSCs did not have a preventive effect on CIA, and the results of day 21 showed the aggravation risks of treating CIA with Flk-1+ MSCs. In conclusion, we propose that elevated IL-6, by enhancing Th17 and plasma cells, is responsible for the aggravation of CIA after day 21 Flk-1+ MSC treatment (Fig. 6). In Phase II clinical trials of Flk-1+ MSCs, special attention should be paid to patients with rheumatoid arthritis.

All flaps survived completely, a success rate of 100%. Advantages GPCR Compound Library clinical trial of this flap are that there is no need to sacrifice any main artery in the lower leg, and minimal morbidity at the donor site. This free perforator flap may be useful for patients with small to medium soft tissue defects of the distal lower extremities and feet. © 2014 Wiley Periodicals, Inc. Microsurgery 34:629–632, 2014. “
“This study was designed to determine if cigarette smoking adversely affects functional recovery following ischemia/reperfusion (I/R) injury in peripheral nerves. Forty Wistar rats were divided evenly among four groups.

Animals in groups A and B were exposed to cigarette smoke via a controlled smoking chamber for 20 minutes daily. On study day 14, all animals underwent a controlled I/R injury to one sciatic nerve. Recovery was assessed with walking track assessments, malondialdehyde (MDA) assay, and histology. Walking track results on study

day 21 did not differ significantly between the smoking and nonsmoking animals. However, by study day 28, the nonsmoking animals showed a greater degree of functional recovery (SFI = −18.0 and −22.8, respectively, P = 0.03). MDA concentration in the smoking group was significantly higher than the nonsmoking group at the 28 day time point (P = 0.04). Exposure to cigarette smoke was associated with a slower functional recovery following peripheral nerve I/R injury. © 2010 Wiley-Liss, Inc. Microsurgery, 2011. “
“Mikko Larsen, MD, PhD, is currently at Department of Plastic and Reconstructive Surgery, Bronovo Hospital and Medisch Centrum Haaglanden, Bronovolaan 5, The Hague, The Netherlands Ethianum Trichostatin A in vivo Klinik Heidelberg, Heidelberg, Germany We previously demonstrated recipient-derived neoangiogenesis to maintain viability of living bone allogeneic transplants without long-term immunosuppression. The effect of cytokine delivery to enhance this process is studied. Vascularized femur transplantation was performed from Dark Agouti to Piebald Virol Glaxo rats. Poly(d,l-lactide-co-glycolide) Sitaxentan microspheres loaded with buffer (N = 11), basic fibroblast growth factor

(FGF2) (N = 10), vascular endothelial growth factor (VEGF) (N = 11), or both (N = 11) were inserted intramedullarly alongside a recipient-derived arteriovenous bundle. FK-506 was administered for 2 weeks. At 18 weeks, bone blood flow, microangiography, histologic, histomorphometric, and alkaline phosphatase measurements were performed. Bone blood flow was greater in the combined group than control and VEGF groups (P = 0.04). Capillary density was greater in the FGF2 group than in the VEGF and combined groups (P < 0.05). Bone viability, growth, and alkaline phosphatase activity did not vary significantly between groups. Neoangiogenesis in vascularized bone allotransplants is enhanced by angiogenic cytokine delivery, with results using FGF2 that are comparable to isotransplant from previous studies.

Therefore, there is a greater chance of bias in these trials, and thus a note of caution in interpretation, as these findings may be related to suboptimal trial conduct. An additional Selleckchem R788 important finding from this review is the observation that the risk of ESKD is significantly reduced with antioxidant therapy. It has been suggested that anti-inflammatory and antioxidant interventions may provide renal benefits in patients with CKD. This effect is further supported by the overall reduction in serum creatinine levels observed in people receiving antioxidant therapy. The available data suggest that these kidney

function benefits of antioxidant therapy may translate into long-term benefits for major kidney outcomes. There was no clear evidence of harm observed among the trials of antioxidants in CKD patients; however, assessment was limited by a lack of consistent reporting or standardized outcomes by the included trials. Taken together, these findings provide a strong rationale for new properly powered trials to be conducted

in the CKD population, particularly in individuals with more advanced kidney dysfunction as there is evidence to suggest greater benefit from antioxidant Metformin therapy in this group. Such trials are needed to confirm if antioxidant therapy could confer both renal and cardiovascular benefits in people with CKD. “
“ADDITIONAL MEETINGS TO BE HELD AT THE ANZSN ANNUAL SCIENTIFIC MEETING 2014 Saturday 23 August 2014 Sunday 24 August 2014 Monday 25 August 2014 Tuesday 26 August 2014 Nephrology and Transplantation Update Course 0830–1645 Meeting Room 213 Nephrology and Transplantation Update Course 0830–1645 Meeting Room 105 (RACP Advanced Trainees meeting in lunch break) AKTN Breakfast Meeting 0715–0815 Meeting Room 104 Renal Dietitian’s Symposium 0930–1615 Meeting Room 104 Renal Scientist’s Workshop 1330–1530 Meeting Room 107 ANZ Paediatric Nephrology Association 1300–1400 Meeting Room 102 Renal Scientist’s Workshop 1100–1130 Meeting Room 205 ANZSN Council Meeting 0900–1700 Meeting Room 101 “
“Central vein catheters are often used in hemodialysis

Florfenicol patients to gain vascular access when the artero-venous or prosthetic fistula becomes unavailable. Catheter insertion and maintenance, while routine, can result in complications of varying severity that include pneumothorax, arterial puncture, arrhythmias, line fracture, malposition, infection, thrombosis, and fibrin sheath formation.[1] Another type of rare complication associated with catheterization involves the fracture of the guide wire of the catheter.[2] We report here not only the fracture of the catheter guide wire during its insertion in the jugular vein but the absence of clinical signs or complications despite its migration in the right ventricle. A 70-year-old women under chronic hemodialysis presented with thrombosis of her artero-venous fistula used for vascular access.

Forty patients met the criteria and gave their written informed consent for participation in this study. All the participants were on

regular haemodialysis three times per see more week for 4 h by low-flux dialyser with polysulfone/polyamide membranes, reverse osmosis purified water and bicarbonate-containing dialysate. The 40 participants were randomized into two equal groups to receive one dose (0.5 mL) of intramuscular Td vaccine (made by Razi Vaccine & Serum Research Institute, Karaj, Iran) supplemented with either levamisole (100 mg) or placebo daily, 6 days before and 6 days after vaccination. This dosage was already shown to be effective in inducing seroprotection against HBV in haemodialysis patients with minimal side effects.[10] Using Random Allocation Software,[11] blocked randomization with a fixed block size of 4 was done by one of the investigators who had no clinical

involvement in the study. Levamisole and placebo tablets were provided by Shiraz School of Pharmacy in prepackaged bottles numbered for each patient according to the randomization sequence. Each patient was given an order number to receive the corresponding levamisole or placebo bottle. Levamisole and placebo tablets were completely similar in shape, size, weight, colour and taste. Patients, clinical investigators and laboratory staff were all blinded to the treatment assignment. Clinical staff inspected adverse events at each haemodialysis session. For all the enrolled patients, the anti-tetanus IgG serum levels were measured at baseline selleck inhibitor and also at 1 and 6 months after vaccination. Before the start of haemodialysis session, 10 cc blood samples were obtained from the patients’ arms used for haemodialysis access. The serum samples were separated by centrifugation at 3000 g/min for 5 min and stored at −70°C

until analysis. Anti-tetanus second IgG levels were measured by a highly sensitive ELISA kit (IBL International GmbH, Hamburg, Germany). The cut-off value for protective level of anti-tetanus IgG was set at 0.1 IU/mL, based on the EPI Program of WHO.[2] The intra- and inter-assay coefficients of variation were 2.1% and 5.5%, respectively. Statistical analyses were done by the SPSS base 15 (SPSS Inc., Chicago, IL, USA) statistical software package. Quantitative data were compared between the two groups using Mann–Whitney U-test; categorical data were compared using chi-squared or Fisher’s exact tests. P-values of less than 0.05 were considered statistically significant. The primary outcome was the rate of the patients who developed protective anti-tetanus IgG levels 1 and 6 months after vaccination. This study was started in March 2008 and was completed in November 2008. As demonstrated in Table 1, the baseline demographic and laboratory characteristics of the patients were similar in the two groups.

The carotid bifurcation is the primary site for atherosclerotic changes, for which extensive clinical trials and pathological analyses on carotid endarterectomy specimens have been performed. Plaque rupture and erosion give rise to thrombus formation, which leads to brain ischaemic injury. These changes have much in common with atherosclerotic lesions of the subepicardial coronary arteries. Emboli of various types of particles are characteristics of brain ischaemic injury. Thrombi rich in fibrin and red blood cells (red thrombi) that develop in the cardiac chambers are common

sources of cerebral emboli. Small-vessel click here disease of the brain induces fibrinoid necrosis, microaneurysm, fibrohyalinosis, lipohyalinosis and microatheroma, changes commonly associated with hypertension. The acute hypertensive small-vessel changes organize to create segmental arterial disorganization and deep LY2157299 chemical structure small infarcts when they escape from rupture. Some specific vascular diseases responsible for brain ischaemic injury are briefly reviewed also. “
“Transactivation response (TAR) DNA-binding protein of Mr 43 kDa (TDP-43) is a major component of the tau-negative and ubiquitin-positive inclusions that characterize amyotrophic

lateral sclerosis (ALS) and frontotemporal lobar degeneration which is now referred to as FTLD-TDP. Concurrent TDP-43 pathology has been reported in a variety of other neurodegenerative disorders such as Alzheimer’s disease, forming a group of TDP-43 proteinopathy. Accumulated TDP-43 is characterized by phosphorylation and fragmentation. There is a close why relationship between the pathological subtypes of FTLD-TDP and the immunoblot pattern of the C-terminal fragments of phosphorylated TDP-43. These results suggest that proteolytic processing of accumulated TDP-43 may play an important role for the pathological process. In cultured cells, transfected C-terminal fragments of TDP-43

are more prone to form aggregates than full-length TDP-43. Transfecting the C-terminal fragment of TDP-43 harboring pathogenic mutations of TDP-43 gene identified in familial and sporadic ALS cases into cells enhanced the aggregate formation. Furthermore, we found that methylene blue and dimebon inhibit aggregation of TDP-43 in these cellular models. Understanding the mechanism of phosphorylation and truncation of TDP-43 and aggregate formation may be crucial for clarifying the pathogenesis of TDP-43 proteinopathy and for developing useful therapeutics. “
“E.-L. von Rüden, J. Avemary, C. Zellinger, D. Algermissen, P. Bock, A. Beineke, W. Baumgärtner, V. M. Stein, A. Tipold and H.

Compared to the more frequent invasive Pexidartinib fungal

infections like cryptococcosis, candidiasis and aspergillosis, infections by mucormycetes (mucormycoses) are rather uncommon.[1] However, the number of mucormycosis cases is increasing, especially in patients with underlying immunosuppression.[2, 3] Treatment of these infections is difficult and requires fast initiation of antifungal therapy, often in combination with extensive surgical debridement. Despite appropriate treatment, overall mortality still reaches approximately 50%.[4, 5] More than 20 mucoralean species are known to cause infections in humans, with R. oryzae as the most frequently isolated species worldwide. In Europe, members of the genus Lichtheimia are the second to third most important cause of mucormycoses.[6, 7] The following review will summarise the current taxonomy of the genus Lichtheimia, its role as human pathogen and cause of disease in other species, and will provide a brief overview of infection models used to study Lichtheimia infections. The genus Lichtheimia (ex Absidia, Mycocladus) belongs to the family Lichtheimiaceae, one of the most basal families in the fungal order Mucorales.[8, 9] To date, six species have been described: L. corymbifera, L. ramosa, L. ornata, L. hyalospora, L. sphaerocystis and L. brasiliensis.[10] The taxonomy of the members of this genus has been changed

repeatedly: L. corymbifera was originally described 1884 as Mucor corymbifer by Cohn[11] before being placed within the mesophilic genus Absidia. Selleck GSK3 inhibitor Based on their higher temperature optimum (>30 °C – 37 °C), morphology and molecular phylogeny, the thermophilic species within Absidia, CYTH4 including current members of Lichtheimia, were reclassified into the genus Mycocladus, resulting in the species designations M. corymbifer, M. hyalosporus and M. blakesleeanus.[8] However, the name had to be corrected to Lichtheimia to comply with the International

Code of Botanical Nomenclature.[12] Finally, Alastruey-Izquierdo et al. described five species, L. corymbifera, L.ramosa, L. ornata, L. hyalospora and L. sphaerocystis, within the genus, based on physiological, morphological and phylogenetic data.[10] Recently, a new species, L. brasiliensis, has been described which represents the most basal species within Lichtheima.[13] All species of Lichtheimia grow well on artificial media and have a growth optimum between 30 °C and 37 °C.[10] Mucoralean fungi are ubiquitous saprophytes and are globally distributed. Soil is believed to be the main habitat of most Mucorales, but some of these fungi can also be found in decaying vegetation and rotting fruits.[14] In addition, Lichtheimia species can be found in a variety of substrates including farming products like hay and straw as well as processed and unprocessed food products like flour and fermented soybeans.[15-21] Interestingly, L. corymbifera and L.

At 2 weeks (primary endpoint), overall cure rate was superior in bifonazole-treated group (54.8% vs. 42.2% for placebo; P = 0.0024). The clinical cure rate was high in both

treatment groups (86.6% bifonazole vs. 82.8% placebo), but proportion with mycological cure was higher with bifonazole treatment (64.5%) vs. placebo treatment 49.0%, (P = 0.0001). We observed higher early overall cure rate with 4 weeks topical bifonazole compared with placebo after removal of infected nail parts with urea. This two stage treatment was well tolerated and offers an additional option in topical onychomycosis therapy. “
“Significant changes in the frequency of candidaemia and the distribution of causative species have been noted worldwide in the last two decades. In this study, we present the results of the first multicentre survey of fungaemia in Polish hospitals. A total of 302 candidaemia episodes in 294 Ku-0059436 supplier patients were identified in 20 hospitals during a 2-year period. The highest number of infections was found in intensive care (30.8%) and surgical (29.5%) units, followed by haematological (15.9%), ‘others’ (19.2%) and neonatological (4.6%) units. Candida albicans was isolated from 50.96% of episodes; its prevalence was higher in intensive care unit and neonatology (61.22% and 73.33%, respectively),

and significantly lower in haematology (22%; P < 0.001). The frequency of C. krusei and C. tropicalis was significantly higher (24% and 18%) in haematology (P < 0.02); Z-VAD-FMK molecular weight whereas, the distribution of C. glabrata (14.1%) and C. parapsilosis (13.1%) did not possess statistically significant differences between compared departments. Obtained data indicates that species distribution of Candida blood isolates in Polish hospitals reflects worldwide trends, particularly a decrease in Ureohydrolase the prevalence of infections due to C. albicans. “
“Diagnostic efficacy of Galactomannan

(GM) assay for invasive aspergillosis (IA) is variably reported. Data from developing countries are scant. Children with haematological malignancies and fever were enrolled prospectively. Blood sample for GM was drawn on the day of admission; levels were measured with Platellia Aspergillus enzyme immunoassay. Diagnostic criteria were adapted from EORTC-MSG-2002. Proven, probable and possible episodes were considered as the disease group. One hundred febrile episodes in 78 patients were evaluated. The mean age was 6.1 years. Majority (75%) episodes were in patients with acute lymphoblastic leukaemia. One episode each was diagnosed with proven and probable IA, while 23 were diagnosed with possible IA. Best results were obtained with a cut-off value of 1.0, with sensitivity, specificity, positive and negative predictive value of 60%, 93%, 75 and 87 respectively. The sensitivity dropped to 40%, at cut-off value of 1.5 and specificity was 38%, at a cut-off of 0.5.

Conclusion: This study suggested that initial use of mPSL accelerates remission of proteinuria and suppresses incidence of relapse of proteinuria in adult-onset MCD patients. Efficacy of mPSL + PSL should be evaluated

in a randomized controlled trial. NAKASATOMI MASAO, MAESHIMA AKITO, SAKURAI NORIYUKI, IKEUCHI HIDEKAZU, SAKAIRI TORU, KANEKO YORIAKI, HIROMURA KEIJU, NOJIMA YOSHIHISA Department of Medicine and Clinical Science, Gunma University Graduate School find more of Medicine Introduction: Epithelial-mesenchymal transition (EMT) in renal fibrosis is generally defined by the loss of epithelial markers and the acquisition of mesenchymal phenotypes by damaged tubules. However, structural details of this process buy Acalabrutinib have not been clarified. Using bromodeoxyuridine (BrdU)

labeling method, we previously reported that renal progenitor-like tubular cells, also called as label-retaining cells, migrated into the interstitium after unilateral ureteral obstruction (UUO) (JASN 16: 2044–51, 2005). By modifying this method, we examined in this study whether EMT process could be detected and quantified in vivo. Methods: Using osmotic pump, BrdU (20 mg/kg/day) was continuously given into 7-week-old Wistar rats for 1, 2, 3 and 4 weeks. UUO was induced in these rats and the kidneys were removed at 4, 6, 8, 10 days after UUO. Localization, phenotype, and number of BrdU-positive cells were examined by immunostaining. Results: The number of BrdU-positive cells was positively associated with labeling period. BrdU-positive cells were detectable in AQP1-positive proximal tubules, but not in the

interstitium of normal rat kidneys. Most proximal tubular cells became BrdU-positive after 4-week labeling. After UUO, some of BrdU-positive tubular cells were protruded from the basement membrane and were migrated into the interstitium. Interstitial BrdU-positive cells were co-localized with alpha-SMA, fibroblast-specific protein Carnitine palmitoyltransferase II 1, and type I collagen. The number of interstitial BrdU-positive cells significantly increased and reached the maximum at 8 days after UUO. Few BrdU-positive cells were observed in the interstitium of normal and sham-operated kidneys. Conclusion: Long-term BrdU treatment labels most proximal tubular cells with BrdU and enabled us to detect and quantify EMT in vivo. This technique will be useful for the search of novel EMT inhibitor(s) for the treatment of renal fibrosis. VILLALOBOS RALPH ELVI M, AHERRERA JAIME ALFONSO, MEJIA AGNES University of the Philippines-Philippine General Hospital Synopsis: Hypertension in the young is commonly due to a primary renal disease. We present a case of a 22- year old male with manifestations of nephrotic syndrome and secondary hypertension. During admission, multiple morbidities plagued him and he expired.