suPAR as a marker of infection in acute kidney injury - a prospective observational study.

BACKGROUND: Soluble urokinase-type plasminogen activator receptor (suPAR) has emerged as a new sepsis biomarker. It is not known whether suPAR has a role in critically ill patients with severe acute kidney injury (AKI). METHODS: Our main aims were to describe serial serum suPAR concentrations in patients with severe AKI, to investigate a potential association between suPAR and C-reactive protein (CRP), and to compare suPAR and CRP as diagnostic markers of infection in patients with AKI. Between April 2013 - April 2014, we recruited adult patients (≥18 years) with AKI KDIGO stage 2/3 admitted to a multidisciplinary Intensive Care Unit (ICU) in a University Hospital in UK. Serial serum suPAR and CRP concentrations were measured for 6 days. We compared the characteristics and serial suPAR and CRP concentrations of patients with and without an infection using Chi-squared, Fisher's exact, t-test and Mann-Whitney tests as appropriate, and calculated the area under the receiver operating characteristics curve (AUC). RESULTS: Data of 55 patients with AKI stage 2/3 were analysed (62% male; mean age 60.5) of whom 43 patients received continuous renal replacement therapy. suPAR was not detectable in effluent fluid. There was no significant correlation between daily suPAR and CRP concentrations. In patients with an infection, suPAR results were significantly higher than in those without an infection across all time points; there was no significant difference in CRP levels between both groups. After exclusion of patients with an infection before or on day of admission to ICU, the AUC of suPAR for predicting an infection later was 0.62 (95% CI 0.43-0.80) compared to 0.50 (95% CI 0.29-0.71) for CRP. CONCLUSIONS: In critically ill patients with AKI stage 2/3, suPAR is a better marker of infection than CRP. TRIAL REGISTRATION: The study was retrospectively registered on the ISRCTN registry on 25 November 2012 ( ISRCTN88354940 ).

Long-term sequelae from acute kidney injury: potential mechanisms for the observed poor renal outcomes.

This article is one of ten reviews selected from the Annual Update in Intensive Care and Emergency Medicine 2015 and co-published as a series in Critical Care. Other articles in the series can be found online at http://ccforum.com/series/annualupdate2015. Further information about the Annual Update in Intensive Care and Emergency Medicine is available from http://www.springer.com/series/8901.

Novel risk factors for acute kidney injury.

PURPOSE OF REVIEW: Acute kidney injury (AKI) is a serious problem. Understanding an individual patient's risk profile may offer opportunities for prevention or early intervention. The aim of this review is to describe novel nontraditional risk factors. RECENT FINDINGS: The risk of AKI is determined by patient factors and nephrotoxic exposures. Hyperuricaemia, obesity, hypoalbuminaemia and certain genetic polymorphism have been found to be associated with an increased susceptibility to AKI, especially in surgical patients. However, there is no convincing evidence that albumin replacement or uric acid lowering ameliorates the risk. Genetic predisposition contributes to AKI in general and also drug-nephrotoxicity. The exact relationship between obesity and AKI has not been fully understood.Patients exposed to starches, chloride-rich fluids or mechanical ventilation have an increased risk of AKI. Starches in particular should be avoided in high-risk patients. Although chloride-rich fluids are associated with AKI based on observational studies, direct proof of harm is lacking. SUMMARY: Novel risk factors for AKI have been identified but more work is necessary to investigate the nature of the association. There is no evidence that correction of hyperuricaemia or hypoalbuminaemia is beneficial but high-risk exposures should be avoided in patients at risk of AKI.

Lymphocyte Function in Human Acute Kidney Injury.

Acute kidney injury (AKI) has been recognised as an inflammatory condition with serious short- and long-term complications. Animal studies primarily using models of ischaemia reperfusion injury or caecal ligation and perforation have clearly demonstrated that inflammatory cells contribute to the initiation, propagation and recovery phase of AKI and that lymphocytes have a key role in these processes. Less is known about their involvement in common types of human AKI. This paper summarises the key findings of experimental AKI studies and limited human data with particular focus on the role of T-lymphocytes.

Fluid Composition and Clinical Effects.

The range of intravenous fluids available for therapeutic use and the differing indications are diverse. A solid understanding of the composition of different types of fluids is essential to understanding the physiologic effects following administration and the appropriate clinical application. In this review, the authors describe the different fluids commonly available and discuss the potential benefits and harms depending on the clinical circumstances.

Increased Fluid Administration After Early Acute Kidney Injury is Associated with Less Renal Recovery.

INTRODUCTION: In acute kidney injury (AKI), fluid accumulation is associated with poor outcome. We aimed to determine whether fluid intake or output had the major role. METHODS: Retrospective analysis of patients admitted to the Intensive Care Unit between July 2007 and June 2009 who had AKI stage I. We collected fluid input, output, and haemodynamic data on day of AKI I and on day of AKI III (if AKI III developed) or 72  h after AKI I (if patients did not progress to AKI III). Univariable and multivariable logistic regression analyses were performed. RESULTS: Among 210 patients with AKI I (median age 70 y; 138 males), 85 had a subsequent mean fluid gain >1 L/day. Their risk of AKI III or death in intensive care unit was significantly higher compared with patients who gained ≤1 L/day (63.5% vs. 23.3%, P = 0.001, and 43.5% vs. 24.8%, P = 0.004, respectively). AKI I patients who gained >1 L/day had a significantly lower urine output (50 vs. 66  mL/h, P = 0.02), lower mean arterial pressure (71 vs. 74  mmHg, P = 0.01), higher arterial lactate level (2.7 vs. 2.0  mmol/L, P < 0.001), and higher Sequential Organ Failure Assessment score (9.4 vs. 8.2, P = 0.002) on day of AKI I compared with those who gained ≤ 1 L/day. Multivariable analysis showed that only fluid intake was independently associated with progression to AKI III (OR 1.8 per 1 L; 95% CI 1.1 - 8.8; P = 0.02), but reduced urine output was not an independent risk factor (OR 0.8; 95% CI 0.3 - 2.2; P = 0.6). CONCLUSION: Increased fluid intake in early AKI was an independent risk factor for AKI III.