Regulación de la liberación de renina durante la hipertensión renovascular

La hipertensión es un síndrome cardiovascular progresivo que surge de etiologías complejas e interrelacionadas. Los marcadores tempranos del síndrome a menudo están presentes antes de que la elevación de la presión sanguínea sea observada. El desarrollo de la hipertensión arterial se asocia con anomalías cardíacas y vasculares funcionales y estructurales que dañan el corazón, los riñones, el cerebro, los vasos, y otros órganos, y conducen a la morbilidad y muerte prematura. El sistema renina angiotensina y los riñones son los principales mecanismos que subyacen para el desarrollo de la hipertensión. La renina es la enzima limitante para la síntesis de la angiotensina II; la liberación de renina está regulada por mecanismos como el barorreceptor intrarrenal, la mácula densa (MD) y el sistema nervioso simpático. Desde la MD son liberadas prostaglandinas vasodilatadoras (PG) como PGI2 y PGE2, generadas por la ciclooxigenasa 2, que inducen la liberación de renina de las células yuxtaglomerulares. En esta revisión, mostramos los mecanismos interrelacionados entre la ciclooxigenasa 2 de la MD y la angiotensina II renal

Efecto hipoglucemiante y nefroprotector de Olea europea, Moringa oleifera y Chicorium intibus var en un modelo experimental de diabetes mellitus

La diabetes mellitus tiene una prevalencia del 14% en la República Mexicana, y la población sigue empleando en su tratamiento plantas medicinales, de las cuales se deben corroborar sus propiedades terapéuticas. Por lo que se estudiaron las propiedades hipoglucemiantes y nefroprotectoras de las hojas frescas de Olea europea, Moringa oleífera, y Chicorium intibus var, en un modelo de diabetes mellitus en ratas. Se trabajó con ratas machos, raza Wistar, a las que se les indujo diabetes mellitus por tratamiento con estreptozotocina 55 mg/kg, vía intraperitoneal. A partir del cuarto día se les administraron a ratas diabéticas los extractos etanólicos de las hojas frescas de las plantas (100 y 200 mg/kg, vía oral) durante 2 semanas. Por HPLC se determinaron flavonoides, ácidos fenólicos y terpenoides en los extractos. Se evaluaron la glucemia, la proteinuria y la hipertrofia renal. Los extractos de O. europea, M. oleífera, y C. intibus var mostraron efectos hipoglucemiantes y renoprotectores en las ratas diabéticas.Diabetes mellitus has a prevalence of 14% in the Mexican Republic, and the population continues to use medicinal plants in their treatment, of which their therapeutic properties must be corroborated. To study the hypoglycemic and nephroprotective properties of fresh leaves of Olea europea, Moringa oleifera, and Chicorium intibus var. in a model of diabetes mellitus in rats. Diabetes mellitus was induced in rats by treatment with streptozotocin 55 mg/kg, intraperitoneally. From the fourth day, ethanolic extracts from fresh leaves of plants (100 and 200 mg/kg, orally) were given to diabetic rats for 2 weeks. Flavonoids, phenolic acids, and terpenoids were determined by HPLC in extracts. Blood glucose, proteinuria and renal hypertrophy were evaluated. Extracts of O. europea, M. oleifera, and C. intibus var showed hypoglycaemic and renoprotective effects in diabetic rats

Efecto de las vitaminas antioxidantes C y E sobre la hipertrofia renal en ratas diabéticas

La estimulación de las enzimas antioxidantes en el riñón puede disminuir las complicaciones renales en la diabetes mellitus (DM). En este trabajo se estudió el efecto de las vitaminas C y E como antioxidantes en el daño renal producido por la DM. La DM se indujo con estreptozotocina 65 mg/kg, vía intraperitoneal. A las ratas DM se les administraron las vitaminas E y C en dosis de 250 y 500 mg/kg, vía oral, durante 2 semanas. Las vitaminas C y E restablecieron la función renal en ratas diabéticas: aumentaron la depuración de creatinina y disminuyeron la proteinuria; se observó una disminución del peso del riñón, del área celular tubular proximal y del coeficiente proteínas/DNA, aumentaron la actividad de las enzimas catalasa, superóxido dismutasa y glutatión peroxidasa. Así, las vitaminas E y C restauran las enzimas antioxidantes y retardan el desarrollo de la hipertrofia renal diabéticaStimulation of antioxidant enzymes in the kidney can decrease kidney complications in diabetes mellitus (DM). This paper studied the effect of vitamins C and E as antioxidants on kidney damage caused by DM. DM was induced with streptozotocin 65 mg/kg, intraperitoneally. DM rats were given vitamins E and C in doses of 250 and 500 mg/kg orally for 2 weeks. Vitamins C and E restored renal function in diabetic rats: they increased creatinine purification and decreased proteinuria; a decrease in kidney weight, proximal tubular cell area and protein/DNA coefficient were observed, increased the activity of the enzymes catalase, superoxide dismutase and glutathione peroxidase. Thus, vitamins E and C restore antioxidant enzymes and slow the development of diabetic renal hypertrophy

Mortality from gastrointestinal congenital anomalies at 264 hospitals in 74 low-income, middle-income, and high-income countries: a multicentre, international, prospective cohort study

Summary Background Congenital anomalies are the fifth leading cause of mortality in children younger than 5 years globally. Many gastrointestinal congenital anomalies are fatal without timely access to neonatal surgical care, but few studies have been done on these conditions in low-income and middle-income countries (LMICs). We compared outcomes of the seven most common gastrointestinal congenital anomalies in low-income, middle-income, and high-income countries globally, and identified factors associated with mortality. Methods We did a multicentre, international prospective cohort study of patients younger than 16 years, presenting to hospital for the first time with oesophageal atresia, congenital diaphragmatic hernia, intestinal atresia, gastroschisis, exomphalos, anorectal malformation, and Hirschsprung’s disease. Recruitment was of consecutive patients for a minimum of 1 month between October, 2018, and April, 2019. We collected data on patient demographics, clinical status, interventions, and outcomes using the REDCap platform. Patients were followed up for 30 days after primary intervention, or 30 days after admission if they did not receive an intervention. The primary outcome was all-cause, in-hospital mortality for all conditions combined and each condition individually, stratified by country income status. We did a complete case analysis. Findings We included 3849 patients with 3975 study conditions (560 with oesophageal atresia, 448 with congenital diaphragmatic hernia, 681 with intestinal atresia, 453 with gastroschisis, 325 with exomphalos, 991 with anorectal malformation, and 517 with Hirschsprung’s disease) from 264 hospitals (89 in high-income countries, 166 in middleincome countries, and nine in low-income countries) in 74 countries. Of the 3849 patients, 2231 (58·0%) were male. Median gestational age at birth was 38 weeks (IQR 36–39) and median bodyweight at presentation was 2·8 kg (2·3–3·3). Mortality among all patients was 37 (39·8%) of 93 in low-income countries, 583 (20·4%) of 2860 in middle-income countries, and 50 (5·6%) of 896 in high-income countries (p<0·0001 between all country income groups). Gastroschisis had the greatest difference in mortality between country income strata (nine [90·0%] of ten in lowincome countries, 97 [31·9%] of 304 in middle-income countries, and two [1·4%] of 139 in high-income countries; p≤0·0001 between all country income groups). Factors significantly associated with higher mortality for all patients combined included country income status (low-income vs high-income countries, risk ratio 2·78 [95% CI 1·88–4·11], p<0·0001; middle-income vs high-income countries, 2·11 [1·59–2·79], p<0·0001), sepsis at presentation (1·20 [1·04–1·40], p=0·016), higher American Society of Anesthesiologists (ASA) score at primary intervention (ASA 4–5 vs ASA 1–2, 1·82 [1·40–2·35], p<0·0001; ASA 3 vs ASA 1–2, 1·58, [1·30–1·92], p<0·0001]), surgical safety checklist not used (1·39 [1·02–1·90], p=0·035), and ventilation or parenteral nutrition unavailable when needed (ventilation 1·96, [1·41–2·71], p=0·0001; parenteral nutrition 1·35, [1·05–1·74], p=0·018). Administration of parenteral nutrition (0·61, [0·47–0·79], p=0·0002) and use of a peripherally inserted central catheter (0·65 [0·50–0·86], p=0·0024) or percutaneous central line (0·69 [0·48–1·00], p=0·049) were associated with lower mortality. Interpretation Unacceptable differences in mortality exist for gastrointestinal congenital anomalies between lowincome, middle-income, and high-income countries. Improving access to quality neonatal surgical care in LMICs will be vital to achieve Sustainable Development Goal 3.2 of ending preventable deaths in neonates and children younger than 5 years by 2030

Regulación de la liberación de renina durante la hipertensión renovascular

Hypertension is a progressive cardiovascular syndrome arising from complex and interrelated etiologies. Early markers of the syndrome are often present before blood pressure elevation is observed. The development of arterial hypertension is associated with functional and structural cardiac and vascular abnormalities that damage the heart, kidneys, brain, vasculature, and other organs, and lead to morbidity and premature death. The kidney and the renin angiotensin system are the principal mechanisms that underlie for development of hypertension. Renin is the rate limiting enzyme for angiotensin II synthesis, and renin release is regulated by mechanisms as the intrarenal baroreceptor, the macula densa (MD) and the sympathetic nervous system. The MD releases vasodilator prostaglandins (PG) as PGI2 and PGE2, generated by cyclooxygenase 2, which induce renin release from juxtaglomerular cells. In this review, we show interrelated mechanisms between cyclooxygenase 2 of MD and renal angiotensin II.La hipertensión es un síndrome cardiovascular progresivo que surge de etiologías complejas e interrelacionadas. Los marcadores tempranos del síndrome a menudo están presentes antes de que la elevación de la presión sanguínea sea observada. El desarrollo de la hipertensión arterial se asocia con anomalías cardíacas y vasculares funcionales y estructurales que dañan el corazón, los riñones, el cerebro, los vasos, y otros órganos, y conducen a la morbilidad y muerte prematura. El sistema renina angiotensina y los riñones son los principales mecanismos que subyacen para el desarrollo de la hipertensión. La renina es la enzima limitante para la síntesis de la angiotensina II; la liberación de renina está regulada por mecanismos como el barorreceptor intrarrenal, la mácula densa (MD) y el sistema nervioso simpático. Desde la MD son liberadas prostaglandinas vasodilatadoras (PG) como PGI2 y PGE2, generadas por la ciclooxigenasa 2, que inducen la liberación de renina de las células yuxtaglomerulares. En esta revisión, mostramos los mecanismos interrelacionados entre la ciclooxigenasa 2 de la MD y la angiotensina II renal