Blood purification
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Fluid overload may occur in critically ill patients as a result of aggressive resuscitation therapies. In such circumstances, persistent fluid overload must be avoided since it does not benefit the patient while it may be harmful. In the septic patient, early volume expansion seems to be beneficial. ⋯ Multiple randomized controlled trials have not shown benefit in the use of diuretics, either to prevent AKI or to treat established AKI. If fluid overload (defined as fluid accumulation >10% over baseline) develops and the patient does not respond to diuretics, persistent use of these drugs will only lead to a delay in the initiation of dialysis or ultrafiltration and an increased risk of negative patient outcomes. In that setting, early initiation of continuous renal replacement therapies may be preferable.
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Acute lung injury (ALI) and acute kidney injury (AKI) are complications often encountered in the setting of critical illness. Both forms of end-organ injury commonly occur in similar settings of systemic inflammatory response syndrome, shock, and evolving multiple organ dysfunction. Recent elucidation of the pathobiology of critical illness has led to a more basic mechanistic understanding of the complex interplay between injured organs in patients with multiple organ dysfunction syndrome; this has been aptly called 'the slippery slope of critical illness' [Kidney Int Suppl 1998;66:S25-S33]. ⋯ In this article, we will review the harmful bidirectional interaction between ALI and AKI, which appears to be a common clinical syndrome with routine clinical implications. We will review the current understanding of lung-kidney interactions from both perspectives, including the renal effects of ALI and mechanical ventilation, and the pulmonary sequelae of AKI. In this review of the emerging evidence of deleterious bidirectional organ cross talk between lung and kidney, we will focus on the role of ventilator-induced kidney injury in the pathogenesis of AKI in patients with ALI.
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Review
The role of peripheral ultrafiltration in the management of acute decompensated heart failure.
Heart failure is a common and highly morbid condition associated with recurrent hospitalizations for disease decompensation. As such, heart failure is a growing public health concern from both a utilization and cost perspective. The current standard of care for the management of volume overload symptoms is underpinned by a diuretic-based treatment regimen. ⋯ Initial research trials have shown that this treatment modality results in improved clinical, biochemical and quality of life parameters. Moreover, these benefits are durable over the long term with decreased recidivism and health care utilization at 1 year. It remains unclear whether these benefits will translate into hard cardiovascular endpoints; greater adoption of this technology coupled with newer clinical trials will help researchers and clinicians identify the optimal strategy for treating symptoms of volume overload among heart failure patients.
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Acute kidney injury (AKI) is a frequent clinical problem in critically ill patients and the associated mortality is high. Standard serum and urine biomarkers are insensitive and nonspecific for the detection of kidney injury in its early stages which limits the therapeutic options and may compromise the outcome. The study presents new candidates for biochemical markers of AKI, with potentially high sensitivity and specificity, causally related to its pathogenesis and development. ⋯ The most promising of the new serum AKI markers are cystatin C, neutrophil gelatinase-associated lipocalin and uric acid. Urinary AKI markers may be classified as enzymes released from damaged tubular cells (alkaline phosphatase, gamma-glutamyl transpeptidase, alanine aminopeptidase, isoenzymes of glutathione transferase, N-acetyl-beta-D-glucosaminidase), low-molecular-weight proteins (alpha(1)-microglobulin, beta(2)-microglobulin, retinol-binding protein, cystatin C) and proteins specifically produced in the kidney and associated with the development of AKI [cysteine-rich protein 61, neutrophil gelatinase-associated lipocalin, kidney injury molecule 1, cytokines and chemokines (Gro-alpha, IL-18), and structural and functional proteins of renal tubules (F-actin, Na(+)/H(+) exchange isoform 3)]. Based on the different expression of these markers, using a panel of serum and urine markers may potentially help to distinguish between various types of insults, establish the duration and severity of injury, predict the clinical outcome and help to monitor response to treatment in AKI.
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Review Comparative Study
Citrate anticoagulation for continuous renal replacement therapy in the critically ill.
Heparins are used for circuit anticoagulation during continuous renal replacement therapy (CRRT). Because heparins cause systemic anticoagulation, they increase the risk of bleeding. Citrate provides regional anticoagulation. Since citrate is a buffer as well, its use has metabolic consequences. The preferential use of citrate therefore remains controversial. ⋯ During critical illness, regional anticoagulation with citrate for CRRT seems superior to heparin anticoagulation concerning tolerance and safety, mainly due to less bleeding. Whether circuit survival is better depends on the modality. In addition, citrate seems to improve patient and kidney survival. This finding needs to be confirmed. Citrate seems to confer a specific benefit in severe organ failure and sepsis. To what extent citrate protects or heparin does harm in the setting of multiple organ failure needs to be unraveled.