Blood purification
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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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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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Large-scale adoption of regional citrate anticoagulation (RCA) is prevented by risks of the technique as practiced traditionally. Safe RCA protocols with automated delivery on customized dialysis systems are needed. ⋯ Using predictive Q(Ca) dosing and integrating control of the infusion pumps with the dialysis machine, SLED-RCA can be near-automated today to provide a user-friendly and safe system.
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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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We have evaluate the effect of slow continuous ultrafiltration (SCUF) on cardiac output (CO) and other hemodynamic parameters related to the overall performance of the cardiovascular system in patients with congestive heart failure (CHF). Minimally invasive hemodynamic monitoring was performed via the radial artery using a pressure recording analytical method (PRAM) during SCUF treatment. ⋯ In CHF patients, ultrafiltration improves not only CO, as previously reported, but also contractile cardiac efficiency and performance. The PRAM system, a minimally invasive method, was able to record hemodynamic changes during SCUF treatment.