Tubular mitochondrial AKT1 is activated during ischemia reperfusion injury and has a critical role in predisposition to chronic kidney disease

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The impact of chronic kidney disease on bariatric perioperative outcome: a MBSAQIP matched analysis

BackgroundMorbid obesity is considered a strong independent risk factor for chronic kidney disease (CKD), and bariatric surgery remains the most effective treatment for obesity-related co-morbidities. Previous large database analyses have suggested that CKD does not independently increase the risk of adverse outcomes after bariatric surgery. The safety of elective bariatric surgery in this patient population remains unclear. To this end, we compared 30-day outcomes in this patient population after laparoscopic sleeve gastrectomy or Roux-en-Y gastric bypass.ObjectivesTo compare 30-day outcomes in CKD patients after laparoscopic sleeve gastrectomy or gastric bypass.SettingUniversity Hospital, United States.MethodsUsing the Metabolic and Bariatric Surgery Accreditation Quality Improvement Program database, we identified patients with CKD who underwent laparoscopic sleeve gastrectomy or Roux-en-Y gastric bypass in 2015 or 2016. An unmatched cohort analysis, a propensity-matched analysis, and a case-control, matched-cohort analysis was performed of patients with and without CKD.ResultsOf the 302,092 patients included in this study, 2362 (.7%) had CKD, of whom 837 (35.4%) required dialysis. CKD patients were older with significantly higher rates of co-morbid conditions. Hospital length of stay, intensive care unit admission, reoperation, readmission, bleeding, cardiopulmonary, infectious complications, and total morbidity were significantly higher in CKD patients. In propensity-matched and case-control matched analyses of 4006 patients and 2264 patients, respectively, poorer outcomes in CKD patients highlight it an independent risk factor for morbidity.ConclusionsIn contrast to previously reported large database analysis, CKD and dependence on dialysis independently increases the risk of 30-day adverse outcomes after primary bariatric surgery. The benefits conferred by bariatric surgery should be carefully weighed against the increased risk of complications in this challenging population.     

Intracellular organelles in health and kidney disease

Subcellular organelles consist of smaller substructures called supramolecular assemblies and these in turn consist of macromolecules. Various subcellular organelles have critical functions that consist of genetic disorders of organelle biogenesis and several metabolic disturbances that occur during non-genetic diseases e.g. infection, intoxication and drug treatments. Mitochondrial damage can cause renal dysfunction as ischemic acute renal injury, chronic kidney disease progression. Moreover, mitochondrial dysfunction is an early event in aldosterone-induced podocyte injury and cardiovascular disease due to oxidative stress in chronic kidney disease. Elevated production of reactive oxygen species could be able to activate NLRP3 inflammasome representing new deregulated biological machinery and a novel therapeutic target in hemodialysis patients. Peroxisomes are actively involved in apoptosis and inflammation, innate immunity, aging and in the pathogenesis of age related diseases, such as diabetes mellitus and cancer. Peroxisomal catalase causes alterations of mitochondrial membrane proteins and stimulates generation of mitochondrial reactive oxygen species. High concentrations of hydrogen peroxide exacerbate organelles and cellular aging. The importance of proper peroxisomal function for the biosynthesis of bile acids has been firmly established. Endoplasmic reticulum stress-induced pathological diseases in kidney cause glomerular injury and tubulointerstitial injury. Furthermore, there is a link between oxidative stress and inflammations in pathological states are associated with endoplasmic reticulum stress. Proteinuria and hyperglycemia in diabetic nephropathy may induce endoplasmic reticulum stress in tubular cells of the kidney. Due to the accumulation in the proximal tubule lysosomes, impaired function of these organelles may be an important mechanism leading to proximal tubular toxicity.