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Background: Cardiovascular complications are the major cause of morbidity and mortality in patients with chronic kidney disease (CKD). One such complication is pulmonary hypertension (PH). Its prevalence in patients in peritoneal dialysis (PD) varies from 12.6-41.7% and its related factors are not well known. The main objective of this multicenter study was to determine the prevalence of PH and its risk factors in patients starting in PD., Methods: Patients incident in PD were studied. Clinical, biochemical, and PD parameters were evaluated. A transthoracic echocardiography was performed and the evaluated according to the American Society of Echocardiography. Systolic pulmonary artery pressure (sPAP) was calculated with tricuspid regurgitation gradient and PH considered if pulmonary artery pressure was ≥35 mmHg., Results: There were 105 men and 72 women included in the study (aged 53.7 ± 12.8 vs. 52.9 ± 15.5 years). PH was found in 69 patients (38.98%), they had sPAP of 49.05 ± 13.80 vs. 18.81 ± 11.15 mmg, in patients without PH (p <0.001). Patients with PH tend to be more frequently men than women (42 vs. 35%, p = 0.33), and were younger (51.0 ± 14.9 vs. 55,1 ± 12.8 years; p = 0.05). Risk factor for PH were diastolic dysfunction of the left ventricle (LV) (OR = 1.46, 95% CI 1.094-1.973), left ventricular hypertrophy (LVF) (OR = 2.56, 95% CI 1.29-5.09); and residual renal function (RRF) was a protector factor (OR = 0.78, 95% CI 0.068-0.915)., Conclusions: Prevalence of PH in patient's incident in PD was 38%. The factors associated with PH were diastolic dysfunction of the LV and LV hypertrophy. RRF was a protector factor., (Copyright © 2020. Published by Elsevier Inc.)

We investigated the regulation of the adhesiveness of the human promonocytic cell line U-937, differentiated along the monocytic pathway either by 1,25-(OH)2-cholecalciferol or a combination of retinoic acid and dibutyryl cAMP. Adhesion to untreated polystyrene plastic was induced by inflammatory agents like PAF, fMLP or LTB4. The response to PAF first appeared after 48hr of differentiation and was inhibited by PAF antagonists and protein kinase C inhibitors indicating involvement of the phosphatidyl-inositol pathway in the stimulating effect. On the other hand, all the c-AMP raising agents tested inhibited PAF-induced cell adhesion, whatever their target membrane receptors, the Gs transducing protein, the catalytic unit of adenylate cyclase or cAMP phosphodiesterase. Direct stimulation of protein kinase A by Br8-cAMP had a similar effect. Moreover, PAF was able to increase cAMP levels. This suggests the existence of a cAMP based negative control mechanism limiting the action of PAF.

Adrenal and plasma corticosterone levels were measured in adult female rats after i.p. administration of specific MAO inhibitors: clorgyline (IMAO-A) and deprenil (IMAO-B). Brain and adrenal MAO activity was also determined. The IMAO effect was found to depend on 3 interrelated factors: (a) dose of drug, (b) time after injection, (c) specificity in MAO inhibition. One hour after injection, clorgyline (1 and 2.5 mg/kg) but not deprenil (20 mg/kg), appeared to inhibit the adrenocortical stress response to i.p. injection. At higher doses, MAO-B inhibition by deprenil (40 mg/kg) induced a moderate but sustained increase in corticosterone levels, while MAO-A inhibition by clorgyline (5, 10, 20 mg/kg) resulted in a large and sharp rise. This effect of clorgyline was potentiated with alpha-methyl-p-tyrosine and blocked with p-chlorophenylalanine. On this basis, the involvement of serotonergic mechanisms could be considered to explain the stimulatory effect of clorgyline on adrenal cortical function.