Introducción: En pacientes con Enfermedad Renal Crónica Terminal (ERCT), la mortalidad cardiovascular está asociada a la presencia de calcificaciones vasculares. Nuestro objetivo fue determinar la asociación entre la modalidad de diálisis y la presencia de calcificación en aorta abdominal en pacientes con ERCT. Métodos: Realizamos un estudio transversal mediante el censo de los pacientes de la unidad renal del Hospital Nacional Edgardo Rebagliati Martins (HNERM), Lima-Perú. Las calcificaciones se evaluaron con radiografías simples de abdomen lateral. Comparamos la proporción de sujetos con calcificaciones según modalidad de diálisis. Calculamos razones de prevalencia mediante la regresión log-binomial. Resultados: Enrolamos 224 pacientes de los cuales 75,4% (169/224) estaban en hemodiálisis y 24.6% (55/224) en diálisis peritoneal. La edad mediana fue 57 años y el 49.1% (110-224) eran mujeres. El 31.3% (70/224) tuvo calcificaciones en aorta abdominal. La modalidad de diálisis no presentó asociación significativa con la presencia de calcificaciones. Sin embargo, la significancia presento valores límites. Los niveles altos de paratohormona estuvieron asociados en forma independiente con las calcificaciones. Conclusiones: Nuestro estudio sugiere que la diálisis peritoneal podría asociarse a una mayor presencia de calcificaciones vasculares a comparación de la hemodiálisis por ser la significancia límite debido al pequeño tamaño muestral. La evaluación rutinaria de calcificaciones a lo largo del tratamiento de soporte dialítico debe ser promovida en esta población. / Background: Presence of vascular calcifications is associated to cardiovascular mortality in patients with terminal chronic renal disease (ESRD). The aim of the present study is to determine the association between dialysis modality and the presence of vascular calcification. Methods: Vascular calcification was detected by plain lateral abdominal radiograph. We calculated the proportion of vascular calcification associated whit dialysis modality obtaining adjusted prevalence ratios from logistic regression models in this cross- sectional study. Results: We studied a total of 224 patients, 75.4 % (169/224) were on hemodialysis and 24.6% (55/224) on continuous ambulatory peritoneal dialysis. The median age was 57 years –old and 49.1% (110-224) were female. Abdominal aortic calcification was detected in 31.3% (70/224). Higher parathyroid hormone level (PTH) was an independent factor associated whit vascular calcification. Conclusions: Our study suggests that peritoneal dialysis could be associated a higher presence of vascular calcification but we did not find a significance result due to small sample. The continuous evaluation in this group of patients must be encouraged to prevent further complications. / Tesis

The triglyceride/high-density cholesterol-lipoprotein (TG/HDL-c) is a biomarker of cardiovascular events and mortality. In hemodialysis patients, the evidence is controversial. A systematic review was carried out in the Medline, Scopus, Embase, Web of Science, and Pubmed databases to identify the relevant cohort studies on cardiovascular events and mortality in hemodialysis patients the role of TG/HDL-c as a risk factor. Four cohort-type studies were evaluated, with a total of 52,579 hemodialysis patients. Three studies conducted in Asian populations and one study in the United States had the highest percentage of the sample (50,673 patients). The elevated TG/HDL-c ratio is associated with better survival, and there is a consistent gradual inverse association between TG/HDL-c and mortality in all analysis subgroups. In the decile categorization of the exposure variable, a 21% decrease in the risk of cardiovascular mortality and a 15% decrease in all-cause mortality in the highest decile compared to the reference group (D10 aHR = 0.79; 95% CI: 0.69–0.91 and D10 aHR = 0.85; 95%CI: 0.78–0.92). Our results show that the TG/HDL-c ratio is a protective factor for cardiovascular outcomes and mortality in the American population and a risk factor for them in the population from Asia. / Revisión por pares

京都大学 / 新制・論文博士 / 博士(医学) / 乙第13556号 / 論医博第2285号 / 新制||医||1067(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 長船 健二, 教授 椛島 健治, 教授 斎藤 通紀 / 学位規則第4条第2項該当 / Doctor of Medical Science / Kyoto University / DFAM

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No description available.

Renal fibrosis, the final endpoint of renal disease of any cause, is characterised by myofibroblast deposition of extracellular matrix (ECM) and commonly studied using the unilateral ureteric obstruction (UUO) model. Macrophages are multifunctional cells and involved in renal injury, repair and scarring. Work in other organs has shown that fibrosis is not necessarily irreversible and we established and characterised the murine model of reversible unilateral ureteric obstruction (R-UUO) to investigate the potential reversibility of fibrosis and the underlying mechanism with a particular focus upon the role of macrophages. Reversal of UUO was performed at day 7 and R-UUO kidneys exhibited rapid and profound loss of α-smooth muscle actin (αSMA) positive myofibroblasts over the subsequent 7 days. Loss of αSMA+ myofibroblasts was accompanied by limited and variable degradation of ECM components including collagens I and III. αSMA/TUNEL double staining suggested that some myofibroblasts underwent apoptosis. Infiltrating macrophages were abundant at D7 UUO and persisted at all time points following reversal, however, there was a reduction in the F4/80+ population at D7 Reversal by flow cytometry. Of the F4/80+ population two distinct subpopulations could be identified, F4/80Hi and F4/80Lo cells. The relative contribution of these macrophage populations to the total renal macrophage pool did not alter in obstruction or reversal. The F4/80Hi population was characterised by increased expression of CD11c and decreased expression of CD11b and Ly6C (F4/80HiCD11cHiCD11bLoLy6CLo), whereas the F4/80Lo population was characterised by increased expression of CD11b and Ly6C and decreased expression of CD11c (F4/80LoCD11cLoCD11bHiLy6CHi). CD11b was decreased in both F4/80+ populations during reversal, with altered Ly6C profiles, indicating that the phenotype of the macrophages in each population is different and may change during reversal. Indeed, macrophages isolated by flow cytometry utilising anti-F4/80-APC conjugated antibodies had altered mRNA profiles with D7 reversal associated with decreased mRNA expression of mannose receptor and TGFβ. Previous work in the liver indicates that macrophages may promote or inhibit tissue scarring. In order to ascertain whether macrophages were involved in the loss of αSMA+ myofibroblasts we depleted macrophages after reversal by either administering diphtheria toxin to transgenic CD11b-DTR mice or antagonising colony stimulating factor-1 (CSF-1), a key macrophage mitogen and growth factor, by administering antibodies to the CSF-1 receptor. Both approaches significantly depleted macrophage infiltration but did not retard the loss of αSMA+ myofibroblasts indicating that myofibroblast loss was macrophage independent. Lastly, we investigated the potential role of tissue stiffness in myofibroblast loss following UUO reversal. Primary renal myofibroblasts were cultured from obstructed kidneys, carefully phenotyped and cultured on matrices of differing stiffness. The susceptibility of myofibroblasts to apoptosis increased as the matrix stiffness fell. These data suggest that the altered mechanical microenvironment of the decompressed kidney may be a key stimulus for the macrophage independent loss of myofibroblasts that follows the reversal of UUO.

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published_or_final_version / Medical Sciences / Master / Master of Medical Sciences

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