Abstract

Pulmonary arterial hypertension (PAH), defined as a systolic pulmonary artery pressure above 35 mm Hg, is another vascular disease entity recently described in patients receiving hemodialysis. It is a major problem due to its high prevalence and morbidity and mortality. Its pathophysiological mechanism is just known and the strategies for its supported not yet defined. To determine the prevalence of PAH in our hemodialysis patients and its risk factors. Single center descriptive and analytical cross-sectional study, including 111 hemodialysis patients who had benefit from a trans-thoracic cardiac Doppler ultrasound during 2014. A value greater than or equal to 35 mm Hg is considered PAH and classified as follows: mild PAH (35 50 mm Hg), moderate PAH (50 70 mm Hg), and severe pulmonary hypertension (> 70 mm Hg). Patients with a high probability of secondary PAH, especially those with the following history: chronic obstructive pulmonary disease, pulmonary embolism, were not included. The mean age was 44.3 ± 14.2 years. Among the 111 patients, 18 had pulmonary arterial pressure above 35 mm Hg corresponding to 16.22% of PAH prevalence. The average pressure was 45 mm Hg. Of these 18 patients, 11.8% had mild PAH, 3.4% moderate PAH and 0.8% severe PAH. The average hemodialysis duration was significantly associated with PAH (p = 0.003), as well as valvular calcification (p = 0.000), mitral regurgitation (p = 0.001) and tricuspid regurgitation (p = 0.002). Primary pulmonary hypertension is a major problem among our hemodialysis because of its high prevalence and its risk factors.

Abstract

Extended use of plant ingredients in Atlantic salmon farming has increased the need for knowledge on the effects of new nutrients and contaminants in plant based feeds on fish health and nutrient-contaminant interactions. Primary Atlantic salmon hepatocytes were exposed to a mixture of PAHs and pesticides alone or in combination with the nutrients ARA, EPA, α-tocopherol, and γ-tocopherol according to a factorial design. Cells were screened for effects using xCELLigence cytotoxicity screening, NMR spectroscopy metabolomics, mass spectrometry lipidomics and RT-qPCR transcriptomics. The cytotoxicity results suggest that adverse effects of the contaminants can be counteracted by the nutrients. The lipidomics suggested effects on cell membrane stability and vitamin D metabolism after contaminant and fatty acid exposure. Co-exposure of the contaminants with EPA or α-tocopherol contributed to an antagonistic effect in exposed cells, with reduced effects on the VTG and FABP4 transcripts. ARA and γ-tocopherol strengthened the contaminant-induced response, ARA by contributing to an additive and synergistic induction of CYP1A, CYP3A and CPT2, and γ-tocopherol by synergistically increasing ACOX1. Individually EPA and α-tocopherol seemed more beneficial than ARA and γ-tocopherol in preventing the adverse effects induced by the contaminant mixture, though a combination of all nutrients showed the greatest ameliorating effect.