Atherosclerotic renovascular disease (ARVD) is the most common cause of renal artery stenosis (RAS). ARVD is associated with an increased risk of progression of kidney disease and high mortality. In this regard, the aim was to evaluate the effects of the factors on kidney functions in short- and long-term follow-ups. Patients with RAS treated with renal artery stenting since January 2015 were evaluated retrospectively in a single center. The primary endpoint was a decline in the estimated glomerular filtration rate (eGFR) of ≥ 20 ml/min and/or evolution to end stage kidney disease. Predictors of the primary endpoint were determined using the Cox regression model. Of the 95 patients included, 57 (56.4

Background Signal transducer and activator of transcription 3 (STAT3) protein is activated in lung fibroblasts and alveolar type II cells (AT-II) and is thought to contribute to fibrosis in lung tissue. Significant JAK/STAT activation was demonstrated in fibroblasts, skin biopsies and scleroderma animal models of patients with Systemic Sclerosis (SSc) [1]. Objectives The aim of this study was to determine whether inhibition of JAK2/STAT3 in the experimental model of scleroderma is a potential therapeutic strategy for this disease and to investigate the effects of the JAK 1-2 inhibitor Baricitinib (BAR) on the experimental model of dermal and pulmonary fibrosis. Methods Thirty-two healthy 6-8 weeks old female C57BL mice with an average weight of 22±3 grams were included in our study. Before the treatment (baseline), day 15 and day 30 (day 30) the same back area was shaved in all mice and skin thickness was measured under the guidance of skin Ultrasound Biomicroscopy (US). US measurements were chosen to be at least >1 cm from the injection area. Whole lung Computed Tomography (CT) scans of each animal were acquired at post-treatment (day 30). H&E and Masson's Trichrome staining were performed to evaluate skin thickness, pulmonary alveolitis, and fibrosis. The Ashcroft score was assessed on Sirius Red stained lung sections post-treatment. For the molecular evaluation of tissue fibrosis, collagen and α-SMA levels were measured in skin and lung tissues by qRTPCR. Results We found that BAR resulted in favorable therapeutic outcomes by affecting the inflammation infiltration and collagen deposition both lung and skin tissues. Immunohistochemical results showed that BAR downregulated the levels of COL1A1 and COL1A2.Treatment with JAK 1-2 selective BAR has been shown to ameliorate BLM-induced skin and lung fibrosis at radiological, pathological and molecular measurements. Conclusion As a result of our study, the effect of JAK1-2 selective inhibitor baricitinib treatment on reducing skin and lung fibrosis in a mouse model created with BLM was demonstrated with radiological and pathological examinations. We conclude that JAKinh treatments will be an important research area for the treatment of SSc and other fibrotic diseases in the future. Reference [1]Wang W, et al. The JAK/STAT pathway is activated in systemic sclerosis and is effectively targeted by tofacitinib. J Scleroderma Relat Disord. 2020;5(1):40–50. Acknowledgements: NIL. Disclosure of Interests None Declared.Figure 1Dermal thickness change with UBM baseline, 2th and 4th week.Table 1Skin and lung measurementsBLM (I)BLM+BAR (II)BLM+PBO (III)PPairwise comparisonMean (SD.)Mean (SD.)Mean (SD.)I vs III vs IIIII vs IIIDermal thickness (with H&E and MT) (μm)430.29 (54.66)308.00 (26.79)452.50 (75.48)0.001 a<0.0010.721<0.001Dermal thickness (with UBM) (μm)524.86 (116.21)304.20 (61.45)505.67 (88.09)<0.001 a<0.0010.919<0.001Median (min-max)Median (min-max)Median (min-max)Ashcroft Score (0-8)5 (2-7)1 (0-4)3 (2-5)0.001 k0.0020.6300.176n (%)n (%)n (%)SSc-ILD in CT0.215 ffAbsent2 (28.6)7 (70)2 (33.3)ns.ns.ns.Present5 (71.4)3 (30)4 (66.7)ns.ns.ns.a OneWay ANOVA (Robuts Statistic:Brown-Forsythe); Post Hoc Test: Tukey HSD, k Kruskal Wallis Test (Monte Carlo); Post Hoc Test: Dunn's Test, ffFisher Freeman Halton (Monte Carlo), ILD: Interstitial lung disease, UBM: Ultrasound biomicroscopy, H&E: hematoxylin and eosin staining, MT: Masson's Trichrome staining, ns.: non significant, min.: minimum, max.: maximum, SD.:Standard deviation, BLM: Bleomycine induced SSc group, BLM+BAR: Bleomycine with Baricitinib group, BLM+PBO: Bleomycine with Placebo group

Acute pancreatitis is a relatively rare complication of continuous ambulatory peritoneal dialysis (CAPD) treatment. Diagnosis of acute pancreatitis may be difficult. It should also be considered in cases of culture-negative perotinitis. We are presenting a 38 year old female with rarely encountered acute pancreatitis resulting in pancreatic pseudocyts and obstruction.

Editor: We read the recent International Society for Peritoneal Dialysis (ISPD) peritonitis guidelines and recommendations (1). In the guideline, only Löwenstein-Jensen culture of peritoneal fluid, mycobacterial DNA PCR (polymerase chain reaction), and laparoscopic peritoneal biopsy are advised as a diagnostic work-up in tuberculous (TB) peritonitis. The principle of the adenosine deaminase (ADA) assay is to detect either hydrogen peroxide or ammonia after enzymatic deamination of adenosine to inosine. Production of the enzyme ADA in bodily fluids reflects the presence of activated T lymphocytes and monocytes (2). Many studies have investigated the usefulness of ADA in ascites for the diagnosis of TB peritonitis (3,4,5). Two metaanalyses suggested that ADA in the ascites can be a sensitive and specific target and a critical criterion for the diagnosis of TB ascites (6,7). Riquelme et al. reported a meta-analysis which included 12 prospective studies. They investigated 264 patients, of whom 50 (18.9%) had peritoneal tuberculosis. Adenosine deaminase levels showed high sensitivity (100%) and specificity (97%) using cut-off values from 36 to 40 IU/L (8). Some studies have shown that ADA assay sensitivity is substantially lower in patients with cirrhosis due to poor humoral and T-cell mediated response (9). A question that arises here is whether the ADA assay is reliable in immunocompromised patients, such as those with chronic kidney and liver diseases. We would therefore like to discuss using the ADA assay for diagnosis of TB peritonitis in peritoneal dialysis (PD) patients. In the literature, there are limited data for using ADA assay in continuous ambulatory PD (CAPD) patients. In one case report, patients with end-stage renal failure were tested for ADA levels in the peritoneal fluid, allowing an early presumptive treatment and a favorable outcome with a 3-year follow-up (10). On the other hand, in a study by Nakav et al., bacterial peritonitis was induced in mice by intraperitoneal injection of Escherichia coli. Following inoculation, ADA mRNA levels and activity in the lavage fluid significantly increased at 48 hours in the late phase of bacterial peritonitis (11). In conclusion, the ADA assay is inexpensive, quick, and simple to perform and has great value for the immediate diagnosis of tuberculous serositis while culture results are pending. It is clear that large-scale studies on the diagnostic value of the ADA assay in chronic renal failure and CAPD patients are needed. In the next guideline, the usefulness of ADA assay should be evaluated in CAPD patients.

Dysregulated expression of matrix metalloproteinases (MMPs) is closely associated with the pathogenesis of renal ischemia/reperfusion injury (I/R). The production of excessive reactive oxygen species (ROS) causes tissue damage. Increased ROS production causes activation of p38 mitogen-activated protein kinase (MAPK) signaling, which participates in gene regulation of MMPs, especially MMP-2 and MMP-9 (gelatinases). Taurine (2-aminoethanesulfonic acid) in mammalian cells functions in bile acid conjugation, maintenance of calcium homeostasis, osmoregulation, membrane stabilization, and antioxidation, antiinflammatory, and antiapoptotic action. We investigated the effects of taurine and the possible role of p38 MAPK signaling on regulation of MMP-2 and MMP-9 in a renal I/R injury model in rats. Rats were divided into three groups: sham, I/R, and I/R + taurine treated. After a right nephrectomy, I/R was induced by clamping the left renal pedicle for 1 h followed by 6 h reperfusion. Taurine was administered 45 min prior to induction of ischemia. Renal function was assessed by serum creatinine and blood urea nitrogen (BUN) levels. Tubule injury and structural changes were evaluated by light microscopy. Malondialdehyde (MDA) levels were analyzed by high performance liquid chromatography (HPLC). Superoxide dismutase (SOD) activity levels were measured using a colorimetric kit. mRNA expression of MMP-2 and MMP-9 was determined by real-time polymerase chain reaction. MMP-2 and MMP-9 activities were measured using a fluorimetric kit. Phosphorylated p38 (p-p38) and total p38 MAPK protein expressions were evaluated by western blot. Taurine pretreatment significantly attenuated renal dysfunction and histologic damage, such as renal tubule dilation and loss of brush borders. The pretreatment also decreased the MDA level and attenuated the reduction of SOD activity in the kidney during I/R. Taurine pretreatment also decreased significantly both MMP-2 and MMP-9 mRNA expression and MMP-9 activity induced by I/R. In addition, the activity of p38 MAPK signaling was down-regulated significantly by taurine administration. Inhibition of MMP-2 and MMP-9 expression and MMP-9 activity caused by taurine may be associated with suppression of p38 MAPK activation during I/R induced renal injury in rats. Therefore, taurine administration may prove to be a strategy for attenuating renal I/R injury.

Objective Hepcidin may be an important mediator in exercise-induced iron deficiency. Despite the studies investigating acute exercise effects on hepcidin and markers of iron metabolism, we found no studies examining the chronic effects of walking exercises (WE) on hepcidin and markers of iron metabolism in premenopausal women. The chronic effects of two 8-week different-intensity WE on hepcidin, interleukin 6 (IL-6), and markers of iron metabolism in pre-menopausal women were examined. Methods Exercise groups (EG) [moderate tempo walking group (MTWG), n = 11; brisk walking group (BWG), n = 11] walked 3 days/week, starting from 30 to 51 min. Control group (CG; n = 8) did not perform any exercises. BWG walked at ∼70%-75%; MTWG at ∼50%-55% of HRRmax. VO2max, hepcidin, IL-6, and iron metabolism markers were determined before and after the intervention. Results VO2max increased in both EGs, favoring the BWG. Hepcidin increased in the BWG (p < 0.01) and CG (p < 0.05). IL-6 decreased in the BWG and the MTWG (p < 0.05; p < 0.01). While iron, ferritin, transferrin, and transferrin saturation levels did not change in any group, total iron binding capacity (p < 0.05), red blood cells (p < 0.05), and hematocrit (p < 0.01) increased only in the BWG. Conclusion Both WE types may be useful to prevent inflammation. However, brisk walking is advisable due to the positive changes in VO2max and some iron metabolism parameters, which may contribute to prevent iron deficiency. The increase in hepcidin levels remains unclear and necessitates further studies.

We aimed to compare the serological profiles of the pups that were housed with their biological mothers and the ones which were transferred to foster-dams after birth, with regard to certain viral agents.The day of delivery for the pregnant rat is recognized as the postnatal day 0 (P0).The pups born from Group 1 [P(0), P(21), P(60)] pregnant rats were housed with their biological mothers.In Group 2 [P(1), P(21), P(60)], however, P(1) consisted of pups housed with their biological mother for 24 hours while P(21) and P(60) consisted of pups transferred from the their biological mother immediately at birth.Antibody response against Lymphocytic Choriomeningitis Virus (LCMV), Rat Parvo Virus (RPV), Sendai Virus (SV) and Toolan's H1 viruses was not detected in dams and pups of all the groups, whereas high rate (45%) of antibody positivity was observed in response to Kilham' Rat Virus (KRV).No statistically significant difference was determined between the pups left with their biological mother and with the foster mothers, except for Murine Adeno Virus type 1, type 2 (MAD 1 and 2), Reovirus type 3 (REO-3) and Theiler's Murine Encephalomyelitis Virus (TMEV).It was conspicuous in terms of REO-3 that for the pups it was essential to stay with their biological mothers and nursed during the first 24 hours.As a result, foster mother usage in breeding laboratory animals is found to be beneficial against a variety of viral agents for the pups particularly in the later period of their lives and we suggest to continue this implementation in routine laboratory practice whenever necessary.

Background: Ischemia-reperfusion injury (IRI) is a leading cause of acute kidney injury (AKI). The inflammatory response that drives IRI involves upregulation of matrix metalloproteinases (MMPs), which results in proteolytic degradation of renal microvascular matrix. Evidence suggests a potential protective role of active vitamin D on ischemic injury by downregulating MMPs. In the present study, we aimed to determine the expression and level of MMP-2 and MMP-9 in renal IRI model and the potential beneficial effect of paricalcitol on both level and expression of MMPs and tubular injury caused by IRI. Materials and methods: 20 Wistar albino rats were divided into three groups: sham-operated, ischemia-reperfusion, and paricalcitol-pretreated. IRI model was induced by bilateral clamping of renal arteries for 45 minutes followed by 24 hours of reperfusion. The analysis of serum creatinine and levels of MMPs were performed after 24 hours of IRI. The effects of paricalcitol on the quantity and expression of MMP-2 and MMP-9 in renal tubular epithelial cells were investigated by enzyme-linked immunosorbent assay and immunohistochemistry, respectively. The pathological examinations were performed to score tubular damage by light microscopy. Results: Creatinine levels decreased in the paricalcitol group, although this was not proven to be significant. Rats in the paricalcitol group showed significant decrease in both level and expression of MMPs and in tubular injury scores as compared to the IRI group. Conclusion: Paricalcitol may attenuate renal tubular injury caused by IRI by decreasing both level and expression of MMPs. Further studies are required to investigate the interplay between activated vitamin D and MMPs in AKI.

INTRODUCTION:Because of the shortage of organs available for transplantation, living related sequential transplantation with the use of liver and a kidney from the same donor has emerged as a reasonable therapeutic alternative. However, there is insufficient literature about the complications that living donors experience after simultaneous kidney and liver transplantations. METHODS:From December 2001 to October 2009, 5 living donors provided simultaneous donation of livers and kidneys and 1 living donor donated first her kidney and then her liver. Demographic data of the donors and information concerning the surgery and postoperative observation were collected prospectively. RESULTS:All of the donors were female. The median age was 27.5 (range, 19-36) years. Indications requiring the simultaneous transplantation of livers and kidneys were primary hyperoxaluria type 1 (PH1) in 5 potential recipients and cirrhosis due to chronic hepatitis B infection and idiopathic chronic renal insufficiency in 1 potential recipient. Four recipients underwent right hepatectomy (segments 5-8) and right nephrectomy; 1 recipient underwent left hepatectomy (segments 2-4) and right nephrectomy; and 1 recipient underwent left lobectomy (segments 2-3) and right nephrectomy. There were no complications except in 1 donor (postoperative ileus). No donor developed hypertension or microalbuminuria. CONCLUSIONS:With the right indications, appropriate preoperative evaluation, meticulous surgical technique, proper postoperative care, and long-term close monitoring to minimize morbidity and mortality risks, liver and kidney donation from the same donor can be considered for simultaneous kidney and liver transplantation.

OBJECTIVE:Ischemia/reperfusion (I/R) injury is a major cause of acute organ dysfunction and I/R related acute renal failure is a common clinical problem. Diabetes mellitus is defined as a risk factor for the development of acute renal injury as diabetic nephropathy compromises the renal tolerance to ischemia. The aim of this study was to investigate the protective effect of magnesium sulfate in a diabetic rat renal I/R injury model.MATERIALS AND METHODS:Diabetes mellitus was induced using streptozotocin. Thirty-five rats were divided into five groups: Group I: Nondiabetic sham group; Group II: Diabetic sham group; Group III: Diabetic I/R group; Group IV: Diabetic I/R + prophylactic (preischemic) MgSO4; and Group V: Diabetic I/R + therapeutic (following reperfusion) MgSO4 group. MgSO4 was administered 200 mg/kg intraperitoneally. Renal I/R (45 min ischemia + 4 h reperfusion) was induced in both kidneys. Histomorphological, immunohistochemical (caspase-3 and iNOS) and biochemical (BUN, Creatinine) methods were performed to assess the blood and tissue samples.RESULTS:Histomorphological injury scores and immunostaining intensities (for both caspase-3 and iNOS) were significantly lower in the MgSO4 administered groups (prophylactic and therapeutic) than in the Diabetic IR group. There were no significant differences in biochemical parameters (BUN, Cr) between the MgSO4 administered groups and the Diabetic IR group.CONCLUSIONS:In the present study, it was demonstrated by histomorphological and immunohistochemical methods that magnesium sulfate administration before ischemia or following reperfusion significantly reduced renal I/R injury in a diabetic rat model.

A 42 year old male patient was admitted to our clinic with complaints of pain, tenderness and mass on the xyphoid process. Radiologic findings indicated benign pathologies. In the follow up, growth in the mass was investigated and surgical exicion was performed. Histopathologic investigation revealed the diagnosis of osteochondroma. Here we report an extremely rare chest wall tumor and different localisation which was an osteochondroma in the xyphoid process. (Tur Toraks Der 2011; 12: 79-80)