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Background: Plasma creatinine (Cr) is a marker of kidney function and typically measured once daily. We hypothesized that Cr measured by point-of-care technology early after ICU admission would be a good predictor of acute kidney injury (AKI) the next day in critically ill patients., Methods: We conducted a retrospective database audit in a single tertiary ICU database. We included patients with normal first admission Cr (Cr F ) and identified a Cr value (Cr P ) obtained within 6-12 hours from ICU admission. We used their difference converted into percentage (delta-Cr-%) to predict subsequent AKI (based on Cr and/or need for renal replacement therapy) the next day. We assessed predictive value by calculating area under the receiver characteristic curve (AUC), logistic regression models for AKI with and without delta-Cr-%, and the category-free net reclassifying index (cfNRI)., Results: We studied 780 patients. Overall, 70 (9.0%) fulfilled the Cr AKI definition by Cr P measurement. On day 2, 148 patients (19.0%) were diagnosed with AKI. AUC (95% CI) for delta-Cr-% to predict AKI on day 2 was 0.82 (95% CI 0.78-0.86), and 0.74 (95% CI 0.69-0.80) when patients with AKI based on the Cr P were excluded. Using a cut-off of 17% increment, the positive likelihood ratio (95% CI) for delta-Cr-% to predict AKI was 3.5 (2.9-4.2). The cfNRI was 90.0 (74.9-106.1)., Conclusions: Among patients admitted with normal Cr, early changes in Cr help predict AKI the following day., (© 2020 The Acta Anaesthesiologica Scandinavica Foundation. Published by John Wiley & Sons Ltd.)

Purpose: We assessed the incidence, characteristics, outcomes and associations of small, short-term point-of-care creatinine increases in critically ill patients., Methods: We prospectively identified the first episode of small (>1 μmol/L/h) short-term (3-4 h) point-of-care creatinine increase between two sequential arterial blood gas measurements. We followed patients for the subsequent development of Kidney Disease: Improving Global Outcomes (KDIGO) defined acute kidney injury (AKI) in the intensive care unit (ICU)., Results: Of 387 patients, 279 (72.1%) developed an episode of small short-term point-of-care creatinine increase and 212 (54.8%) developed AKI. Such episodes occurred at a median of 5 (IQR 2-10) hours after ICU admission, while AKI occurred at a median of 15 (IQR 9-28) hours after admission. Patients with such episodes were more likely to be mechanically ventilated on admission (83.9 vs. 44.4%; p < .001) and had higher hospital mortality (10.9 vs. 3.7%, p = .03). Creatinine increase episodes had a sensitivity of 86% (95% CI 78-95) and specificity of 31% (95% CI 26-36) for subsequent AKI stages 2 and 3 in 24 h., Conclusions: Small, short-term point-of-care creatinine increase episodes are common. They are associated with illness severity, occur early, precede AKI by 10 h and are sensitive rather than specific markers of AKI., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Acute kidney injury (AKI) and sepsis carry consensus definitions. The simultaneous presence of both identifies septic AKI. Septic AKI is the most common AKI syndrome in ICU and accounts for approximately half of all such AKI. Its pathophysiology remains poorly understood, but animal models and lack of histological changes suggest that, at least initially, septic AKI may be a functional phenomenon with combined microvascular shunting and tubular cell stress. The diagnosis remains based on clinical assessment and measurement of urinary output and serum creatinine. However, multiple biomarkers and especially cell cycle arrest biomarkers are gaining acceptance. Prevention of septic AKI remains based on the treatment of sepsis and on early resuscitation. Such resuscitation relies on the judicious use of both fluids and vasoactive drugs. In particular, there is strong evidence that starch-containing fluids are nephrotoxic and decrease renal function and suggestive evidence that chloride-rich fluid may also adversely affect renal function. Vasoactive drugs have variable effects on renal function in septic AKI. At this time, norepinephrine is the dominant agent, but vasopressin may also have a role. Despite supportive therapies, renal function may be temporarily or completely lost. In such patients, renal replacement therapy (RRT) becomes necessary. The optimal intensity of this therapy has been established, while the timing of when to commence RRT is now a focus of investigation. If sepsis resolves, the majority of patients recover renal function. Yet, even a single episode of septic AKI is associated with increased subsequent risk of chronic kidney disease.

Importance: Saline (0.9% sodium chloride) is the most commonly administered intravenous fluid; however, its use may be associated with acute kidney injury (AKI) and increased mortality., Objective: To determine the effect of a buffered crystalloid compared with saline on renal complications in patients admitted to the intensive care unit (ICU)., Design and Setting: Double-blind, cluster randomized, double-crossover trial conducted in 4 ICUs in New Zealand from April 2014 through October 2014. Three ICUs were general medical and surgical ICUs; 1 ICU had a predominance of cardiothoracic and vascular surgical patients., Participants: All patients admitted to the ICU requiring crystalloid fluid therapy were eligible for inclusion. Patients with established AKI requiring renal replacement therapy (RRT) were excluded. All 2278 eligible patients were enrolled; 1152 of 1162 patients (99.1%) receiving buffered crystalloid and 1110 of 1116 patients (99.5%) receiving saline were analyzed., Interventions: Participating ICUs were assigned a masked study fluid, either saline or a buffered crystalloid, for alternating 7-week treatment blocks. Two ICUs commenced using 1 fluid and the other 2 commenced using the alternative fluid. Two crossovers occurred so that each ICU used each fluid twice over the 28 weeks of the study. The treating clinician determined the rate and frequency of fluid administration., Main Outcomes and Measures: The primary outcome was proportion of patients with AKI (defined as a rise in serum creatinine level of at least 2-fold or a serum creatinine level of ≥3.96 mg/dL with an increase of ≥0.5 mg/dL); main secondary outcomes were incidence of RRT use and in-hospital mortality., Results: In the buffered crystalloid group, 102 of 1067 patients (9.6%) developed AKI within 90 days after enrollment compared with 94 of 1025 patients (9.2%) in the saline group (absolute difference, 0.4% [95% CI, -2.1% to 2.9%]; relative risk [RR], 1.04 [95% CI, 0.80 to 1.36]; P = .77). In the buffered crystalloid group, RRT was used in 38 of 1152 patients (3.3%) compared with 38 of 1110 patients (3.4%) in the saline group (absolute difference, -0.1% [95% CI, -1.6% to 1.4%]; RR, 0.96 [95% CI, 0.62 to 1.50]; P = .91). Overall, 87 of 1152 patients (7.6%) in the buffered crystalloid group and 95 of 1110 patients (8.6%) in the saline group died in the hospital (absolute difference, -1.0% [95% CI, -3.3% to 1.2%]; RR, 0.88 [95% CI, 0.67 to 1.17]; P = .40)., Conclusions and Relevance: Among patients receiving crystalloid fluid therapy in the ICU, use of a buffered crystalloid compared with saline did not reduce the risk of AKI. Further large randomized clinical trials are needed to assess efficacy in higher-risk populations and to measure clinical outcomes such as mortality., Trial Registration: clinicaltrials.gov Identifier: ACTRN12613001370796.

Background: Changes in mean perfusion pressure (MPP) from premorbid resting values may contribute to the progression of septic acute kidney injury (AKI)., Objectives: In patients with septic shock, we aimed to investigate the association of changes from premorbid values with AKI severity and progression., Methods: We obtained premorbid resting mean arterial pressure (MAP), central venous pressure (CVP), and MPP, and then recorded data from intensive care unit admission 2 hourly for the first 24 hours to calculate hemodynamic deficits. We recorded 4-hourly creatinine measurements for 96 hours. The association of hemodynamic variables with progression of AKI by Kidney Disease: Improving Global Outcomes ≥2 stages was explored by multivariate logistic regression., Results: Of 107 patients, 55 (51.4%) had severe AKI. Median MAP deficit was similar for patients with or without severe AKI. Median MPP deficit was 29% in patients with severe AKI and 24% in those without (P = .04), a difference determined by greater CVP levels. Central venous pressure was independently associated with worsening AKI (odds ratio, 1.26 [95% confidence interval, 1.01-1.58]; P = .04)., Conclusions: Mean arterial pressure and MPP deficits were substantial in septic shock patients, with patients with severe AKI having a greater MPP deficit. However, only CVP was independently associated with AKI progression. These findings suggest a possible role for venous congestion in septic AKI., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Background and Objectives: AKI is a major clinical problem and predictor of outcome in hospitalized patients. In 2013, the Kidney Disease: Improving Global Outcomes (KDIGO) group published the third consensus AKI definition and classification system after the Risk, Injury, Failure, Loss of Kidney Function, and End-Stage Kidney Disease (RIFLE) and the Acute Kidney Injury Network (AKIN) working group systems. It is unclear which system achieves optimal prognostication in hospital patients., Design, Setting, Participants, & Measurements: A retrospective observational study using hospital laboratory, admission, and discharge databases was performed that included adult patients admitted to a teaching hospital in Tokyo, Japan between April 1, 2008, and October 31, 2011. AKI occurring during each hospital stay was identified, and discriminative ability of each AKI classification system based on serum creatinine for the prediction of hospital mortality was assessed. The receiver operating characteristic curve, a graphical measure of test performance, and the area under the curve were used to evaluate how classifications preformed on the study population., Results: In total, 49,518 admissions were studied, of which 11.0% were diagnosed with RIFLE criteria and 11.6% were diagnosed with KDIGO criteria, but only 4.8% were diagnosed with AKIN criteria. Overall hospital mortality was 3.0%. AKI staging and hospital mortality were closely correlated in all systems. Discrimination for hospital mortality was similar for RIFLE and KDIGO criteria (area under the curve=0.77 versus 0.78; P=0.02), whereas AKIN discrimination was inferior (area under the curve=0.69 versus RIFLE [P<0.001] versus KDIGO [P<0.001])., Conclusion: Among hospital patients, KDIGO and RIFLE criteria achieved similar discrimination, but the discrimination of AKIN was inferior.

Background: A pre-morbid 'baseline' creatinine is required in order to diagnose and stage acute kidney injury (AKI) using the RIFLE classification. Estimation of baseline creatinine by solving the Modification of Diet in Renal Disease (MDRD) equation assuming a glomerular filtration rate of 75 ml/min/1.73 m(2) has been widely used but never validated., Methods: We analysed four cohorts of intensive care unit (ICU) patients from three centres (two from Pittsburgh and one from Mayo and Austin). Three cohorts consisted of preselected patients without AKI (Pittsburgh 1 n = 1048, Mayo n = 737, Austin n = 333), and measured creatinine values in these cohorts were taken to represent baseline creatinine values. The last cohort (Pittsburgh 2 n = 468) consisted of unselected ICU patients with baseline creatinine values recorded within 1 year before ICU admission. Using the Pittsburgh 1 cohort, we derived an equation using the same anthropometric variables as the MDRD equation: baseline creatinine = 0.74 - 0.2 (if female) + 0.08 (if black) + 0.003 × age (in years). We then compared measured creatinine in the Mayo and Austin cohorts and recorded creatinine in the Pittsburgh 2 cohort to the estimated creatinine from: (i) the MDRD equation; (ii) our new equation; (iii) a gender-fixed creatinine of 0.8 mg/dl for females and 1.0 mg/dl for males., Results: Using any of the three methods, the median absolute error of the estimates was of the order of 0.1-0.2 mg/dl, and overall accuracy was similar. When the definition of AKI was limited to the severity grades of Injury and Failure, all three methods were able to generate 78-90% reliable results for preselected normal range cohorts, and 63-70% for the unselected cohort of ICU patients., Conclusions: Estimates of incidence of AKI in the critically ill using RIFLE classification can be affected by the bias and limited accuracy of methods to estimate baseline creatinine. Whenever possible, recorded creatinine values should be used as a reference of baseline. The use of the MDRD equation to estimate baseline creatinine when it is unknown may over- or underestimate some mild (Risk) AKI cases but is unlikely to misclassify patients in Injury and Failure.

Acute kidney injury (AKI) is a common complication of critical illness. While the etiology of AKI in critically ill patients is likely often multifactorial, sepsis has consistently been found an important contributing factor and has been associated with high attributable morbidity and mortality. Accordingly, the timely identification of septic AKI in critically ill patients is clearly a clinical priority. The diagnosis of AKI has traditionally depended upon biochemical measurements such as serum creatinine, urea, and urine output. In addition, several urinary biochemical tests, derived indices and microscopy have also been widely cited as valuable in the diagnosis and classification of AKI. However, the value of these urinary tests in the diagnosis, classification, prognosis and clinical management in septic AKI remains unclear, due in part to a lack of kidney morphologic changes and histopathology in human studies of septic AKI. This review will summarize the urinary biochemistry and microscopy in septic AKI., (2010 S. Karger AG, Basel.)

Background: The RIFLE classification scheme for acute kidney injury (AKI) is based on relative changes in serum creatinine (SCr) and on urine output. The SCr criteria, therefore, require a pre-morbid baseline value. When unknown, current recommendations are to estimate a baseline SCr by the MDRD equation. However, the MDRD approach assumes a glomerular filtration rate of approximately 75 mL/min/1.73 m(2). This method has not been validated., Methods: Data from the Beginning and Ending Supportive Therapy for the Kidney (BEST Kidney) study, a prospective observational study from 54 ICUs in 23 countries of critically ill patients with severe AKI, were analysed. The RIFLE class was determined by using observed (o) pre-morbid and estimated (e) baseline SCr values. Agreement was evaluated by correlation coefficients and Bland-Altman plots. Sensitivity analysis by chronic kidney disease (CKD) status was performed., Results: Seventy-six percent of patients (n = 1327) had a pre-morbid baseline SCr, and 1314 had complete data for evaluation. Forty-six percent had CKD. The median (IQR) values were 97 micromol/L (79-150) for oSCr and 88 micromol/L (71-97) for eSCr. The oSCr and eSCr determined at ICU admission and at study enrolment showed only a modest correlation (r = 0.49, r = 0.39). At ICU admission and study enrolment, eSCr misclassified 18.8% and 11.7% of patients as having AKI compared with oSCr. Exclusion of CKD patients improved the correlation between oSCr and eSCr at ICU admission and study enrolment (r = 0.90, r = 0.84) resulting in 6.6% and 4.0% being misclassified, respectively., Conclusions: While limited, estimating baseline SCr by the MDRD equation when pre-morbid SCr is unavailable would appear to perform reasonably well for determining the RIFLE categories only if and when pre-morbid GFR was near normal. However, in patients with suspected CKD, the use of MDRD to estimate baseline SCr overestimates the incidence of AKI and should not likely be used. Improved methods to estimate baseline SCr are needed.

Objective: To assess the effect of high-dose N-acetylcysteine on renal function in cardiac surgery patients at higher risk of postoperative renal failure., Design: Multiblind, placebo-controlled, randomized, phase II clinical trial., Setting: Operating rooms and intensive care units of two tertiary referral hospitals., Patients: A total of 60 cardiac surgery patients at higher risk of postoperative renal failure., Interventions: Patients were allocated to either 24 hrs of high-dose N-acetylcysteine infusion (300 mg/kg body weight in 5% glucose, 1.7 L) or placebo (5% glucose, 1.7 L)., Measurements and Main Results: The primary outcome measure was the absolute change in serum creatinine from baseline to peak value within the first five postoperative days. Secondary outcomes included the relative change in serum creatinine, peak serum creatinine level, serum cystatin C, and in urinary output. Further outcomes were needed for renal replacement therapy, length of ventilation, and length of stay in the intensive care unit and hospital. Randomization was successful and patients were well balanced for preoperative and intraoperative characteristics. There was no significant attenuation in the increase in serum creatinine from baseline to peak when comparing N-acetylcysteine with placebo (64.5 +/- 91.2 and 38.0 +/- 42.4 mumol/L, respectively; p = .15). Also, there was no attenuation in the increase in serum cystatin C from baseline to peak for N-acetylcysteine compared with placebo (0.45 +/- 0.43 and 0.30 +/- 0.33 mg/L, respectively; p = .40). Likewise, there was no evidence for differences in any other clinical outcome., Conclusions: In this phase II, randomized, controlled trial, high-dose N-acetylcysteine was no more effective than placebo in attenuating cardiopulmonary bypass-related acute renal failure in high-risk cardiac surgery patients.

Background and Objectives: Different techniques of continuous renal replacement therapy (CRRT) might have different effects on azotemic control. Accordingly, we tested whether continuous veno-venous hemodiafiltration (CVVHDF) or continuous veno-venous hemofiltration (CVVH) would achieve better control of serum creatinine and plasma urea levels., Design: Retrospective controlled study., Setting: Two tertiary Intensive Care Units., Patients: Critically ill patients with acute renal failure (ARF) treated with CVVHDF (n = 49) or CVVH (n = 50)., Interventions: Retrieval of daily morning urea and creatinine values before and after the initiation of CRRT for up to 2 weeks of treatment., Measurements and Results: Before treatment, serum urea and creatinine concentrations were significantly lower in the CVVH group than in CVVHDF group (urea: 31.0 +/- 15.0 mmol/L for CVVHDF and 24.7 +/- 16.1 mmol/L for CVVH, p = 0.01, creatinine: 547 +/- 308 micromol/L vs. 326 +/- 250 micromol/L, p < 0.0001). These differences were still significant after 48 h of treatment (urea: 20.1 +/- 8.3 mmol/L vs. 14.1 +/- 6.1 mmol/L; p = 0.0003, creatinine: 360 +/- 189pmol/L vs. 215 +/- 118 micromol/L; p < 0.0001). Throughout the duration of therapy, mean urea levels (22.3 +/- 9.0 mmol/L for CVVHDF vs. 16.7 +/- 7.8 mmol/L for CVVH, p < 0.0001) and mean creatinine levels (302 +/- 167 vs. 211 +/- 103 micromol/L, p < 0.0001) were better controlled in the CVVH group., Conclusions: CRRT strategies based on different techniques might have a significantly different impact on azotemic control.

Background: Nephrocheck® was approved for acute kidney injury (AKI) risk assessment in critically illness. However, new studies suggest that urinary concentration affects Nephrocheck® and previous studies did not provide data on urinary output (UO) at the time of measurement. Methods: We performed a prospective cohort study of the Nephrocheck® in intensive care unit patients fulfilling standard inclusion criteria. The primary outcome was Stage 2 or 3 AKI defined by both UO and creatinine Kidney Disease Improving Global Outcomes (KDIGO) criteria in the subsequent 12 h. The secondary outcome was the relationship of UO with Nephrocheck® measurement. Results: Among 98 patients, the primary outcome occurred in 53 (54.1%) overall, but in 23 (23.5%) by creatinine criteria alone. The median (interquartile range) Nephrocheck® in patients with subsequent Stage 2 or 3 AKI was greater than in Stage 1 or no‐AKI patients (0.97 [0.48–1.99] vs. 0.46 [0.22–1.17]; p =.005). However, its area under the receiver characteristic curve was 0.66 (95% confidence interval [CI], 0.56–0.77). Moreover, Nephrocheck® was significantly and inversely correlated with UO (ρ = −.46, p <.001) at the time of measurement and, on a multivariable logistic regression, Nephrocheck® was not associated with subsequent Stage 2 or 3 AKI (OR 1.06 [95% CI, 0.74–1.53], p =.73). In contrast, the UO had an OR of 0.98 for each ml/h increase (95% CI, 0.97–1.00, p =.007). Conclusion: Nephrocheck®'s predictive performance was limited and its value was inversely correlated with UO. Nephrocheck® had no independent relationship with outcome once UO at measurement was considered. [ABSTRACT FROM AUTHOR]

Background: Survivors of acute kidney injury (AKI) are at increased risk of major adverse kidney events and international guidelines recommend individuals be evaluated 3 months following AKI. Aim: We describe practice patterns and predictors of post‐AKI care in an Australian tertiary hospital. Methods: A retrospective analysis was undertaken of adults with AKI (defined by KDIGO criteria) admitted to a single centre between 2012 and 2016. The primary outcome was outpatient nephrology review at 3 months. Secondary outcomes included inpatient nephrology review, and outpatient serum creatinine and urinary protein measurements. Data were analysed using multivariable logistic and competing risk regression. Results: Only 117 of 2111 (6%) patients with AKI were reviewed by a nephrologist at 3 months. Reviewed patients were more likely to have a higher discharge serum creatinine (odds ratio (OR) 1.20 per 10 μmol/L increase; 95% confidence interval (CI) 1.16–1.25) or a history of peripheral vascular disease (OR 1.77; 95% CI 1.00–3.14). They were less likely to be older (OR 0.66 per decade; 95% CI 0.57–0.76) or to have a history of liver (OR 0.47; 95% CI 0.26–0.87) or ischaemic heart (OR 0.50; 95% CI 0.27–0.94) disease. AKI stage did not predict follow up. The median time from discharge to outpatient serum creatinine testing was 12 days (interquartile range 4–47) and proteinuria was measured in 538 (25%) patients. Conclusions: A minority of admitted AKI patients receive recommended post‐AKI care. Studies in other Australian institutions are required to confirm or refute these concerning findings. [ABSTRACT FROM AUTHOR]

Modern CRRT machines can deliver therapy that resembles IHD, and IHD treatments can be slowed to deliver therapy over 10-12 hours, which resembles CRRT. Bellomo R, Cass A, Cole L, et al; RENAL Replacement Therapy Study Investigators: Intensity of continuous renalreplacement therapy in critically ill patients. RRT was performed in 96.8% of accelerated-strategy patients and 61.8% of patients in the standard therapy patients, where RRT was discouraged unless conventional indications developed or AKI persisted for greater than 72 hours. Initially, dialysis nurses were consulted for ICU patients, but due to their high workload, they were often unable to respond in a timely manner to the increasing needs associated with a therapy that was delivered 24 hr/d in sicker and sicker patients. [Extracted from the article]

Background: Acute kidney injury (AKI) in traumatic brain injury (TBI) is poorly understood and it is unknown if it can be attenuated using erythropoietin (EPO).Methods: Pre-planned analysis of patients included in the EPO-TBI (ClinicalTrials.gov NCT00987454) trial who were randomized to weekly EPO (40 000 units) or placebo (0.9% sodium chloride) subcutaneously up to three doses or until intensive care unit (ICU) discharge. Creatinine levels and urinary output (up to 7 days) were categorized according to the Kidney Disease Improving Global Outcome (KDIGO) classification. Severity of TBI was categorized with the International Mission for Prognosis and Analysis of Clinical Trials in TBI.Results: Of 3348 screened patients, 606 were randomized and 603 were analyzed. Of these, 82 (14%) patients developed AKI according to KDIGO (60 [10%] with KDIGO 1, 11 [2%] patients with KDIGO 2, and 11 [2%] patients with KDIGO 3). Male gender (hazard ratio [HR] 4.0 95% confidence interval [CI] 1.4-11.2, P = 0.008) and severity of TBI (HR 1.3 95% CI 1.1-1.4, P < 0.001 for each 10% increase in risk of poor 6 month outcome) predicted time to AKI. KDIGO stage 1 (HR 8.8 95% CI 4.5-17, P < 0.001), KDIGO stage 2 (HR 13.2 95% CI 3.9-45.2, P < 0.001) and KDIGO stage 3 (HR 11.7 95% CI 3.5-39.7, P < 0.005) predicted time to mortality. EPO did not influence time to AKI (HR 1.08 95% CI 0.7-1.67, P = 0.73) or creatinine levels during ICU stay (P = 0.09).Conclusions: Acute kidney injury is more common in male patients and those with severe compared to moderate TBI and appears associated with worse outcome. EPO does not prevent AKI after TBI. [ABSTRACT FROM AUTHOR]

Importance: Acute kidney injury (AKI) is characterized by severe loss of glomerular filtration rate (GFR) and is associated with a prolonged intensive care unit (ICU) stay and increased risk of death. No interventions have yet been shown to prevent AKI or preserve GFR in critically ill patients. Evidence from mammalian physiology and small clinical trials suggests higher amino acid intake may protect the kidney from ischemic insults and thus may preserve GFR during critical illness. Objective: To determine whether amino acid therapy, achieved through daily intravenous (IV) supplementation with standard amino acids, preserves kidney function in critically ill patients. Design, setting, and participants: Multicenter, phase II, randomized clinical trial conducted between December 2010 and February 2013 in the ICUs of 16 community and tertiary hospitals in Australia and New Zealand. Participants were adult critically ill patients expected to remain in the study ICU for longer than 2 days. Interventions: Random allocation to receive a daily supplement of up to 100 g of IV amino acids or standard care. Main outcomes and measures: Duration of renal dysfunction (primary outcome); estimated GFR (eGFR) derived from creatinine; eGFR derived from cystatin C; urinary output; renal replacement therapy (RRT) use; fluid balance and other measures of renal function. Results: 474 patients were enrolled and randomized (235 to standard care, 239 to IV amino acid therapy). At time of enrollment, patients allocated to receive amino acid therapy had higher APACHE II scores (20.2 ± 6.8 vs. 21.7 ± 7.6, P = 0.02) and more patients had pre-existing renal dysfunction (29/235 vs. 44/239, P = 0.07). Duration of renal dysfunction after enrollment did not differ between groups (mean difference 0.21 AKI days per 10 patient ICU days, 95 % CI −0.27 to 1.04, P = 0.45). Amino acid therapy significantly improved eGFR (treatment group × time interaction, P = 0.004), with an early peak difference of 7.7 mL/min/1.73 m (95 % CI 1.0-14.5 mL/min/1.73 m, P = 0.02) on study day 4. Daily urine output was also significantly increased (+300 mL/day, 95 % CI 145-455 mL, P = 0.0002). There was a trend towards increased RRT use in patients receiving amino acid therapy (13/235 vs. 25/239, P = 0.062); however, this trend was not present after controlling for baseline imbalance ( P = 0.21). Conclusion and relevance: Treatment with a daily IV supplement of standard amino acids did not alter our primary outcome, duration of renal dysfunction. Trial registration: anzctr.org.au Identifier: ACTRN12609001015235. [ABSTRACT FROM AUTHOR]

Background: Different molecular forms of urinary neutrophil gelatinase-associated lipocalin (NGAL) have recently been discovered. We aimed to explore the nature, source and discriminatory value of urinary NGAL in intensive care unit (ICU) patients. Methods: We simultaneously measured plasma NGAL (pNGAL), urinary NGAL (uNGAL), and estimated monomeric and homodimeric uNGAL contribution using Western blotting-validated enzyme-linked immunosorbent assays [uNGAL and uNGAL] and their calculated ratio in 102 patients with the systemic inflammatory response syndrome and oliguria, and/or a creatinine rise of >25 μmol/L. Measurements and main results: Bland-Altman analysis demonstrated that, despite correlating well ( r = 0.988), uNGAL and uNGAL were clinically distinct, lacking both accuracy and precision (bias: 266.23; 95 % CI 82.03-450.44 ng/mg creatinine; limits of agreement: −1,573.86 to 2,106.32 ng/mg creatinine). At best, urinary forms of NGAL are fair (area under the receiver operating characteristic [AUROC] ≤0.799) predictors of renal or patient outcome; most perform significantly worse. The 44 patients with a primarily monomeric source of uNGAL had higher pNGAL (118.5 ng/ml vs. 72.5 ng/ml; p < 0.001), remaining significant following Bonferroni correction. Conclusions: uNGAL is not a useful predictor of outcome in this ICU population. uNGAL patterns may predict distinct clinical phenotypes. The nature and source of uNGAL are complex and challenge the utility of NGAL as a uniform biomarker. [ABSTRACT FROM AUTHOR]

Abstract: Purpose: It is controversial whether all critically ill patients with risk, injury, failure, loss, and end-stage renal failure (RIFLE) F class acute kidney injury (AKI) should receive renal replacement therapy (RRT). We reviewed the outcome of open heart surgery patients with severe RIFLE-F AKI who did not receive RRT. Materials and Methods: We identified all patients with AKI after cardiac surgery over 4 years and obtained baseline characteristics, intraoperative details, and in-hospital outcomes. We analyzed physiologic and biochemical features at RRT initiation or at peak creatinine if no RRT was provided. Results: We reviewed 1504 patients. Of these, 137 (9.1%) developed postoperative AKI with 71 meeting RIFLE-F criteria and 23 (32.4% of RIFLE-F cases) not receiving RRT. Compared with RRT-treated RIFLE-F patients, “no-RRT” patients had lower Acute Physiology and Chronic Health Evaluation III scores, less intra-aortic balloon pump requirements, shorter intensive care stay, and a trend toward lower mortality. At peak RIFLE score, their urinary output, arterial pH, and Pao 2/fraction of inspired oxygen ratio were all significantly higher. Their serum creatinine was also higher (304 vs 262 μmol/L; P = .02). Only 3 RIFLE-F no-RRT patients died in-hospital. Detailed review of cause and mode of death was consistent with non–RRT-preventable deaths. In contrast, 27 patients with RIFLE-R or RIFLE-I class received RRT. Compared with RRT-treated RIFLE-F patients, such RIFLE-R or RIFLE-I treated patients had a more severe presentation and higher mortality (51.8% vs 29.2%; P = .02). Conclusions: After cardiac surgery, RRT was typically applied to patients with the most severe clinical presentation irrespective of creatinine levels. A RIFLE score–based trigger for RRT is unlikely to improve patient survival. [Copyright &y& Elsevier]

Background. A blood urea nitrogen (BUN)/creatinine ratio (BCR) >20 (0.081 in international unit) is used to distinguish pre-renal azotemia (PRA) and acute tubular necrosis (ATN). However, there is little evidence that BCR can distinguish between these two conditions and/or is clinically useful. Methods. We conducted a retrospective study using a large hospital database. Patients were divided into three groups: ‘low BCR’ (if BCR when acute kidney injury (AKI) developed was ≤20), ‘high BCR’ (if BCR when AKI developed was >20) and ‘no AKI’ if patients did not satisfy any of the Risk, Injury, Failure, Loss and End-stage kidney disease criteria for AKI during hospitalization. Results. Among 20 126 study patients, 3641 (18.1%) had AKI. Among these patients, 1704 (46.8%) had a BCR <20 at AKI diagnosis (‘low BCR’) and 1937 (53.2%) had a BCR >20 (‘high BCR’). The average BCR for the two groups was 15.8 versus 26.1 (P < 0.001). Hospital mortality was significantly less in the ‘low-BCR’ group (18.4 versus 29.9%, P < 0.001). Multivariable logistic regression analysis for hospital mortality (‘no AKI’ as a reference) showed that the odds ratio of ‘high BCR’ (5.73) was higher than that of ‘low BCR’ (3.32). Conclusions. Approximately half of the patients with AKI have a BCR >20, the traditional threshold of diagnosing PRA. Unlike PRA patients who have a lower mortality than ATN patients, high BCR patients had higher hospital mortality compared with low BCR patients, which was confirmed with multivariable analysis. These findings do not support BCR as a marker of PRA. [ABSTRACT FROM PUBLISHER]

Objective: To test the precision and limits of agreement of point-of-care testing (POCT)-based measurement of serum creatinine (Cr) in critically ill patients. Methods: We studied 250 paired blood samples from 82 critically ill patients from a general intensive care unit by simultaneous POCT and central laboratory testing (Jaffé method). Correlation, precision, bias, and limits of agreement were assessed. Possible confounders for interference of noncreatinine chromogens were evaluated by multivariate linear regression analysis. Results: The mean difference in serum Cr measured by central laboratory and POCT was ++9.6 μmol/L (95%% limits of agreement: −11.2 to ++30.4 μmol/L). The mean percentage difference between the two techniques was 8.7%% (95%% limits of agreement −7.8%% to ++25.1%%). On multivariate regression, the difference in serum Cr was increased with greater hemoglobin and lactate levels but decreased with greater bilirubin, albumin, and calcium levels. Conclusions: Compared with the central laboratory testing, POCT-based measurement of serum Cr in critically ill patients carried a small negative bias. This difference appeared affected by the blood levels of biochemical variables known to affect the Jaffé method. POCT-based Cr measurement appears sufficiently accurate for clinical use. [ABSTRACT FROM AUTHOR]

Objective: To measure renal blood flow (RBF) and renal function during recovery from experimental septic acute kidney injury (AKI).Design: Controlled experimental study.Subjects: Nine merino ewes.Setting: University physiology laboratory.Intervention: We recorded systemic and renal hemodynamics during a 96-h observation period (control) via implanted transit-time flow probes. We then compared this period with 96[Symbol: see text]h of septic AKI (48 h of Escherichia coli infusion) and subsequent recovery (48 h of observation after stopping E. coli).Measurements and Results: Compared with the control period, E. coli infusion induced hyperdynamic sepsis (increased cardiac output and decreased blood pressure) and septic AKI (serum creatinine 65.4 +/- 8.7 vs. 139.9 +/- 33.0 micromol/l; creatinine clearance 73.8 +/- 12.2 vs. 40.2 +/- 17.2 ml/min; p < 0.05) with a mortality of 22%. RBF increased (278.8 +/- 33.9 vs. 547.9 +/- 124.8 ml/min; p < 0.05) as did renal vascular conductance (RVC). During recovery, we observed a decrease in RVC and RBF with all values returning to control levels. Indices of tubular function [fractional excretion of sodium (FENa) and urea (FEUn) and urinary sodium concentration (UNa)], which had been affected by sepsis, returned to control values after 18 h of recovery, as did serum creatinine.Conclusions: Infusion of E. coli induced a hyperdynamic circulatory state with hyperemic AKI. Recovery was associated with relative renal vasoconstriction and reduction in RBF and RVC back to control levels. Indices of tubular function normalized more rapidly than changes in RBF. [ABSTRACT FROM AUTHOR]

Background: The association between intraoperative oliguria during major abdominal surgery and the subsequent development of postoperative acute kidney injury (AKI) remains poorly defined. We hypothesised that, in such patients, intraoperative oliguria would be an independent predictor of subsequent AKI.Methods: We performed a post hoc analysis of data from the Restrictive versus Liberal Fluid Therapy in Major Abdominal Surgery (RELIEF) trial of conservative vs liberal fluid therapy during and after major abdominal surgery. We used χ2, logistic regression, and fractional polynomials to study the association between intraoperative oliguria defined as a urinary output <0.5 ml kg-1 h-1 and the development of postoperative AKI defined by the Kidney Disease Improving Global Outcomes consensus criteria.Results: We included 2444 of 2983 patients from the RELIEF trial in this study. A total of 889 patients (36%) met oliguric criteria intraoperatively. Oliguria occurred in 35% of those without AKI, and 44%, 48%, and 45% of those who developed postoperative AKI Stages 1-3, respectively (P<0.001 for trend). Intraoperative oliguria was associated with an increased risk of AKI, risk ratio: 1.38 (95% confidence interval: 1.14-1.44; P<0.001), but greater intensity of oliguria (urine output <0.3 ml kg-1 h-1) did not increase this risk further. Most patients with oliguria did not develop AKI; the positive predictive value of oliguria was 25.5%, and the negative predictive value was 81.6%.Conclusions: Intraoperative oliguria, defined as urine output <0.5 ml kg-1 h-1, was relatively common and was associated with postoperative AKI. However, the predictive utility of oliguria for AKI was low, whilst its absence had a good predictive value for an AKI-free postoperative course.Clinical Trial Registration: NCT01424150. [ABSTRACT FROM AUTHOR]

Objectives: Cardiac surgery-associated acute kidney injury occurs in up to 50% of patients and is associated with increased mortality and morbidity. This study aimed to discover if perioperative urinary alkalinization with sodium bicarbonate infusion reduces the prevalence of cardiac surgery-associated acute kidney injury. Design: This study was a phase lib multicenter double-blind randomized controlled trial. Setting: This study was conducted in three tertiary hospitals in New Zealand and Australia. Patients: A total of 427 patients scheduled to undergo elective cardiac surgery, who were at increased risk of development of cardiac surgery-associated acute kidney injury using recognized risk factors. Measurements and Main Results: Patients were randomly allocated to receive either sodium bicarbonate (n = 215) or sodium chloride (n = 212) infusion, commencing at the start of anesthesia, in a dose of 0.5 mEq/kg/hr for the first hour and then 0.2 mmol/kg/hr for 23 hours. The primary outcome measure was the number of patients with development of cardiac surgery-associated acute kidney injury, defined as an increase in creatinine greater than 25% or 0.5 mg/dL (44 µmol/L) from baseline to peak value within the first five postoperative days. Significant differences among the groups in both plasma and urinary biochemistry were achieved 6 hours after commencement of the infusion, and these changes persisted for more than 24 hours. A total of 100 out of 215 patients (47% [95% CI, 40%-53%]) in the sodium bicarbonate group and 93 of 212 patients (44% [95% CI, 37%-51%]) in the sodium chloride group with development of acute kidney injury within the first five postoperative days (p = 0.58). There were also no significant differences in ventilation hours, ICU or hospital length of stay, or mortality. Conclusions: Perioperative alkalinization of blood and urine using an infusion of sodium bicarbonate did not result in a decrease in the prevalence of acute kidney injury in patients following cardiac surgery. [ABSTRACT FROM AUTHOR]

Objectives: To examine the effects of fluid bolus therapy on systemic hemodynamics, renal blood flow, intrarenal perfusion and oxygenation, PO2, renal function, and fluid balance in experimental early septic acute kidney injury.Design: Interventional study.Setting: Research institute.Subjects: Adult Merino ewes.Interventions: Implantation of flow probes on the pulmonary and renal arteries and laser Doppler oxygen-sensing probes in the renal cortex, medulla, and within a bladder catheter in sheep. Infusion of Escherichia coli to induce septic acute kidney injury (n = 8). After 24, 25, and 26 hours of sepsis, fluid bolus therapy (500 mL of Hartmann's solution over 15 min) was administered.Measurements and Main Results: In conscious sheep, infusion of Escherichia coli decreased creatinine clearance and increased plasma creatinine, renal blood flow (+46% ± 6%) and cortical perfusion (+25% ± 4%), but medullary perfusion (-48% ± 5%), medullary PO2 (-56% ± 4%), and urinary PO2 (-54% ± 3%) decreased (p < 0.01). The first fluid bolus therapy increased blood pressure (+6% ± 1%), central venous pressure (+245% ± 65%), cardiac output (+11% ± 2%), medullary PO2 (+280% ± 90%), urinary PO2 (+164% ± 80%), and creatinine clearance (+120% ± 65%) at 30 minutes. The following two boluses had no beneficial effects on creatinine clearance. The improvement in medullary oxygenation dissipated following the third fluid bolus therapy. Study animals retained 69% of the total volume and 80% of sodium infused. Throughout the study, urinary PO2 correlated significantly with medullary PO2.Conclusions: In early experimental septic acute kidney injury, fluid bolus therapy transiently improved renal function and medullary PO2, as also reflected by increased urinary PO2. These initial effects of fluid bolus therapy dissipated within 4 hours, despite two additional fluid boluses, and resulted in significant volume retention. [ABSTRACT FROM AUTHOR]

The article discusses a study which measured renal blood flow in septic patients with acute kidney injury using cine phase-contrast magnetic resonance imaging. Results show that there was no rank correlation between renal blood flow index and creatinine clearance in patients with septic acute kidney injury. It concluded that cine phase-contrast magnetic resonance imaging can be used to noninvasively and safely assess renal perfusion in critically ill patients.