Seminars in nephrology
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Seminars in nephrology · Jan 2015
ReviewEntanglement of sepsis, chronic kidney disease, and other comorbidities in patients who develop acute kidney injury.
Acute kidney injury (AKI) is a common and severe complication for patients in the intensive care setting, often occurring in the setting of sepsis. Both sepsis and AKI are complex and heterogeneous syndromes with overlapping risk factors. Comorbidities - such as chronic kidney disease, diabetes mellitus, liver disease, cardiac disease and cancer - may contribute to the development of these syndromes and complicate their management. Recognition of the complex interplay between comorbid conditions, sepsis, and AKI is key to the successful management of these syndromes.
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The renal microcirculation plays a major role in the delivery of blood and oxygen to the kidney. In sepsis, alterations in renal microvascular perfusion, in conjunction with increased oxygen requirements, may contribute to renal failure even when renal macrovascular perfusion is preserved. In this review, we discuss the pathophysiology of the renal microcirculation during sepsis and how it contributes to acute kidney injury. ⋯ Coagulative disorders and glycocalyx disruption also may contribute to the microcirculatory dysfunction. New technologies in experimental models and human beings are being developed to explore renal microcirculation in vivo. These technologies will allow a better understanding of the pathophysiopathology of the renal microcirculation and will help guide specific therapeutic strategies in sepsis-induced acute kidney injury.
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Seminars in nephrology · Jan 2015
ReviewEmerging therapeutic targets of sepsis-associated acute kidney injury.
Sepsis-associated acute kidney injury (SA-AKI) is linked to high morbidity and mortality. To date, singular approaches to target specific pathways known to contribute to the pathogenesis of SA-AKI have failed. ⋯ In this review, we discuss the clinical and experimental basis of emerging therapeutic approaches that focus on targeting early proinflammatory and late anti-inflammatory processes, as well as therapeutics that may enhance cellular survival and recovery. Finally, we include ongoing clinical trials in sepsis.
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Acute kidney injury (AKI) occurs frequently in critically ill patients with sepsis, in whom it doubles the mortality rate and half of the survivors suffer permanent kidney damage or chronic kidney disease. Failure in the development of viable therapies has prompted studies to better elucidate the cellular and molecular etiologies of AKI, which have generated novel theories and paradigms for the mechanisms of this disease. ⋯ It is becoming clear that a major etiologic effector of all these inputs is the renal tubule epithelial cell (RTEC). This review discusses these elements and their effects on RTECs, and reviews the current hypotheses of how these effects may determine the fate of RTECs during sepsis-induced AKI.
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Seminars in nephrology · May 2014
ReviewPrediction and management of hyperkalemia across the spectrum of chronic kidney disease.
Hyperkalemia commonly limits optimizing treatment to slow stage 3 or higher chronic kidney disease (CKD) progression. The risk of hyperkalemia is linked to dietary potassium intake, level of kidney function, concomitant diseases that may affect potassium balance such as diabetes, and use of medications that influence potassium excretion. The risk predictors for developing hyperkalemia are an estimated glomerular filtration rate of less than 45 mL/min/1.73 m(2) and a serum potassium level greater than 4.5 mEq/L in the absence of blockers of the renin-angiotensin-aldosterone system (RAAS). ⋯ Moreover, dual RAAS blockade further reduces albuminuria by 25% to 30% compared with monotherapy, it has failed to show a benefit on CKD progression or cardiovascular outcome, and thus is not indicated in such patients because of its marked increase in hyperkalemia potential. Although sodium polystyrene resins exist to manage hyperkalemia in patients requiring therapy that increases serum potassium levels, they are not well tolerated. Newer, more predictable, better-tolerated polymers to bind potassium are on the horizon and may be approved within the next 1 to 2 years.