Retroperitoneal fibrosis (RPF) is a rare disease. It is characterized by the presence of fibro-inflammatory tissue involving retroperitoneal structures. The usual mode of presentation of this disease is with lumbar pain, kidney failure, and a biological inflammatory syndrome. The aim of our study is to describe the diagnostic, etiologic, therapeutic aspects and outcomes of RPF in a nephrology unit in Morocco. Twelve cases of RPF were included in our study. The mean age was 57 ± 10 years (32.70). Nine patients were male and three were female. Symptoms were highly variable, dominated by pain that was present in all patients. Venous compressive signs were described in four patients (33.3%), anuria in one patient (8.3%), and hematuria in two patients (16.6%). Laboratory examinations found an inflammatory syndrome in all patients and renal failure in nine patients (75%), with a mean serum creatinine at 35 mg/L ± 8.5. Diagnosis was suspected on the ultrasound data and confirmed by computed tomography or magnetic resonance imaging. RPF was idiopathic in nine patients (75%). It was secondary to aortic aneurysm in one patient (8.3%), Riedel’s thyroiditis in one patient (8.3%), and drug induced in another patient (8.3%). All patients received surgical treatment along with corticosteroids. At six months, remission was achieved in nine patients, whereas three others had steroid resistance. These patients were treated by mycophenolate mofetil (MMF) at a dose of 2 g/day; two of them had intestinal intolerance to MMF and thus were treated by tamoxifen at a dose of 40 mg/day. At 24 months, they stabilized their renal function with incomplete regression of the fibrotic plate. No cases of recurrence were observed during the study period.Thrombotic microangiopathy (TMA) after kidney transplant is rather uncommon but an important reversible cause of graft loss. This retrospective study of biopsy-proven posttransplant TMA was done to identify the important etiological factors, clinical features, and outcomes of post transplant TMA in a tertiary care referral hospital in northern India. This retrospective study was conducted among all renal transplant recipients who presented with graft dysfunction between 1989 and 2015. All the cases were looked for their etiology, clinical course, treatment modalities, and renal outcomes. The study was conducted in accord with prevailing ethical principles and reviewed by our own institutional review board. Seventeen patients out of 2000 (0.008%) transplants done during the study period had posttransplant TMA, out of which all the patients had de novo TMA, and the median time of presentation after transplantation was four months. Systemic TMA was noted in only four patients. Biopsy revealed associated rejection in five patients and associated calcineurin inhibitor (CNI) toxicity in 12 patients. Patients with TMA due to CNI toxicity were managed with CNI reduction or switching to alternate CNI or mammalian target of rapamycin inhibitors. In addition, antithymocyte globulin and plasma exchange were used in rejection-associated TMA. While four out of 12 patients (33%) in CNI-related TMA developed end-stage renal disease (ESRD), all patients in rejection-associated TMA developed ESRD. The overall one-year graft survival was 47%, whereas five- and 10-year survival was 35%. There was no significant difference in graft survival between localized and systemic TMAs (P = 0.4). Posttransplant TMA should be suspected even if there are no systemic features of hemolysis and early graft biopsy and prompt action is needed. The occurrence of TMA in the setting of rejection is associated with grave prognosis.Today, we witness an increase in the prevalence of chronic kidney disease, which is a very stressful process. In order to cope with the stress caused by this disease, the first step is to appraise the stressful situation correctly. Therefore, the present study was conducted with the aim of investigating the effect of training on the basis of Lazarus and Folkman transactional model on stress appraisal for hemodialysis (HD) patients. The present quasi-experimental study was conducted on 116 filed HD patients in two dialysis centers in Tehran. The patients were randomly divided into two groups experimental and control groups. The data were collected using a researcher-made questionnaire whose validity and reliability were confirmed. After performing the intervention, the primary and secondary appraisals’ scores were investigated before and three months after the intervention. The data were analyzed using independent /?-test, paired /-test, and covariance at a significant level of 0.05 using software Statistical Package for the Social Sciences version 16.0. selleck inhibitor The mean age of participants in the study was 52.86 years. In this study, the difference between the mean score of the primary appraisal and substructure of perceived susceptibility, motivational relevance, self-blame (casual focus), and secondary appraisal and self-efficacy substructure after the intervention was significant in the experimental group. However, these differences were not significant in the control group. According to the study results, it can be concluded that the use of training based on Lazarus and Folkman tran- sactional model can be useful for improving the correct appraisal of individuals for stressful situations.Nephrotic syndrome (NS) is characterized by proteinuria in children. Steroid- resistant NS (SRNS) is defined by resistance to standard steroid therapy, and it continues to be one of the most common causes of chronic renal failure. Molecular studies have revealed specialized molecules in different regions of the podocytes that play a role in proteinuria. Mutations in NPHS2 that encode for podocin constitute a frequent cause of SRNS worldwide. This study aimed to screen for podocin mutations in Azerbaijani patients with SRNS. Our study included 21 pediatric patients with SRNS aged between 0 and 18 years and the same number of healthy control groups. Mutational analysis of the NPHS2 gene was performed using direct sequencing methods. Disease-causing mutations in the NPHS2 gene were detected in eight patients (38%). Thirteen patients (62%) had NPHS2 mutations without causing the disease. Two patients had p.Val290Met homozygous mutation; two had p.Arg229Gln homozygous mutations; and one each had p.Pro20Leu homozygote, p.