Evolución a largo plazo del hiperparatiroidismo primario con tratamiento quirúrgico o médico. Bases para la indicación terapéutica

Tesis doctoral inédita. Universidad Autónoma de Madrid. Facultad de Medicina, Departmento de Medicina. Fecha de lectura: 21 de Junio de 199

Importancia del bisfenol A, una toxina urémica de origen exógeno, en el paciente en hemodiálisis

The Kidney Disease and Diabetes Research Group (IIS-FJD) is funded by the following agencies: Health Research Fund (PI14/00386; PIE13/00051 and PI16/01298), the Spanish Society of Nephrology (SENEFRO) and Fundación Renal Íñiigo Álvarez de Toledo (FRIAT)

Preparing for generation Z:how can technology enhanced learning be firmly embedded in our students' learning experience? A case study from Abertay University

Abertay is a relatively small, modern university (undergraduate population of around 4000) with a wide portfolio and a diverse student population. Around 35% of our students are direct entry from local partner colleges to years 2 and 3 of our programmes and a significant number are first generation higher education within their families. As such, partnership working with colleges and support to aid student transitions are key aspects of Abertay’s provision. Since 2013/14, the university has developed and implemented a new Teaching and Learning Enhancement strategy that has catalysed wholescale transformation across the institution. This paper provides an overview of technology enhanced learning at the university with the drivers for change being to the quality of our students' learning experience, improve student retention and progression and enhance learners’ engagement

Gut microbiota in chronic kidney disease

La microflora intestinal mantiene una relación simbiótica con el huésped en condicionesnormales, sin embargo, su alteración se ha asociado recientemente con numerosas enfer-medades.En la enfermedad renal crónica (ERC) se ha descrito una disbiosis en la microflora intesti-nal con un aumento de la flora patógena sobre la simbionte. Además, la permeabilidad de labarrera intestinal está aumentada, lo que permite el paso de endotoxinas y otros productosbacterianos a la sangre. La microflora intestinal, mediante la fermentación de productosno digeridos que alcanzan el colon, produce indoles, fenoles, o aminas, entre otros, queson absorbidos por el huésped, se acumulan en la ERC y tienen efectos deletéreos sobre elorganismo. Estas toxinas urémicas generadas en el intestino y el aumento de la permeabi-lidad de la barrera intestinal en la ERC se han asociado a un aumento de la inflamación y elestrés oxidativo, y están implicados en diversas complicaciones asociadas a la ERC, como laenfermedad cardiovascular, la anemia, las alteraciones del metabolismo mineral o la progre-sión de la ERC. El uso de prebióticos, probióticos o simbióticos, entre otras aproximaciones,podrían mejorar la disbiosis o el aumento de la permeabilidad de la barrera intestinal en laERC.En este artículo se revisan la situación de la microflora intestinal en la ERC, la alteraciónde la barrera intestinal y sus consecuencias clínicas, los efectos deletéreos de las toxinasurémicas derivadas de la microflora intestinal, así como las posibles opciones terapéuticaspara mejorar esta disbiosis y reducir las complicaciones de la ERCThe intestinal microflora maintains a symbiotic relationship with the host under normal conditions, but its imbalance has recently been associated with several diseases. In chronic kidney disease (CKD), dysbiotic intestinal microflora has been reported with an increase in pathogenic flora compared to symbiotic flora. An enhanced permeability of the intestinal barrier, allowing the passage of endotoxins and other bacterial products to the blood, has also been shown in CKD. By fermenting undigested products that reach the colon, the intestinal microflora produce indoles, phenols and amines, among others, that are absorbed by the host, accumulate in CKD and have harmful effects on the body. These gut-derived uraemic toxins and the increased permeability of the intestinal barrier in CKD have been associated with increased inflammation and oxidative stress and have been involved in various CKD-related complications, including cardiovascular disease, anaemia, mineral metabolism disorders or the progression of CKD. The use of prebiotics, probiotics or synbiotics, among other approaches, could improve the dysbiosis and/or the increased permeability of the intestinal barrier in CKD. This article describes the situation of the intestinal microflora in CKD, the alteration of the intestinal barrier and its clinical consequences, the harmful effects of intestinal flora- derived uraemic toxins, and possible therapeutic options to improve this dysbiosis and reduce CKD-related complicationsEste trabajo ha sido financiado con becas del Fondo de Investigaciones Sanitarias (PI16/01298) y de la Sociedad Madrileña de Nefrología y REDinREN

Phosphorus and Nutrition in Chronic Kidney Disease

Patients with renal impairment progressively lose the ability to excrete phosphorus. Decreased glomerular filtration of phosphorus is initially compensated by decreased tubular reabsorption, regulated by PTH and FGF23, maintaining normal serum phosphorus concentrations. There is a close relationship between protein and phosphorus intake. In chronic renal disease, a low dietary protein content slows the progression of kidney disease, especially in patients with proteinuria and decreases the supply of phosphorus, which has been directly related with progression of kidney disease and with patient survival. However, not all animal proteins and vegetables have the same proportion of phosphorus in their composition. Adequate labeling of food requires showing the phosphorus-to-protein ratio. The diet in patients with advanced-stage CKD has been controversial, because a diet with too low protein content can favor malnutrition and increase morbidity and mortality. Phosphorus binders lower serum phosphorus and also FGF23 levels, without decreasing diet protein content. But the interaction between intestinal dysbacteriosis in dialysis patients, phosphate binder efficacy, and patient tolerance to the binder could reduce their efficiency

Vegetable-Based Diets for Chronic Kidney Disease? It Is Time to Reconsider

Traditional dietary recommendations to renal patients limited the intake of fruits and vegetables because of their high potassium content. However, this paradigm is rapidly changing due to the multiple benefits derived from a fundamentally vegetarian diet such as, improvement in gut dysbiosis, reducing the number of pathobionts and protein-fermenting species leading to a decreased production of the most harmful uremic toxins, while the high fiber content of these diets enhances intestinal motility and short-chain fatty acid production. Metabolic acidosis in chronic kidney disease (CKD) is aggravated by the high consumption of meat and refined cereals, increasing the dietary acid load, while the intake of fruit and vegetables is able to neutralize the acidosis and its deleterious consequences. Phosphorus absorption and bioavailability is also lower in a vegetarian diet, reducing hyperphosphatemia, a known cause of cardiovascular mortality in CKD. The richness of multiple plants in magnesium and vitamin K avoids their deficiency, which is common in these patients. These beneficial effects, together with the reduction of inflammation and oxidative stress observed with these diets, may explain the reduction in renal patients' complications and mortality, and may slow CKD progression. Finally, although hyperkalemia is the main concern of these diets, the use of adequate cooking techniques can minimize the amount absorbed

Reactions to synthetic membranes dialyzers: Is there an increase in incidence?

Background: Reactions to dialyzers used in dialysis have been reported more frequently in recent years. Evidence, however, shows that the reaction rate has remained stable for years. Summary: One explanation for the apparent increase in publication frequency could be the lack of knowledge that dialyzer reactions may well occur with biocompatible membranes. Studies showed that the cause of these reactions is very diverse and varied, involving multiple materials. However, polyvinylpyrrolidone continues to be the main suspect, but without conclusive results. There are no differences between the different fibers, and although polysulfone is the most described, it is also the most used. Key Messages: The change to cellulose triacetate continues to be the most appropriate form of treatment. The classification of these reactions into type A and B complicates the diagnosis, and its true usefulness is in doubtThe research presented in this article is supported by the grants from the Spanish Ministry of Economy and Competitiveness and European Regional Development Funds (ERDF/FEDER) through ISCIII/FIS grants PI16/01298, PI17/01495, CIBERDEM and REDINREN RD016/0019 and through the Madrid Renal Society (SOMANE) grant

Bisfenol (A) una toxina a tener en cuenta en el enfermo renal en hemodiálisis

Introduction: Most uremic toxins are by-products of protein metabolism by action of intestinal flora. The metabolism of aromatic amino acids originates phenolic type residues. The most studied is p-cresol that is associated with renal function and vascular damage. Bisphenol A (BPA) is an exogenous molecule with characteristics similar to these aromatic uremic toxins. BPA is an estrogenic endocrine disruptor, found in tin cans, plastic bottles, epoxy resins and in some dialyzers. This molecule accumulates in patients who have impaired renal function. Observational studies have shown that exposure of BPA is linked to renal and cardiovascular injury, among many others in humans, and in animal studies a causal link has been described. Kidneys with normal renal function rapidly excrete BPA, but insufficient excretion in patients with CKD results in accumulation of BPA in the body.Muchas toxinas urémicas son originadas como consecuencia del catabolismo proteico por la flora intestinal. El metabolismo de aminoácidos aromáticos origina residuos de tipo fenólico. De estas toxinas, la más estudiada es el p-cresol, que se asocia a la función renal y daño vascular. El Bisfenol A (BPA) es una molécula exógena de características semejantes a estas toxinas urémicas aromáticas. El BPA es un disruptor endocrino estrogénico que se encuentra en latas de conserva, botellas de plástico, resinas epoxi y en algunos dializadores. Esta molécula se acumula en pacientes que tienen deteriorada la función renal. Estudios observacionales han demostrado que una exposición a BPA está vinculada, entre otras muchas, a lesión renal y cardiovascular en los seres humanos; en estudios en animales se ha descrito un vínculo causal. Los riñones con función renal normal excretan rápidamente BPA, pero una excreción insuficiente en pacientes con ERC da lugar a la acumulación del BPA en el organismo

Bisphenol A in chronic kidney disease

Phenols are uremic toxins of intestinal origin formed by bacteria during protein metabolism. Of these molecules, p-cresol is the most studied and has been associated with renal function impairment and vascular damage. Bisphenol A (BPA) is a molecule with structural similarity with phenols found in plastic food and beverage containers as well as in some dialyzers. BPA is considered an environmental toxicant based on animal and cell culture studies. Japanese authorities recently banned BPA use in baby bottles based on observational association studies in newborns. BPA is excreted in urine and uremic patients present higher serum levels, but there is insufficient evidence to set cut-off levels or to link BPA to any harmful effect in CKD. However, the renal elimination and potential exposure during dialysis warrant the monitoring of BPA exposure and the design of observational studies in which the potential health risks of BPA for end-stage renal disease patients are evaluated.This research was supported by a grant from ISCIII and FEDER funds PS09/00447, Sociedad Española de Nefrologia, ISCIII-RETICREDinREN/RD06/0016, RD12/0021/,Comunidad de Madrid/CIFRA/S2010/BMD-2378, and salary support was from ERA/EDTA to Usama Elewa and Programa Intensificación Actividad Investigadora (ISCIII/Agencia Laín-Entralgo/CM) to Alberto Ortiz Arduán. ISC III (PI10/ 00072), RECAVA (RD06/0014/0038) and Lilly Foundation to Jesús Egido

Uso del sevelamer en la enfermedad renal crónica: Más allá del control del fósforo

Sevelamer is a non-calcium phosphate binder used in advanced chronic kidney disease (CKD) and in dialysis for hyperphosphataemia control. Several experimental, observational studies and clinical trials have shown that sevelamer has pleiotropic effects, beyond hyperphosphataemia control, including actions on inflammation, oxidative stress, lipid profile and atherogenesis, vascular calcification, endothelial dysfunction and the reduction of several uremic toxins. This is the biological basis for its global effect on cardiovascular morbidity and mortality in patients with chronic kidney disease. This review focuses on these pleiotropic actions of sevelamer and their impact on cardiovascular health, with the experience published after more than ten years of clinical expertiseEl sevelamer es un captor no cálcico de fósforo que se utiliza en la ERC avanzada y en diálisis para el control de la hiperfosforemia. Varios estudios experimentales, observacionales y ensayos clínicos han mostrado que el sevelamer tiene efectos pleiotrópicos, más allá del control de la hiperfosforemia, incluyendo acciones sobre la inflamación, el estrés oxidativo, el perfil lipídico y la aterogénesis, la calcificación vascular, la disfunción endotelial y la disminución de diversas toxinas urémicas, todo lo cual sería la base biológica de su efecto global sobre la morbilidad y la mortalidad cardiovascular en pacientes con enfermedad renal crónica. En esta revisión, se hace énfasis en estas acciones pleiotrópicas del sevelamer y su impacto en la salud cardiovascular, con la experiencia publicada después de más de 10 años de experiencia clínicaInstituto de Salud Carlos III [Carlos III Health Institute] (PI10/00072), REDINREN (Red de Investigación Renal [Renal Research Network]) (RD012/0021