AT1 receptor antagonism before ischemia prevents the transition of acute kidney injury to chronic kidney disease.

Despite clinical recovery of patients from an episode of acute kidney injury (AKI), progression to chronic kidney disease (CKD) is possible on long-term follow-up. However, mechanisms of this are poorly understood. Here, we determine whether activation of angiotensin-II type 1 receptors during AKI triggers maladaptive mechanisms that lead to CKD. Nine months after AKI, male Wistar rats develop CKD characterized by renal dysfunction, proteinuria, renal hypertrophy, glomerulosclerosis, tubular atrophy, and tubulointerstitial fibrosis. Renal injury was associated with increased oxidative stress, inflammation, α-smooth muscle actin expression, and activation of transforming growth factor ß; the latter mainly found in epithelial cells. Although administration of losartan prior to the initial ischemic insult did not prevent or reduce AKI severity, it effectively prevented eventual CKD. Three days after AKI, renal dysfunction, tubular structural injury, and elevation of urinary biomarkers were present. While the losartan group had similar early renal injury, renal perfusion was completely restored as early as day 3 postischemia. Further, there was increased vascular endothelial growth factor expression and an early activation of hypoxia-inducible factor 1 α, a transcription factor that regulates expression of many genes that help reduce renal injury. Thus, AT1 receptor antagonism prior to ischemia prevented AKI to CKD transition by improving early renal blood flow recovery, lesser inflammation, and increased hypoxia-inducible factor 1 α activity.

Short-term effects of burn severity on ecosystem multifunctionality in the northwest Iberian Peninsula.

Severe wildfires cause important changes in vegetation and soil properties in Mediterranean ecosystems. The aim of this work was to evaluate ecosystem multifunctionality through the study of burn severity short-term effects on different ecosystem functions and services. We selected the Cabrera wildfire (2017) in northwest Spain. Burn severity was quantified using CBI index, differentiating four categories: unburned, low, moderate, and high severity. We established a total of 126 field plots, where one year after fire the vegetation was evaluated and soil samples for the analysis of chemical, biochemical, and microbiological properties were collected. Sentinel-2 images were used to obtain vegetation biophysical variables. Vegetation and soil variables were directly applied as indicators, or used to calculate other indicators, which were standardized and selected to define ecosystem functions and services: (1) photosynthetic activity, soil fertility, nutrient cycling, and soil quality (supporting ecosystem service); (2) grass production for livestock and wood production (provisioning ecosystem service); (3) climate regulation and erosion protection (regulating ecosystem services), and (4) woody species diversity and aesthetic value (cultural ecosystem services). The combination of these functions and services defined ecosystem multifunctionality. The main results showed that burn severity negatively affected most ecosystem functions, as well as the ecosystem services of supporting, provisioning, and regulating, and hence, ecosystem multifunctionality. However, the soil fertility function significantly increased with high burn severity, while woody species diversity and aesthetic value functions and, consequently, the cultural ecosystem service, only decreased under the effect of moderate severity. These results provide a starting point to study burn severity effects from a multifunctional approach in Mediterranean ecosystems.

[Cytogenetic diagnosis of first trimester spontaneous abortion]. / Diagnóstico citogenético en aborto espontáneo del primer trimestre.

BACKGROUND: About 15% of all pregnancies end in abortion. In approximately 60% of all losses are chromosomal abnormalities as a cause of pregnancy loss. OBJECTIVE: To determine the importance of cytogenetic study in patients with spontaneous abortion. MATERIALS AND METHODS: A series of cases of women diagnosed with spontaneous abortion less than 12 weeks and cytogenetic studies. Two groups, one group of women with normal cytogenetics and group 2 patients with abnormal cytogenetic result. 44 patients were excluded by cytogenetic study failed. RESULTS: We included 164 women, 55 and 65 for groups 1 and 2, respectively. In 44 cases the material was not suitable for performing karyotype. Of the 120 cases included, had abnormal karyotypes in 65 cases (54%), of which 34 cases (52.3%) were trisomy, 16 cases (24.6%) to polyploidy and 9 cases (13.8%) a monosomy. In addition, we found six cases (8.7%) with recurrent pregnancy loss. The maternal age limit increased incidence of chromosomal abnormalities occurred in the group of 31 and 35 years with 20 cases (30%). Of trisomies, the 16 were the mostfrequent with 11 cases (32.3%). CONCLUSIONS: The finding of 54% of chromosomal abnormalities in spontaneous abortion products demonstrates the importance of cytogenetic study, regardless of patient age and number of previous pregnancy losses.

Urinary prolactin as a reliable marker for preeclampsia, its severity, and the occurrence of adverse pregnancy outcomes.

CONTEXT: It has been proposed that preeclampsia may result from of an imbalance in angiogenic factors. Although prolactin (PRL) is mainly related to lactation, it is also involved in other biological functions, including angiogenesis. OBJECTIVE: Our objective was to determine the relationship among preeclampsia, serum and urinary PRL (uPRL) levels, and excretion of antiangiogenic PRL fragments in urine. STUDY DESIGN: Using a cross-sectional design, uPRL and serum PRL levels, and the presence of PRL isoforms were determined in 546 pregnant women: 207 healthy pregnant, 124 with gestational hypertension, 48 with mild preeclampsia, and 167 with severe preeclampsia (sPE). RESULTS: uPRL concentrations were significantly (P < 0.001) higher in preeclampsia (11.99 ng/mg creatinine) than in healthy pregnancy (0.20 ng/mg creatinine) and gestational hypertension (0.19 ng/mg creatinine), and were even higher in sPE compared with mild preeclampsia (21.20 vs. 2.77 ng/mg creatinine, respectively; P < 0.001). Antiangiogenic PRL fragments (14-16 kDa) were detected in 21.6% of urine samples from women with sPE but in none from other groups. Patients with hemolysis, elevated liver enzymes, low platelet count syndrome, and/or eclampsia, placental abruption, acute renal failure, and pulmonary edema exhibited highest uPRL concentrations (P < or = 0.028) and frequency of antiangiogenic PRL fragments in urine (P < or = 0.036). High-serum PRL levels were associated with sPE independently of gestational age, proteinuria, and prolactinuria (P = 0.032). CONCLUSIONS: Preeclampsia is characterized by increased uPRL excretion. uPRL concentrations and their isoforms appear to be suitable markers to assess the severity of preeclampsia and occurrence of adverse outcomes. PRL and and/or its isoforms might be involved in the pathophysiology of preeclampsia.

Intestinal polyp formation in the Apcmin mouse: effects of levels of dietary calcium and altered vitamin D homeostasis.

This study evaluated the effects of various levels of dietary calcium on polyp formation, vitamin D homeostasis, and fecal bile acids in the Apcmin mouse. Female Apcmin mice were randomized to three groups and fed a purified diet with either half or double the level of calcium in control AIN-93G. Serum 25-OH-D and fecal bile acids were measured at weeks 0 and 12 of treatment. Mice were killed for polyp scoring by two observers blinded to treatment after 12 weeks. Results show there was no difference in polyp number or tumor load with dietary calcium in any treatment group. Serum 25-OH-D was reduced and total fecal bile acids were increased in animals that received the high calcium diet. We have previously shown that vitamin D supplementation diminishes polyp load; the lack of effect of an altered calcium diet seen here may be due to a disturbance in vitamin D homeostasis.