RESUMEN
Obesity and the corresponding burden of related diseases is a major public health issue worldwide that is reaching pandemic proportions. Bariatric surgery is the only intervention that has been shown to result in substantial and lasting weight loss, and a decrease in overall mortality for patients with severe obesity. Consequently, the population of patients having undergone this procedure is increasing. Multifactorial weight-dependent and independent mechanisms underlying metabolic diseases could also drive preventable, but potentially life-threatening, long-term nutritional complications. However, given post-bariatric patients are prone to functional gastrointestinal symptoms and substantial weight loss, nutritional complications might be challenging. This Review is focused on the prevention and treatment of nutritional complications after bariatric surgery in the clinical setting.
Asunto(s)
Cirugía Bariátrica/efectos adversos , Desnutrición/epidemiología , Enfermedades Metabólicas/prevención & control , Obesidad Mórbida/cirugía , Cirugía Bariátrica/métodos , Femenino , Enfermedades Gastrointestinales/etiología , Humanos , Desnutrición/etiología , Desnutrición/fisiopatología , Obesidad Mórbida/complicaciones , Obesidad Mórbida/epidemiología , Complicaciones Posoperatorias/epidemiología , Complicaciones Posoperatorias/fisiopatología , Pérdida de PesoRESUMEN
Acute kidney injury (AKI) is strongly associated with mortality, independently of its cause. The kidney contributes to up to 40% of systemic glucose production by gluconeogenesis during fasting and under stress conditions. Whether kidney gluconeogenesis is impaired during AKI and how this might influence systemic metabolism remain unknown. Here we show that glucose production and lactate clearance are impaired during human and experimental AKI by using renal arteriovenous catheterization in patients, lactate tolerance testing in mice and glucose isotope labelling in rats. Single-cell transcriptomics reveal that gluconeogenesis is impaired in proximal tubule cells during AKI. In a retrospective cohort of critically ill patients, we demonstrate that altered glucose metabolism during AKI is a major determinant of systemic glucose and lactate levels and is strongly associated with mortality. Thiamine supplementation increases lactate clearance without modifying renal function in mice with AKI, enhances glucose production by renal tubular cells ex vivo and is associated with reduced mortality and improvement of the metabolic pattern in a retrospective cohort of critically ill patients with AKI. This study highlights an unappreciated systemic role of renal glucose and lactate metabolism under stress conditions, delineates general mechanisms of AKI-associated mortality and introduces a potential intervention targeting metabolism for a highly prevalent clinical condition with limited therapeutic options.
Asunto(s)
Lesión Renal Aguda/metabolismo , Lesión Renal Aguda/mortalidad , Glucosa/metabolismo , Túbulos Renales Proximales/metabolismo , Adulto , Anciano , Animales , Enfermedad Crítica , Femenino , Gluconeogénesis , Humanos , Ácido Láctico/metabolismo , Masculino , Ratones , Ratones Endogámicos C57BL , Persona de Mediana Edad , Cultivo Primario de Células , Puntaje de Propensión , Circulación Renal , Estudios Retrospectivos , Tiamina/uso terapéutico , Complejo Vitamínico B/uso terapéutico , Adulto JovenRESUMEN
We report the case of a 70-year-old woman who developed life-threatening arrhythmia as a result of acute and severe hypokalaemia, which she developed after consuming large quantities of a liquorice-rich herb tea. She had no previous heart condition. We also discuss the legislative discrepancy in both the USA and in Europe, whereby consumers are warned about the risk of chronic hypertension whenever they buy a product containing liquorice, yet the risk of hypokalaemia may not be mentioned at all.