Haur Poesia dramatizatzeko aukera bat: proposamen didaktikoa

42 p. : il. -- Bibliogr.: p. 32-35[EUS] Gradu Amaierako Lan (GrAL) hau Haur Poesiaren inguruan eta Haur Poesiaren dramatizazioaren ingurukoa da. Izan ere, poesia eta dramatizazioa elkarloturik lantzea garrantzitsua da Haur Hezkuntzan hainbat eduki eta gaitasun eskuratzeko: gorputz adierazpena, hizkuntza, musikaltasuna, erritmoa, etab, uneoro jolasa baliabide nagusitzat hartuz. GrAL hau aurrera eramateko Haur Hezkuntzan 4 eta 5 urteko haurrekin egingo dut, haurrek poesiaren inguruan dituzten jakintza ezberdinak ikusteko aukera egokia delako. Lan hau egiteko, Zurriola Ikastolan egindako praktikak eta San Ignazio Ikastetxean baimen esplizituaz egindako esku-hartze pedagogikoa baliatu izan ditut. Arestiko bi esperientzien ondorioz, poesiaren eta dramatizazioaren inguruko proposamen didaktikoa sortzea erabaki dut. Haur Hezkuntzako profesionalentzat baliabide interesgarria izan daitekeelakoan.[ES] Este Trabajo de Fin de Grado (TFG) trata sobre la poesía infantil y la dramatización de la poesía infantil. Trabajar conjuntamente la poesía y la dramatización es importante en Educación Infantil para el desarrollo de diversos contenidos: expresión corporal, el lenguaje, la musicalidad, el ritmo, etc. y en todo momento teniendo el juego como principal recurso. Para llevar a cabo este TFG lo hare con niños de 4 y 5 años de Educación Infantil para saber cuáles son los conocimientos de cada niño a cerca de la poesía. Durante las prácticas echas en la Zurriola Ikastola y gracias a la intervención explicita echa en San Ignazio Ikastetxea he tenido la ocasión de ponerlo en práctica. Gracias al resultado de las dos anteriores experiencias, he decidido crear una propuesta didáctica a cerca de la poesía y la dramatización pensando en que será útil para los profesionales de Educación Infantil.[EN] This Final Degree Paper (TFG) is about children´s poetry and the dramatization of children´s poetry. Working together with poetry and drama is important in Infant Education for the development of various contents: body expression, language, musicality, rhythm, etc. and at all time with the game as the main resource. To carry out this TFG I will do it with children of 4 and 5 years of Infant Education to know what are the knowledge of each child about poetry. During the internship at the Zurriola Ikastola and thanks to the explicit intervention in San Ignazio Ikastetxea I had the opportunity to put it into a practice. Thanks to the result of the two previous experiences, I have decided to create a didactic proposal about poetry and drama, thinking that it will be useful for the professionals of Infant Education

Sodium-glucose cotransporter inhibitors: beyond glycaemic control

SGLT2; Chronic kidney disease; Diabetic nephropathySGLT2; Malaltia renal crònica; Nefropatia diabèticaSGLT2; Enfermedad renal crónica; Nefropatía diabéticaDiabetes increases the risk of adverse cardiovascular and renal events. Recently, sodium-glucose co-transporter 2 (SGLT2) inhibitors have been demonstrated to reduce cardiovascular complications and slow diabetic kidney disease progression in patients with type 2 diabetes. The glycaemic control exerted by these drugs is not greater than the one achieved with other classical glucose-lowering medications such as sulphonylureas. For that reason, plausible renoprotective mechanisms independent from glycaemic control have been proposed such as blood pressure control, body weight loss, intraglomerular pressure reduction and a decrease in urinary proximal tubular injury biomarkers. Interestingly, the hypothesis that SGLT2 inhibitors have a direct renoprotective effect has been addressed in diabetic and non-diabetic models. In this editorial, we update the different postulated mechanisms involved in the cardiorenal protection afforded by SGLT2 inhibition in chronic kidney disease.The authors are current recipients of research grants from the FONDO DE INVESTIGACIÓN SANITARIA-FEDER, ISCIII, PI17/00257 and REDINREN, RD16/0009/0030

Sodium-glucose cotransporter inhibitors : beyond glycaemic control

Diabetes increases the risk of adverse cardiovascular and renal events. Recently, sodium-glucose co-transporter 2 (SGLT2) inhibitors have been demonstrated to reduce cardiovascular complications and slow diabetic kidney disease progression in patients with type 2 diabetes. The glycaemic control exerted by these drugs is not greater than the one achieved with other classical glucose-lowering medications such as sulphonylureas. For that reason, plausible renoprotective mechanisms independent from glycaemic control have been proposed such as blood pressure control, body weight loss, intraglomerular pressure reduction and a decrease in urinary proximal tubular injury biomarkers. Interestingly, the hypothesis that SGLT2 inhibitors have a direct renoprotective effect has been addressed in diabetic and non-diabetic models. In this editorial, we update the different postulated mechanisms involved in the cardiorenal protection afforded by SGLT2 inhibition in chronic kidney disease

Urinary angiotensin-converting enzyme 2 and metabolomics in COVID-19-mediated kidney injury

COVID-19; Angiotensin-converting enzyme 2; MetabolomicsCOVID-19; Enzim convertidor d'angiotensina 2; MetabolòmicaCOVID-19; Enzima convertidora de angiotensina 2; MetabolómicaBackground Angiotensin-converting enzyme 2 (ACE2), the receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is highly expressed in the kidneys. Beyond serving as a crucial endogenous regulator of the renin–angiotensin system, ACE2 also possess a unique function to facilitate amino acid absorption. Our observational study sought to explore the relationship between urine ACE2 (uACE2) and renal outcomes in coronavirus disease 2019 (COVID-19). Methods In a cohort of 104 patients with COVID-19 without acute kidney injury (AKI), 43 patients with COVID-19-mediated AKI and 36 non-COVID-19 controls, we measured uACE2, urine tumour necrosis factor receptors I and II (uTNF-RI and uTNF-RII) and neutrophil gelatinase-associated lipocalin (uNGAL). We also assessed ACE2 staining in autopsy kidney samples and generated a propensity score–matched subgroup of patients to perform a targeted urine metabolomic study to describe the characteristic signature of COVID-19. Results uACE2 is increased in patients with COVID-19 and further increased in those that developed AKI. After adjusting uACE2 levels for age, sex and previous comorbidities, increased uACE2 was independently associated with a >3-fold higher risk of developing AKI [odds ratio 3.05 (95% confidence interval 1.23‒7.58), P = .017]. Increased uACE2 corresponded to a tubular loss of ACE2 in kidney sections and strongly correlated with uTNF-RI and uTNF-RII. Urine quantitative metabolome analysis revealed an increased excretion of essential amino acids in patients with COVID-19, including leucine, isoleucine, tryptophan and phenylalanine. Additionally, a strong correlation was observed between urine amino acids and uACE2. Conclusions Elevated uACE2 is related to AKI in patients with COVID-19. The loss of tubular ACE2 during SARS-CoV-2 infection demonstrates a potential link between aminoaciduria and proximal tubular injury.This work was supported by the Heart and Stroke Foundation (grant 855632 to G.Y.O.) and the Canada Foundation for Innovation (grant 35456). A.V. is a current recipient of a Fundacion Alfonso Martin Escudero–2020 Research Grant

Antioxidant Roles of SGLT2 Inhibitors in the Kidney

Diabetic kidney disease; Mitochondrial dysfunction; Oxidative stressMalaltia renal diabètica; Disfunció mitocondrial; Estrès oxidatiuEnfermedad renal diabética; Disfunción mitocondrial; Estrés oxidativoThe reduction-oxidation (redox) system consists of the coupling and coordination of various electron gradients that are generated thanks to serial reduction-oxidation enzymatic reactions. These reactions happen in every cell and produce radical oxidants that can be mainly classified into reactive oxygen species (ROS) and reactive nitrogen species (RNS). ROS and RNS modulate cell-signaling pathways and cellular processes fundamental to normal cell function. However, overproduction of oxidative species can lead to oxidative stress (OS) that is pathological. Oxidative stress is a main contributor to diabetic kidney disease (DKD) onset. In the kidney, the proximal tubular cells require a high energy supply to reabsorb proteins, metabolites, ions, and water. In a diabetic milieu, glucose-induced toxicity promotes oxidative stress and mitochondrial dysfunction, impairing tubular function. Increased glucose level in urine and ROS enhance the activity of sodium/glucose co-transporter type 2 (SGLT2), which in turn exacerbates OS. SGLT2 inhibitors have demonstrated clear cardiovascular benefits in DKD which may be in part ascribed to the generation of a beneficial equilibrium between oxidant and antioxidant mechanisms.The authors are current recipients of grants from FONDO DE INVESTIGACIÓN SANITARIA-FEDER, ISCIII (PI17/00257 and RICORS RD21/0005/0016), and Fundació la Marató de TV3 (421/C/2020, 759/U/2020 and 215/C/2021)

Cardiorenal syndrome and diabetes: an evil pairing

Cardiorenal syndrome; Diabetes mellitus; Heart failureSíndrome cardiorrenal; Diabetes mellitus; Insuficiencia cardiacaSíndrome cardiorenal; Diabetis mellitus; Insuficència cardíacaCardiorenal syndrome (CRS) is a pathology where the heart and kidney are involved, and the deterioration of one of them leads to the malfunction of the other. Diabetes mellitus (DM) carries a higher risk of HF and a worse prognosis. Furthermore, almost half of people with DM will have chronic kidney disease (CKD), which means that DM is the main cause of kidney failure. The triad of cardiorenal syndrome and diabetes is known to be associated with increased risk of hospitalization and mortality. Cardiorenal units, with a multidisciplinary team (cardiologist, nephrologist, nursing), multiple tools for diagnosis, as well as new treatments that help to better control cardio-renal-metabolic patients, offer holistic management of patients with CRS. In recent years, the appearance of drugs such as sodium-glucose cotransporter type 2 inhibitors, have shown cardiovascular benefits, initially in patients with type 2 DM and later in CKD and heart failure with and without DM2, offering a new therapeutic opportunity, especially for cardiorenal patients. In addition, glucagon-like peptide-1 receptor agonists have shown CV benefits in patients with DM and CV disease in addition to a reduced risk of CKD progression

A Nephrologist Perspective on Obesity: From Kidney Injury to Clinical Management

Malaltia renal crònica; Obesitat; Trasplantament de ronyóEnfermedad renal crónica; Obesidad; Trasplante de riñónChronic kidney disease; Obesity; Kidney transplantationObesity is one of the epidemics of our era. Its prevalence is higher than 30% in the U.S. and it is estimated to increase by 50% in 2030. Obesity is associated with a higher risk of all-cause mortality and it is known to be a cause of chronic kidney disease (CKD). Typically, obesity-related glomerulopathy (ORG) is ascribed to renal hemodynamic changes that lead to hyperfiltration, albuminuria and, finally, impairment in glomerular filtration rate due to glomerulosclerosis. Though not only hemodynamics are responsible for ORG: adipokines could cause local effects on mesangial and tubular cells and podocytes promoting maladaptive responses to hyperfiltration. Furthermore, hypertension and type 2 diabetes mellitus, two conditions generally associated with obesity, are both amplifiers of obesity injury in the renal parenchyma, as well as complications of overweight. As in the native kidney, obesity is also related to worse outcomes in kidney transplantation. Despite its impact in CKD and cardiovascular morbility and mortality, therapeutic strategies to fight against obesity-related CKD were limited for decades to renin-angiotensin blockade and bariatric surgery for patients who accomplished very restrictive criteria. Last years, different drugs have been approved or are under study for the treatment of obesity. Glucagon-like peptide-1 receptor agonists are promising in obesity-related CKD since they have shown benefits in terms of losing weight in obese patients, as well as preventing the onset of macroalbuminuria and slowing the decline of eGFR in type 2 diabetes. These new families of glucose-lowering drugs are a new frontier to be crossed by nephrologists to stop obesity-related CKD progression

The New Era for Reno-Cardiovascular Treatment in Type 2 Diabetes

Diabetes; Diabetic kidney disease; Dipeptidyl peptidase 4 inhibitorsDiabetis; Nefropatia diabètica; Inhibidors de la dipeptidil peptidasa 4Diabetes; Nefropatía diabética; Inhibidores de la dipeptidil peptidasa 4Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease in the developed world. Until 2016, the only treatment that was clearly demonstrated to delay the DKD was the renin-angiotensin system blockade, either by angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. However, this strategy only partially covered the DKD progression. Thus, new strategies for reno-cardiovascular protection in type 2 diabetic patients are urgently needed. In the last few years, hypoglycaemic drugs, such as sodium-glucose co-transporter 2 inhibitors and glucagon-like peptide-1 receptor agonists, demonstrated a cardioprotective effect, mainly in terms of decreasing hospitalization for heart failure and cardiovascular death in type 2 diabetic patients. In addition, these drugs also demonstrated a clear renoprotective effect by delaying DKD progression and decreasing albuminuria. Another hypoglycaemic drug class, dipeptidyl peptidase 4 inhibitors, has been approved for its use in patients with advanced chronic kidney disease, avoiding, in part, the need for insulinization in this group of DKD patients. Studies in diabetic and non-diabetic experimental models suggest that these drugs may exert their reno-cardiovascular protective effect by glucose and non-glucose dependent mechanisms. This review focuses on newly demonstrated strategies that have shown reno-cardiovascular benefits in type 2 diabetes and that may change diabetes management algorithms.The authors are current recipients of research grants from the FONDO DE INVESTIGACIÓN SANITARIA-FEDER, ISCIII, PI17/00257, and REDINREN, RD16/0009/0030

The Impact of Age on Mortality in Chronic Haemodialysis Population with COVID-19

Coronavirus SARS-CoV-2; COVID-19; 2019-nCoV; Hemodiàlisi; MortalitatCoronavirus SARS-CoV-2; COVID-19; 2019-nCoV; Hemodiálisis; MortalidadCoronavirus SARS-CoV-2; COVID-19; 2019-nCoV; Haemodialysis; MortalityAge and chronic kidney disease have been described as mortality risk factors for coronavirus disease 2019 (COVID-19). Currently, an important percentage of patients in haemodialysis are elderly. Herein, we investigated the impact of age on mortality among haemodialysis patients with COVID-19. Data was obtained from the Spanish COVID-19 chronic kidney disease (CKD) Working Group Registry. From 18 March 2020 to 27 August 2020, 930 patients on haemodialysis affected by COVID-19 were included in the Registry. A total of 254 patients were under 65 years old and 676 were 65 years or older (elderly group). Mortality was 25.1% higher (95% CI: 22.2–28.0%) in the elderly as compared to the non-elderly group. Death from COVID-19 was increased 6.2-fold in haemodialysis patients as compared to the mortality in the general population in a similar time frame. In the multivariate Cox regression analysis, age (hazard ratio (HR) 1.59, 95% CI: 1.31–1.93), dyspnea at presentation (HR 1.51, 95% CI: 1.11–2.04), pneumonia (HR 1.74, 95% CI: 1.10–2.73) and admission to hospital (HR 4.00, 95% CI: 1.83–8.70) were identified as independent mortality risk factors in the elderly haemodialysis population. Treatment with glucocorticoids reduced the risk of death (HR 0.68, 95% CI: 0.48–0.96). In conclusion, mortality is dramatically increased in elderly haemodialysis patients with COVID-19. Our results suggest that this high risk population should be prioritized in terms of protection and vaccination.The authors are current recipients of FONDOS DE INVESTIGACIÓN SANITARIA—FEDER (ISCIII) PI17/00257, REDINREN RD16/0009/0030, RD/16/0009/0026, and EIN2020-112338