HUGO ABENSUR
Projetos de Pesquisa
Unidades Organizacionais
Instituto Central, Hospital das Clínicas, Faculdade de Medicina - Médico
5 resultados
Resultados de Busca
Agora exibindo 1 - 5 de 5
bookPart Esclerose peritoneal encapsulante(2016) ERNANES NETO, Miguel; ABENSUR, Hugo- Interactions between kidney disease and diabetes: dangerous liaisons(2016) PECOITS-FILHO, Roberto; ABENSUR, Hugo; BETONICO, Carolina C. R.; MACHADO, Alisson Diego; PARENTE, Erika B.; QUEIROZ, Marcia; SALLES, Joao Eduardo Nunes; TITAN, Silvia; VENCIO, SergioBackground: Type 2 diabetes mellitus (DM) globally affects 18-20 % of adults over the age of 65 years. Diabetic kidney disease (DKD) is one of the most frequent and dangerous complications of DM2, affecting about one-third of the patients with DM2. In addition to the pancreas, adipocytes, liver, and intestines, the kidneys also play an important role in glycemic control, particularly due to renal contribution to gluconeogenesis and tubular reabsorption of glucose. Methods: In this review article, based on a report of discussions from an interdisciplinary group of experts in the areas of endocrinology, diabetology and nephrology, we detail the relationship between diabetes and kidney disease, addressing the care in the diagnosis, the difficulties in achieving glycemic control and possible treatments that can be applied according to the different degrees of impairment. Discussion: Glucose homeostasis is extremely altered in patients with DKD, who are exposed to a high risk of both hyperglycemia and hypoglycemia. Both high and low glycemic levels are associated with increased morbidity and shortened survival in this group of patients. Factors that are associated with an increased risk of hypoglycemia in DKD patients include decreased renal gluconeogenesis, deranged metabolic pathways (including altered metabolism of medications) and decreased insulin clearance. On the other hand, decrease glucose filtration and excretion, and inflammation-induce insulin resistance are predisposing factors to hyperglycemic episodes. Conclusion: Appropriate glycaemic monitoring and control tailored for diabetic patients is required to avoid hypoglycaemia and other glycaemic disarrays in patients with DM2 and kidney disease. Understanding the renal physiology and pathophysiology of DKD has become essential to all specialties treating diabetic patients. Disseminating this knowledge and detailing the evidence will be important to initiate breakthrough research and to encourage proper treatment of this group of patients.
bookPart Doença Renal Crônica(2016) SILVA, Bruno Caldin; ABENSUR, Hugo- Nebivolol, a beta(1)-adrenergic blocker, protects from peritoneal membrane damage induced during peritoneal dialysis(2016) LIAPPAS, Georgios; GONZALEZ-MATEO, Guadalupe; AGUIRRE, Anna Rita; ABENSUR, Hugo; ALBAR-VIZCAINO, Patricia; PARRA, Emilio Gonzalez; SANDOVAL, Pilar; RAMIREZ, Laura Garcia; PESO, Gloria del; ACEDO, Juan Manuel; BAJO, Maria A.; SELGAS, Rafael; TOMERO, Jose A. Sanchez; LOPEZ-CABRERA, Manuel; AGUILERA, AbelardoPeritoneal dialysis (PD) is a form of renal replacement treatment, which employs the peritoneal membrane (PM) to eliminate toxins that cannot be removed by the kidney. The procedure itself, however, contributes to the loss of the PM ultrafiltration capacity (UFC), leading consequently to the technique malfunction. beta-blockers have been considered deleterious for PM due to their association with loss of UFC and induction of fibrosis. Herein we analyzed the effects of Nebivolol, a new generation of beta(1)-blocker, on PM alterations induced by PD fluids (PDF). In vitro: We found that mesothelial cells (MCs) express beta(1)-adrenergic receptor. MCs were treated with TGF-beta to induce mesothelial-to-mesenchymal transition (MMT) and co-treated with Nebivolol. Nebivolol reversed the TGF-beta effects, decreasing extracellular matrix synthesis, and improved the fibrinolytic capacity, decreasing plasminogen activator inhibitor-1 (PAI-1) and increasing tissue-type plasminogen activator (tPA) supernatant levels. Moreover, Nebivolol partially inhibited MMT and decreased vascular endothelial growth factor (VEGF) and IL-6 levels in supernatants. In vivo: Twenty-one C57BL/6 mice were divided into 3 groups. Control group carried a catheter without PDF infusion. Study group received intraperitoneally PDF and oral Nebivolol during 30 days. PDF group received PDF alone. Nebivolol maintained the UFC and reduced PM thickness, MMT and angiogenesis promoted by PDF. It also improved the fibrinolytic capacity in PD effluents decreasing PAI-1 and IL-8 and increased tPA levels. Conclusion: Nebivolol protects PM from PDF-induced damage, promoting antifibrotic, anti-angiogenic, anti-inflammatory and pro-fibrinolytic effects.
- Acometimento renal na doença de Fabry(2016) ABENSUR, Hugo; REIS, Marlene Antônia dosAbstract Every cell in the human body has globotriaosylceramide accumulation (Gb3) in Fabry disease due to the mutation in gene of the enzyme α-galactosidase A. It is a disease linked to sex. The main clinical features are: cutaneous angiokeratomas; acroparestesias and early strokes; decreased sweating and heat intolerance; ocular changes; myocardial hypertrophy, arrhythmias; gastrointestinal disorders and renal involvement. Renal involvement occurs due to Gb3 accumulation in all types of renal cells. Therefore, patients may present glomerular and tubular function disorders. Podocytes are particularly affected, with pedicels effacement and development of proteinuria. The diagnosis is made by detection of reduced plasma or leukocyte α-galactosidase activity and genetic study for detecting the α-galactosidase gene mutation. Treatment with enzyme replacement contributes to delay the progression of kidney disease, especially if initiated early.