Acute kidney disease (AKD), or renal dysfunction persisting >7 days after an initiating event of acute kidney injury, is a rising concern. This study aimed to elucidate the clinical course of AKD after cardiac surgery with data on post-cardiac surgery patients admitted to intensive care units (ICU) at 18 Japanese hospitals during 2012-2014. Using multivariable logistic models, we evaluated the association of AKD with 90-day mortality and the 50% eGFR decline during 2-year follow-up compared to eGFR at 90 days. AKD was defined as an elevation in serum creatinine to at least 1.5-fold from baseline in >7 days after ICU admission. Of the 3,605 eligible patients undergoing cardiac surgery, 403 patients (11.2%) had AKD. Multivariable analysis revealed that the adjusted odds ratio (OR) of AKD for 90-day mortality was 63.0 (95% confidence interval [CI], 27.9-180.6). In addition, the adjusted OR of AKD for 50% eGFR decline was 3.56 (95% CI, 2.24-5.57) among hospital survivors. In conclusion, AKD after cardiac surgery was associated with higher 90-day mortality and renal function decline after hospital discharge.It is well known that acute kidney injury (AKI) is a significant risk of developing subsequent proteinuria and chronic kidney disease (CKD) 1,2 . AKI and CKD seem to be separate conceptualized models because AKI refers to a clinical syndrome characterized by a rapid decrease in renal function while CKD refers to the presence of kidney damage or decreased kidney function for three months or more 3,4 . However, recent studies show that AKI and CKD are not always discrete and can form a continuum with patients who have a sustained renal dysfunction, having an increased risk of developing de novo CKD or deteriorating underlying CKD 5 .Acute kidney disease (AKD), a condition in which renal dysfunction persists over seven days or more after an exposure, is a rising concern because it could play a key role in AKI to CKD transition 6-8 . The term AKD describes the clinical course of acute or subacute damage and/or loss of renal function for a duration of between 7 and 90 days after an AKI-initiating event 6,7 . It is considered that AKD is mostly a consequence of AKI in patients whose renal function is not fully recovered within seven days and progresses to CKD if the AKD is not fully recovered 6,7 . However, the trajectory of AKD remains poorly elucidated.Cardiac surgery-associated AKI (CSA-AKI) is the second most common type of AKI (next to septic shock) and is associated with high in-hospital mortality 9,10 . In addition, CSA-AKI is proven to be a risk for CKD [11][12][13] . Among the characteristics of CSA-AKI are the various timings of occurrence (early or late phase after cardiac surgery) and the various clinical courses (transient or persistent renal dysfunction) due to the complex pathophysiology of CSA-AKI, which includes hemodynamic instability, mechanical stress such as cardiopulmonary bypass, inflammation, oxidative stress, neurohormonal factors, nephrotoxic agents and postoperative complications such as infect...
BackgroundFurosemide responsiveness (FR) is determined by urine output after furosemide administration and has recently been evaluated as a furosemide stress test (FST) for predicting severe acute kidney injury (AKI) progression. Although a standardized furosemide dose is required for FST, variable dosing is typically employed based on illness severity, including renal dysfunction in the clinical setting. This study aimed to evaluate whether FR with different furosemide doses can predict AKI progression. We further evaluated the combination of an AKI biomarker, plasma neutrophil gelatinase-associated lipocalin (NGAL), and FR for predicting AKI progression.ResultsWe retrospectively analyzed 95 patients who were treated with bolus furosemide in our medical–surgical intensive care unit. Patients who had already developed AKI stage 3 were excluded. A total of 18 patients developed AKI stage 3 within 1 week. Receiver operating curve analysis revealed that the area under the curve (AUC) values of FR and plasma NGAL were 0.87 (0.73–0.94) and 0.80 (0.67–0.88) for AKI progression, respectively. When plasma NGAL level was < 142 ng/mL, only one patient developed stage 3 AKI, indicating that plasma NGAL measurements were sufficient to predict AKI progression. We further evaluated the performance of FR in 51 patients with plasma NGAL levels > 142 ng/mL. FR was associated with AUC of 0.84 (0.67–0.94) for AKI progression in this population with high NGAL levels.ConclusionsAlthough different variable doses of furosemide were administered, FR revealed favorable efficacy for predicting AKI progression even in patients with high plasma NGAL levels. This suggests that a combination of FR and biomarkers can stratify the risk of AKI progression in a clinical setting.Electronic supplementary materialThe online version of this article (10.1186/s13613-018-0355-0) contains supplementary material, which is available to authorized users.
This study evaluated kinetic eGFR as a predictive parameter for CRRT discontinuation. Kinetic eGFR combined with urine volume was a better predictor for CRRT discontinuation. Evaluation of kinetic eGFR utility in other clinical settings will be necessary.
IntroductionThe renal angina index (RAI) is determined based on changes in the creatinine and condition scores of patients. The aim of this study is to evaluate the efficacy of the RAI in predicting persistent acute kidney injury (AKI) in Asian intensive care unit (ICU) patients.MethodsThis is a subanalysis of 3 prospective studies conducted in Japan and Thailand. The RAI was calculated for all enrolled patients using the method of Goldstein and colleagues, with a minor modification for adults on day 2. To determine the accuracy of RAI further, we evaluated a subgroup of patients for whom baseline serum creatinine values were available at ICU admission (i.e., those with hospital-acquired AKI). AKI biomarkers were evaluated for their efficacy in improving the performance of RAI. The outcome was defined as AKI stage 2 or 3 over 48 hours.ResultsOf the 263 patients analyzed, a total of 22 progressed to stage 2 or 3 AKI over 48 hours. The RAI was associated with an area under the curve (AUC) of 0.63 in receiver-operating characteristics analysis, with a cutoff of 10. In those admitted from general wards, the RAI had good performance, with an AUC of 0.73 and a cutoff of 6. A combination of L-type fatty acid–binding protein with the RAI improved the predictive performance for assessing persistent AKI with an AUC of 0.79.ConclusionThe RAI may be effective in predicting persistent AKI in adult patients admitted from general wards. Incorporation of AKI biomarkers into the RAI may potentially improve prediction.
Acute kidney injury (AKI) is a major clinical problem that still has no established treatment. We investigated the efficacy of cultured human peripheral blood mononuclear cells (PBMNCs) for AKI. Ischemia/reperfusion injury (IRI) was used to induce AKI in male nonobese diabetic (NOD/severe combined immunodeficiency) mice aged 7 to 8 wk. PBMNCs were isolated from healthy volunteers and were subjected to quality and quantity controlled (QQc) culture for 7 d in medium containing stem cell factor, thrombopoietin, Flt-3 ligand, vascular endothelial growth factor, and interleukin 6. IRI-induced mice were divided into 3 groups and administered (1) 1 × 106 PBMNCs after QQc culture (QQc PBMNCs group), (2) 1 × 106 PBMNCs without QQc culture (non-QQc PBMNCs group), or (3) vehicle without PBMNCs (IRI control group). PBMNCs were injected via the tail vein 24 h after induction of IRI, followed by assessment of renal function, histological changes, and homing of injected cells. Blood urea nitrogen and serum creatinine (Cr) 72 h after induction of IRI in the QQc PBMNCs group dramatically improved compared with those in the IRI control and the non-QQc PBMNCs groups, accompanied by the improvement of tubular damages. Interstitial fibrosis 14 d after induction of IRI was also significantly improved in the QQc PBMNCs group compared with the other groups. The renoprotective effect noted in the QQc PBMNCs group was accompanied by reduction of peritubular capillary loss. The change of PBMNCs’ population (increase of CD34+ cells, CD133+ cells, and CD206+ cells) and increased endothelial progenitor cell colony-forming potential by QQc culture might be one of the beneficial mechanisms for restoring AKI. In conclusion, an injection of human QQc PBMNCs 24 h after induction of IRI dramatically improved AKI in mice.
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