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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.)

Reliable estimates of the long-term outcomes of acute kidney injury (AKI) are needed to inform clinical practice and guide allocation of health care resources. This systematic review and meta-analysis aimed to quantify the association between AKI and chronic kidney disease (CKD), end-stage kidney disease (ESKD), and death. Systematic searches were performed through EMBASE, MEDLINE, and grey literature sources to identify cohort studies in hospitalized adults that used standardized definitions for AKI, included a non-exposed comparator, and followed patients for at least 1 year. Risk of bias was assessed by the Newcastle-Ottawa Scale. Random effects meta-analyses were performed to pool risk estimates; subgroup, sensitivity, and meta-regression analyses were used to investigate heterogeneity. Of 4973 citations, 82 studies (comprising 2,017,437 participants) were eligible for inclusion. Common sources of bias included incomplete reporting of outcome data, missing biochemical values, and inadequate adjustment for confounders. Individuals with AKI were at increased risk of new or progressive CKD (HR 2.67, 95% CI 1.99-3.58; 17.76 versus 7.59 cases per 100 person-years), ESKD (HR 4.81, 95% CI 3.04-7.62; 0.47 versus 0.08 cases per 100 person-years), and death (HR 1.80, 95% CI 1.61-2.02; 13.19 versus 7.26 deaths per 100 person-years). A gradient of risk across increasing AKI stages was demonstrated for all outcomes. For mortality, the magnitude of risk was also modified by clinical setting, baseline kidney function, diabetes, and coronary heart disease. These findings establish the poor long-term outcomes of AKI while highlighting the importance of injury severity and clinical setting in the estimation of risk., (Copyright © 2018 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.)

Acute kidney injury (AKI) is common, although commonly used clinical diagnostic markers are imperfect. Intravenous fluid administration remains a cornerstone of therapy worldwide, but there is minimal evidence of efficacy for the use of fluid bolus therapy outside of specific circumstances, and emerging evidence associates fluid accumulation with worse renal outcomes and even increased mortality among critically ill patients. Artificial colloid solutions have been associated with harm, and chloride-rich solutions may adversely affect renal function. Large trials to provide guidance regarding the optimal fluid choices to prevent or ameliorate AKI, and promote renal recovery, are urgently required., (Copyright © 2017 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.

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.)

Purpose: In a previous study, restricting intravenous chloride administration in ICU patients decreased the incidence of acute kidney injury (AKI). To test the robustness of this finding, we extended our observation period to 12 months., Methods: The study extension included a 1-year control period (18 August 2007 to 17 August 2008) and a 1-year intervention period (18 February 2009 to 17 February 2010). During the extended control period, patients received standard intravenous fluids. During the extended intervention period, we continued to restrict all chloride-rich fluids. We used the Kidney Disease: Improving Global Outcomes (KDIGO) staging to define AKI., Results: We studied 1,476 control and 1,518 intervention patients. Stages 2 and 3 of KDIGO defined AKI decreased from 302 (20.5 %; 95 % CI, 18.5-22.6 %) to 238 (15.7 %; 95 % CI, 13.9-17.6 %) (P < 0.001) and the use of RRT from 144 (9.8 %; 95 % CI, 8.3-11.4 %) to 103 (6.8 %; 95 % CI, 5.6-8.2 %) (P = 0.003). After adjustment for relevant covariates, liberal chloride therapy remained associated with a greater risk of KDIGO stages 2 and 3 [hazard ratio 1.32 (95 % CI 1.11-1.58); P = 0.002] and use of RRT [hazard ratio 1.44 (95 % CI 1.10-1.88); P = 0.006]. However, on sensitivity assessment of each 6-month period, KDIGO stages 2 and 3 increased in the new extended intervention period compared with the original intervention period., Conclusions: On extended assessment, the overall impact of restricting chloride-rich fluids on AKI remained. However, sensitivity analysis suggested that other unidentified confounders may have also contributed to fluctuations in the incidence of AKI.

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(E1) and uNGAL(E2)] 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(E1) 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.

Purpose: Choice of renal replacement therapy (RRT) modality may affect renal recovery after acute kidney injury (AKI). We sought to compare the rate of dialysis dependence among severe AKI survivors according to the choice of initial renal replacement therapy (RRT) modality applied [continuous (CRRT) or intermittent (IRRT)]., Methods: Systematic searches of peer-reviewed publications in MEDLINE and EMBASE were performed (last update July 2012). All studies published after 2000 reporting dialysis dependence among survivors from severe AKI requiring RRT were included. Data on follow-up duration, sex, age, chronic kidney disease, illness severity score, vasopressors, and mechanical ventilation were extracted when available. Results were pooled using a random-effects model., Results: We identified 23 studies: seven randomized controlled trials (RCTs) and 16 observational studies involving 472 and 3,499 survivors, respectively. Pooled analyses of RCTs showed no difference in the rate of dialysis dependence among survivors (relative risk, RR 1.15 [95 % confidence interval (CI) 0.78-1.68], I(2) = 0 %). However, pooled analyses of observational studies suggested a higher rate of dialysis dependence among survivors who initially received IRRT as compared with CRRT (RR 1.99 [95 % CI 1.53-2.59], I (2) = 42 %). These findings were consistent with adjusted analyses (performed in 7/16 studies), which found a higher rate of dialysis dependence in IRRT-treated patients [odds ratio (OR) 2.2-25 (5 studies)] or no difference (2 studies)., Conclusions: Among AKI survivors, initial treatment with IRRT might be associated with higher rates of dialysis dependence than CRRT. However, this finding largely relies on data from observational trials, potentially subject to allocation bias, hence further high-quality studies are necessary.

Aim: Cardiac arrest (CA) in humans causes warm renal ischemia-reperfusion injury, similar to animal models of ischemic acute kidney injury (AKI). We aimed to investigate the incidence and risk associations of AKI after CA, with or without post-resuscitation cardiogenic shock (PRCS)., Methods: We examined the renal outcomes of adult patients admitted to the intensive care unit (ICU), who survived for more than 48 h following successful resuscitation after CA., Results: Of 105 patients (median age 65 years; 69% male), 58 (55.2%) had PRCS and were on vasoactive drugs beyond 24h; and 9 (8.6%) (all of whom had PRCS) received renal replacement therapy. Only 3 (6.4%) of 47 patients without PRCS had RIFLE-'I'/'F' AKI, compared to 30 (51.7%) of 58 patients with PRCS (p<0.001). Median peak serum creatinine in the non-PRCS group was 102 μmol/L (interquartile range 85-115), compared to 155 μmol/L (interquartile range 112-267) (p<0.001) in the PRCS group. On multivariate analysis, cumulative noradrenaline dose during the first 24h in ICU, PRCS, and pre-CA renin-angiotensin-aldosterone-system blockade were independently associated with RIFLE-'I'/'F' AKI; while higher serum lactate 12h after CA, baseline creatinine, and PRCS were independently associated with greater rise in creatinine from pre-CA levels. Estimated time without spontaneous circulation, total adrenaline dose and initial cardiac rhythm during CA, had no independent associations with renal outcomes., Conclusions: In the absence of PRCS, CA in isolation is uncommonly associated with significant AKI. The human kidney may be more resistant to warm ischemia-reperfusion injury than previously thought., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

Purpose of Review: Successful renal recovery is a key goal of patient management during acute kidney injury in critically ill patients. However, limited information exists to guide clinicians as to what interventions might either decrease or increase the likelihood of renal recovery and especially renal recovery to dialysis independence. The purpose of this review is to analyse recent data and help clinicians with relevant therapeutic choices., Recent Findings: Two large trials, the Acute Renal Failure Trial Network (ATN) and Randomized Evaluation of Normal versus Augmented Level Renal Replacement Therapy (RENAL), provide important evidence on the possible impact of choice of renal replacement therapy on renal recovery to dialysis independence. In the ATN trial in which intermittent haemodialysis (IHD) was delivered 5077 times, continued dialysis dependence by day 28 occurred in 45.2% of survivors, whereas in the RENAL study in which IHD was used 314 times, dialysis dependence at 28 days was 13.3%. These striking differences in favour of using continuous renal replacement therapy are supported by observational studies and a randomized controlled trial. Similarly the association of a positive fluid balance with poor outcomes has now been supported by multiple observational studies and multivariable logistic regression analysis. Both use of IHD and a positive fluid balance can delay renal recovery., Summary: Available evidence from randomized controlled trials and comparative analysis of their results as well as data from large observational studies suggest that the avoidance of IHD and of a positive fluid balance are likely to increase the speed of renal recovery and may prevent end-stage renal failure in selected high-risk patients with acute kidney injury.

Objectives To determine the ability of urinary neutrophil gelatinase-associated lipocalin (uNGAL) to predict cardiac surgery-associated acute kidney injury (CSA-AKI), continuous renal replacement therapy (CRRT), mortality, and a composite outcome of major adverse kidney events at 365 days (MAKE 365 ), and to investigate the influence of cardiopulmonary bypass (CPB) on NGAL release. Design A prospective observational study. Setting A single-center university hospital. Participants A cohort of 288 adult cardiac surgery patients. Interventions uNGAL was measured at baseline, immediately after surgery, and on days 1 and 2 postoperatively. The authors used the recent Kidney Disease Improving Global Outcomes consensus criteria to define CSA-AKI. Measurements and Main Results CSA-AKI occurred in 36.1% of patients. uNGAL rapidly became significantly higher in patients who developed AKI, with peak value immediately after surgery (349.9 [76.6-1446.6] v 90.1 [20.8-328] ng/mg creatinine; p<0.001). No measure of uNGAL (peak, postsurgery, day 1 or 2 postsurgery) accurately predicted CSA-AKI, CRRT, mortality, or MAKE 365 . However, immediately after surgery, CPB induced greater uNGAL release compared with off-pump surgery (265.5 µmol/L [71-989.6] v 48.7 ng/mg creatinine [17-129.8]; p<0.001). Moreover, such early uNGAL release correlated with CPB duration (r = 0.505; p<0.001) but not with peak serum creatinine values on day 3 or 7 after surgery. Conclusions uNGAL had a limited predictive ability for CSA-AKI or other relevant clinical outcomes after cardiac surgery and appeared to be more closely related to the use and duration of CPB. Thus, its levels may represent the aggregate effect of an inflammatory response to CPB as well as a renal response to cardiac surgery and inflammation. [ABSTRACT FROM AUTHOR]