IgA nephropathy (IgAN) is a heterogeneous disease with highly variable clinical and histopathological features. We investigated the effects of Oxford classification and clinical features on renal survival in patients with IgAN. This retrospective observational study conducted from 2013 to 2017. Ninety-seven patients who were followed up more than six months were examined. A total of 97 patients (68% male and median age 40 years) were enrolled in this study. 13% of patients developed end stage renal disease (ESRD) within the median of 37 months of follow-up. Need for renal replacement therapy at the time of diagnosis, serum creatinine level of higher than 1.97 mg/dl, serum albumin level less than 3.5 gr/dl, 24-hour urine protein level of higher than>3.5 g/day, the percentage of glomerulosclerosis higher than 53%, T2 score and total MEST-C score higher than two were found to be significant predictors of development of ESRD. None of the clinical or histopathological features were found to be significant predictor of steroid treatment sensitivity except T1-2 scores. We think that IgA nephropathy is a heterogeneous disease that requires clinical and histopathological features to be evaluated together, but not individually, to determine renal survival.We think that IgA nephropathy is a heterogeneous disease that requires clinical and histopathological features to be evaluated together, but not individually, to determine renal survival. COVID-19 disease was associated with both thrombo-embolic events and in-situ thrombi formation in small vessels. Antiphospholipidic antibodies were found in some studies. Assessment of protein S activity in patients with COVID-19 as a cause this prothrombotic state, and of the association of protein S activity with worse outcome. All patients admitted for COVID-19 disease in a university hospital between 15th of May and 15th of July 2020 were prospectively enrolled into this cohort study. Patients treated with antivitamin K anticoagulants and with liver disease were excluded. All patients had protein S activity determined at admission. The main outcome was survival, secondary outcomes were clinical severity and lung damage. 91 patients were included, of which 21 (23.3%) died. Protein S activity was decreased in 65% of the patients. Death was associated with lower activity of protein S (median 42% vs. 58%, p<0.001), and the association remained after adjustment for age, inflammation markers and ALAT. There was a dose-response relationship between protein S activity and clinical severity (Kendall_tau coefficient = -0.320, p < 0.001; Jonckheere-Terpstra for trend p<0.001) or pulmonary damage on CT scan (Kendall_tau coefficient = -0.290, p<0.001; Jonckheere-Terpstra for trend p<0.001). High neutrophil count was also independently associated with death (p=0.002). Protein S activity was lower in COVID-19 patients, and its level was associated with survival and disease severity, suggesting that it may have a role in the thrombotic manifestations of the disease.Protein S activity was lower in COVID-19 patients, and its level was associated with survival and disease severity, suggesting that it may have a role in the thrombotic manifestations of the disease. Congenital cytomegalovirus (cCMV) infection can be easily prevented by hygienic measures. Up to date the majority of the studies in literature highlighted a reduction in cCMV antenatal counseling and its prevention. Our purpose was to evaluate obstetrics providers' knowledge about cCMV infection, management and the behavioral practices to avoid it. This is a cross-sectional survey carried out in Umberto I Hospital, "Sapienza" University of Rome between November 2019 and January 2020. We recruited 148 specialists and residents in Obstetrics and Gynecology through online anonymous multiple-choice 13-questions, 10min-survey comparing responses between the two groups. A total of 94.6% of all participants said they always prescribe cytomegalovirus (CMV) serum screening 73.6% of them regularly counsel about preventive practices, with specialists recording higher percentages (85.4 vs. 65.1%, p<0.005). We identified a good knowledge about the diagnostic pathway, but only 58.1% of our population knows the correct time of late amniocentesis. 12.2% of providers do not consider magnetic resonance (MRI) as a complementary exam. Prevention of maternal seroconversion is crucial even if our data show an acceptable knowledge about antenatal counseling, we encourage clinicians to firmly inform and educate women about behavioral measures.Prevention of maternal seroconversion is crucial even if our data show an acceptable knowledge about antenatal counseling, we encourage clinicians to firmly inform and educate women about behavioral measures.Introduction Primary adrenal insufficiency is a potentially life-threatening condition that can have many underlying causes. find more Mutations in the steroidogenic acute regulatory protein (StAR) gene produce lipoid congenital adrenal hyperplasia (LCAH) which usually presents in the infantile period with severe symptoms of adrenal insufficiency. Less commonly, a non-classical form is identified which may present at a later age in affected individuals. Till date, around 30 individuals with the non-classical form have been described. Case presentation We describe a 4-year-old 46, XX Indian girl who presented with hypoglycemic seizures and was subsequently diagnosed as non-classical LCAH on genetic analysis, with homozygous R188C mutation in the StAR gene. Conclusions StAR mutations may have a variety of clinical presentations and are likely under-diagnosed. Genetic diagnosis is important for treatment as well as monitoring of reproductive function.Objectives Hyperinsulinemic hypoglucemia (HH) is characterized by a dysregulation of insulin secretion from pancreatic β cells. Congenital hyperinsulinism has been associated with specific genes in monogenic forms and also with other diseases with a yet unknown genetic cause. In 2017, Rubio Cabezas et al. described the association of HH and autosomal recessive polycystic kidney disease (ARPKD) with a promoter mutation in the PMM2 gene. They found that all the patients carried a promoter mutation (c-167G>T) in PMM2, either homozygous or in trans with a second PMM2 coding mutation. Methods We performed the study of the PMM2 gene in six patients from four unrelated families, previously diagnosed with ARPKD and HH. Results All these patients had in common the heterozygous variant c-167G>T in the promoter region for PMM2. Additionally, each patient carried a compound heterozygote for a second missense mutation in this gene (p.Arg141His, p.Asp148Asn or p.Phe157Ser), previously reported as pathogenic for congenital disorder of glycosylation type Ia, with an autosomal recessive inheritance pattern.