Nephron. Physiology
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Nephron. Physiology · Jan 2014
Randomized Controlled TrialBolus administration of intravenous glucose in the treatment of hyperkalemia: a randomized controlled trial.
Hyperkalemia is a common medical emergency that may result in serious cardiac arrhythmias. Standard therapy with insulin plus glucose reliably lowers the serum potassium concentration ([K(+)]) but carries the risk of hypoglycemia. This study examined whether an intravenous glucose-only bolus lowers serum [K(+)] in stable, nondiabetic, hyperkalemic patients and compared this intervention with insulin-plus-glucose therapy. ⋯ Infusion of a glucose-only bolus caused a clinically significant decrease in serum [K(+)] without any episodes of hypoglycemia.
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Nephron. Physiology · Jan 2014
ReviewRole of renal oxygenation and mitochondrial function in the pathophysiology of acute kidney injury.
There are unique features of renal oxygenation that render the kidney susceptible to oxygen demand-supply mismatch and hypoxia. Renal oxygen consumption by oxidative metabolism is closely coupled to and driven by tubular transport, which is linked to the filtered solute load and glomerular filtration rate (GFR). In turn, filtered solute load and GFR are dependent on the renal blood flow. ⋯ Here we review the published literature characterizing renal oxygenation and mitochondrial function in ischemic and sepsis-associated acute kidney injury (AKI). However, the coupling of transport and metabolism in AKI has not been examined. This is a potentially fruitful area of research that should become increasingly active given the emerging data linking renal oxygenation and hypoxia to acute and chronic dysfunction in the kidney.
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Nephron. Physiology · Jan 2014
ReviewTargeting recovery from acute kidney injury: incidence and prevalence of recovery.
Since the creation of Risk, Injury, Failure, Loss of Kidney Function, and End-Stage Renal Disease (RIFLE) criteria in the last 10 years, the use of a standardized definition of acute kidney injury (AKI) has made it possible for epidemiologic studies to document the increasing incidence of AKI, especially in the critical care setting. In addition, several studies applying the criteria of RIFLE, Acute Kidney Injury Network, and, more recently, the Kidney Disease: Improving Global Outcome, were able to establish the association of severity of AKI with adverse clinical outcomes, including the development of chronic kidney disease (CKD) and end-stage renal disease (ESRD). Although, until recently, it was thought that survivors from an AKI episode frequently recover kidney function, cumulative observational data over the past decade have confirmed the association of AKI with the increased risk for permanent kidney damage, with subsequent development of CKD. The epidemiological studies that we will present and discuss in this review confirm and clarify the association of AKI with the development of CKD and ESRD.
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Nephron. Physiology · Jan 2014
Central venous oxygen saturation: a potential new marker for circulatory stress in haemodialysis patients?
Haemodialysis causes recurrent haemodynamic stress with subsequent ischaemic end-organ dysfunction. As dialysis prescriptions/schedules can be modified to lessen this circulatory stress, an easily applicable test to allow targeted interventions in vulnerable patients is urgently required. ⋯ This initial study demonstrates ScvO2 sampling is practical, with a potential clinical utility as an indicator of circulatory stress during dialysis.
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Nephron. Physiology · Jan 2014
ReviewThe central role of renal microcirculatory dysfunction in the pathogenesis of acute kidney injury.
Acute kidney injury (AKI) is a rapidly developing condition often associated with critical illness, with a high degree of morbidity and mortality, whose pathophysiology is ill understood. Recent investigations have identified the dysfunction of the renal microcirculation and its cellular and subcellular constituents as being central to the etiology of AKI. ⋯ Effective therapies expected to resolve AKI will have to control inflammation and restore this homeostasis. In order to apply and guide these therapies effectively, diagnostic tools aimed at physiological biomarkers of AKI for monitoring renal microcirculatory function in advance of changes in pharmacological biomarkers associated with structural damage of the kidney will need to be developed.