The attributable mortality of new-onset acute kidney injury among critically ill patients: a propensity-matched analysis based on a multicentre prospective cohort study

Purpose This study aimed to evaluate the attributable mortality of new-onset acute kidney injury (AKI). Methods The data in the present study were derived from a multi-center, prospective cohort study in China that was performed at 18 Chinese ICUs. A propensity-matched analysis was performed between matched patients with and without AKI selected from all eligible patients to estimate the attributable mortality of new-onset AKI. Results A total of 2872 critically ill adult patients were eligible. The incidence of new-onset AKI was 29.1% (n = 837). After propensity score matching, 788 patients with AKI were matched 1:1 with 788 controls (patients without AKI). Thirty-day mortality was significantly higher among the patients with AKI than among their matched controls (25.5% versus 17.4%, p < 0.001). Subgroup analysis in terms of AKI classification showed that there was no significant difference (p = 0.509) in 30-day mortality between patients with stage 1 AKI and their matched controls. The attributable mortality values of stage 2 and stage 3 AKI were 12.4% [95% confidence interval (CI) 2.6–21.8%, p = 0.013] and 16.1% (95% CI 8.2–23.8%, p < 0.001), respectively. The attributable mortality of persistent AKI was 15.7% (95% CI 8.8–22.4%, p = 0.001), while no observable difference in 30-day mortality was identified between transient AKI patients and their matched non-AKI controls (p = 0.229). Conclusion The absolute excess 30-day mortality that is statistically attributable to new-onset AKI is substantial (8.1%) among general ICU patients. However, neither stage 1 AKI nor transient AKI increases 30-day mortality.

Risk factors, clinical features and outcome of new-onset acute kidney injury among critically ill patients: a database analysis based on prospective cohort study

Background Acute kidney injury (AKI) newly-emerged in intensive care unit (ICU), has not been thoroughly studied in previous researches, is likely to differ from AKI developed before ICU admission. This study aimed to evaluate the incidence, risk factors, clinical features and outcome of new-onset AKI in critically ill patients. Methods The data of present study derived from a multicenter, prospective cohort study in17 Chinese ICUs (January 2014 - August 2015). The incidence, risk factors, clinical features and survival analysis of new-onset AKI were assessed. Results A total of 3374 adult critically ill patients were eligible. The incidence of new-onset AKI was 30.0 % (n = 1012). Factors associated with a higher risk of new-onset AKI included coronary heart disease, hypertension, chronic liver disease, use of nephrotoxic drugs, sepsis, SOFA score, APACHEII score and use of vasopressors. The new-onset AKI was an independent risk factor for 28-day mortality (adjusted hazard ratio, 1.643; 95 % CI, 1.370–1.948; P < 0.001). 220 (21.7 %) patients received renal replacement therapy (RRT), 71 (32.3 %) of them were successfully weaning from RRT. More than half of the new-onset AKI were transient AKI (renal recovery within 48 h). There was no statistical relationship between transient AKI and 28-day mortality (hazard ratio, 1.406; 95 % CI, 0.840–1.304; P = 0.686), while persistent AKI (non-renal recovery within 48 h) was strongly associated with 28-day mortality (adjusted hazard ratio, 1.486; 95 % CI, 1.137–1.943; P < 0.001). Conclusions New-onset AKI is common in ICU patients and is associated with significantly higher 28-day mortality. Only persistent AKI, but not transient AKI is associated with significantly higher 28-day mortality.

Duration of Acute Kidney Injury and in-hospital Mortality in Elder Patients With Severe COVID-19: a Retrospective Cohort Study

Background Patients with severe coronavirus disease 2019 (COVID-19) who develop acute kidney injury (AKI) in the intensive care unit (ICU) have extremely high rates of mortality. This study evaluated the prognostic impact of AKI duration on in-hospital mortality in elder patients.Methods We performed a retrospective study of 126 patients with confirmed COVID-19 with severe or critical disease who treated in the ICU from February 4, 2020, to April 16, 2020. AKI was defined according to the Kidney Disease Improving Global Outcomes serum creatinine (Scr) criteria. AKI patients were divided into transient AKI and persistent AKI groups based on whether Scr level returned to baseline within 48 h post-AKI.Results In total, 107 patients were included in the final analysis. The mean age was 70 (64–78) years, and 69 (64.5%) patients were men. AKI occurred in 48 (44.9%) during their ICU stay. Of these, 11 (22.9%) had transient AKI, 37 (77.9%) had persistent AKI. In-hospital mortality was 18.6% (n =11) for patients without AKI, 72.7% (n=8) for patients with transient AKI, and 86.5% (n=32) for patients with persistent AKI (P<0.001). Kaplan–Meier curve analysis revealed that patients with both transient AKI and persistent AKI had significantly higher death rates than those without AKI (log-rank P<0.001). Multivariate Cox regression analysis revealed that transient and persistent AKI were an important risk factor for in-hospital mortality in older patients with severe COVID-19 even after adjustment for variables (hazard ratio [HR]=2.582; 95% CI: 1.025–6.505; P=0.044; and HR=6.974; 95% CI: 3.334–14.588; P<0.001).Conclusions AKI duration is a useful parameter to predict of worse clinical outcomes in elder patients with COVID-19 in the ICU. Among AKI patients, those persistent AKI have a lower in-hospital survival rate than those transient AKI, emphasizing the importance of identifying an appropriate treatment window for early intervention.

MO372IN-HOSPITAL MORTALITY IN ACUTE CARDIAC DISEASES IS ASSOСIATED WITH CERTAIN PHENOTYPES OF ACUTE KIDNEY INJURY

Background and Aims Impaired renal function is a common finding in patients with cardiac diseases and confers an adverse prognosis in this population. To evaluate the incidence, phenotypes and prognostic value of cardiorenal interrelations in patients with acute decompensated heart failure (ADHF) and non-ST-elevation acute coronary syndrome (NSTE-ACS). Method we examined 278 patients with ADHF (85.3% had anamnesis of symptomatic HF with frequent hospitalizations, 20.1% had ejection fraction &lt;35%) and 288 with NSTE-ACS (64.9% developed myocardial infarction (MI)). In ADHF group in comparison with NSTE-ACS the patients were younger (69.7±10.2 vs 72±12.1 years, p&lt;0.01), there were more males (55.4 vs 36.5%, p&lt;0.001), smokers and alcohol abusers (47.8 and 30.6% vs 8 and 5.6%, p&lt;0.001). The comorbidities were more typical for ADHF group: atrial fibrillation 46 vs 24% (p&lt;0.001), obesity 55.8 vs 30.9% (p&lt;0.001), anemia 40.6 vs 25.3% (p&lt;0.001), diabetes mellitus 33.1 vs 23.3% (p&lt;0.01). Chronic kidney disease (CKD) and acute kidney injury (AKI) were diagnosed according to KDIGO 2012 Guidelines. AKI phenotypes were identified depending on time of development (community- or hospital-acquired), persistency (transient or persistent), history of CKD (AKI de novo or AKI on CKD). Results Incidence of CKD in patients with ADHF and NSTE-ACS was 45 and 46.5%, CKD was first diagnosed on admission in 57.6 and 64.2% of patients respectively. In 7.6% cases of ADHF and 14.2% of NSTE-ACS groups the duration of impaired kidney function was unknown. No associations of existing CKD and in-hospital mortality were detected. Incidence of AKI in ADHF and NSTE-ACS groups was 43.5 and 37.2%. The hospital-acquired AKI, AKI on CKD and persistent AKI were found in 52.9, 47.9 and 46.3% of ADHF patients, and in 57.9, 58.9 and 50.5% in NSTE-ACS group respectively. In-hospital mortality was higher in patients with AKI in ADHF and NSTE-ACS groups (12.4 vs 5%, p&lt;0.01 and 17.8 vs 3.3%, p&lt;0.001). Mortality in patients with ADHF and hospital-acquired persistent AKI de novo and community-acquired persistent AKI on CKD was 41 and 29%, and in community-acquired transient AKI on CKD in the NSTE-ACS group – 29%. Conclusion Different cardiorenal interrelations were revealed in 75.2% of patients with ADHF and in 61.8% with NSTE-ACS. In patients with acute cardiac diseases high in-hospital mortality is tightly associated with phenotypes of hospital-acquired persistent AKI de novo and community-acquired persistent AKI on CKD in ADHF, and in community-acquired transient AKI on CKD in the NSTE-ACS.

Prognosis of acute kidney injury during acute heart failure: the role of diuretics

Background Acute kidney injury (AKI) frequently occurs after diuretic treatment initiation during acute heart failure (AHF). Treatment-induced hemoconcentration seems associated with improved prognosis. Transient AKI, with or without hemoconcentration, is of unsettled prognosis. Purpose We aimed to determine the independent prognostic values of transient AKI, persistent AKI and hemoconcentration in the context of hospitalized AHF. Methods Data were obtained from our institution's Clinical Data Warehouse. Patients that visited our unit at least once were screened. All hospitalizations in our institution were examined (&gt;30 hospitals). Inclusion criteria were: ≥1 hospitalization with ≥1 recorded furosemide administration and ≥1 AHF ICD-10 code. Only the first hospitalization fulfilling these criteria was considered. AKI during 1–13 days following first furosemide administration was defined based on Kidney Disease Improving Global Outcome guidelines. Hemoconcentration was defined as an increase in serum proteins ≥5 g/l during the same period. We performed multivariate logistic regression to determine which characteristics were predictive of AKI. We used Cox regression of 100-days all-cause mortality using several confounders to determine the prognostic values of transient AKI (lasting &lt;14 days), persistent AKI (lasting ≥14 days) and hemoconcentration. To account for immortality bias, AKI and hemoconcentration were treated as time-dependent covariates. Results We included 579 patients in the study. Median follow-up was 114 days. AKI following furosemide initiation occurred in 234 patients (40.4%). Patients that experienced AKI more frequently suffered from chronic kidney disease (43.6% vs. 33%, p=0.01) or presented with right ventricular dilatation (12% vs. 6.7%, p=0.04). Independent predictors of AKI were arterial hypertension (adjusted OR: 1.86 [1.08–3.22]), elevated serum creatinine at baseline (adjusted OR: 1.07 [1.01–1.14] per 10 μmol/l increase) and initial intravenous furosemide (adjusted OR: 2.42 [1.39–4.29]). Death during follow-up occurred in 35% of patients in the AKI group compared to 21% in the non-AKI group (p&lt;0.001). In Cox regression, persistent AKI was independently associated with increased mortality in a period of 100 days following furosemide initiation (adjusted HR: 2.31 [1.07–4.99]). Transient AKI was not significantly associated with mortality (adjusted HR: 0.64 [0.34–1.19]). Hemoconcentration was independently associated with decreased mortality (adjusted HR: 0.46 [0.27–0.79]). Conclusion In the context of hospitalized AHF, AKI that developed 1–13 days after furosemide initiation and that lasted ≥14 days was independently associated with decreased 100 days survival. Hemoconcentration, using a clinically relevant definition, was independently associated with improved survival. These findings show that serum creatinine and proteins, routinely used and with limited cost, accurately stratify mortality risk during AHF. Kaplan-Meier curves Funding Acknowledgement Type of funding source: None

A high urea-to-creatinine ratio predicts long-term mortality independent of acute kidney injury among patients hospitalized with an infection

Acute kidney injury (AKI) occurs frequently in patients with sepsis. Persistent AKI is, in contrast to transient AKI, associated with reduced long-term survival after sepsis, while the effect of AKI on survival after non-septic infections remains unknown. As prerenal azotaemia is a common cause of transient AKI that might be identified by an increased urea-to-creatinine ratio, we hypothesized that the urea-to-creatinine ratio may predict the course of AKI with relevance to long-term mortality risk. We studied the association between the urea-to-creatinine ratio, AKI and long-term mortality among 665 patients presented with an infection to the ED with known pre-existent renal function. Long-term survival was reduced in patients with persistent AKI. The urea-to-creatinine ratio was not associated with the incidence of either transient or non-recovered AKI. In contrast, stratification according to the urea-to-creatinine-ratio identifies a group of patients with a similar long-term mortality risk as patients with persistent AKI. Non-recovered AKI is strongly associated with all-cause long-term mortality after hospitalization for an infection. The urea-to-creatinine ratio should not be employed to predict prerenal azotaemia, but identifies a group of patients that is at increased risk for long-term mortality after infections, independent of AKI and sepsis.

Acute kidney injury in hospitalized patients with COVID-19

Introduction: The incidence of AKI in coronavirus disease 2019 (COVID-19) patients ranges from 0.5 to 35% and has been associated with worse prognosis. The purpose of this study was to evaluate the incidence, severity, duration, risk factors and prognosis of AKI in hospitalized patients with COVID-19.Methods: We conducted a retrospective single-center analysis of 192 hospitalized COVID-19 patients from March to May of 2020. AKI was diagnosed using the Kidney Disease Improving Global Outcome (KDIGO) classification based on serum creatinine (SCr) criteria. Persistent and Transient AKI were defined according to the Acute Disease Quality Initiative (ADQI) workgroup definitions.Results: In this cohort of COVID-19 patients, 55.2% developed AKI (n=106). The majority of AKI patients had persistent AKI (n=64, 60.4%). Overall, in-hospital mortality was 18.2% (n=35) and was higher in AKI patients (28.3% vs 5.9%, p<0.001, unadjusted OR 6.03 (2.22-16.37), p<0.001). On a multivariate analysis, older age (adjusted OR 1.08 (95% CI 1.02-1.13), p=0.004), lower Hb level (adjusted OR 0.69 (95% CI 0.53-0.91), p=0.007) and acidemia at presentation (adjusted OR 5.53 (95% CI 1.70-18.63), p=0.005), duration of AKI (adjusted OR 7.91 for persistent AKI (95% CI 2.39-26.21), p=0.001) and severity of AKI (adjusted OR 2.30 per increase in KDIGO stage (95% CI 1.10-4.82), p=0.027) were independent predictors of mortality.Conclusion: AKI was frequent in hospitalized patients with COVID-19. Persistent AKI and higher severity of AKI were independent predictors of in-hospital mortality.

TO019PROGNOSTIC VALUE OF ACUTE KIDNEY INJURY AND HEMOCONCENTRATION DURING ACUTE HEART FAILURE

Background and Aims Acute kidney injury (AKI) occurring after diuretic treatment initiation for acute heart failure (AHF) is a common phenomenon, with an incidence estimated between 20 and 50% of AHF hospitalizations. Previous studies found that persistent AKI is associated with poor prognosis. Treatment-induced hemoconcentration is associated with improved prognosis, but several definitions previously used are not suited for clinical practice. Transient AKI, with or without hemoconcentration, is of unsettled prognosis. We aim to determine the independent prognostic value of transient AKI, persistent AKI and hemoconcentration in the context of AHF hospitalization, using practical definitions. Method Data were obtained from the Greater Paris University Hospitals (GPUH) Clinical Data Warehouse. Patients hospitalized for AHF in various GPUH units were included. AHF hospitalization was defined as hospitalization with at least one AHF ICD-10 code and at least one recorded furosemide administration. Bumetanide is rarely used in GPUH hospitals hence it was not considered. AKI in a period of 14 days following first furosemide administration was defined based on KDIGO guidelines. Hemoconcentration was defined as an increase in serum proteins ≥ 5 g/l during the same period. Multivariate logistic regression was performed to determine which characteristics were predictive of AKI. Cox regression of 100 days all-cause mortality using multiple confounders was performed to determine the prognostic value of transient AKI (&lt; 14 days), persistent AKI (≥ 14 days) and hemoconcentration. Patients with AKI upon hospital entry were excluded from regression analyses. AKI and hemoconcentration were treated as time-dependent covariates to adjust for immortality bias. Results Five hundred seventy nine patients were included. Among them, 529 had no AKI upon hospital entry and 513 had at least one recorded serum proteins and creatinine value following furosemide initiation. Median follow-up was 114 days. AKI in a period of 14 days following furosemide initiation occurred in 234 patients (40.4%). At baseline, patients in the AKI group more frequently suffered from chronic kidney disease or presented with clinical and echocardiographic signs of right heart failure. Independent predictors of AKI were arterial hypertension upon furosemide initiation (adjusted OR 1.86 [1.08 – 3.22]), elevated serum creatinine upon furosemide initiation (adjusted OR 1.07 [1.01 – 1.14] per 10 µmol/l increase) and initial intravenous administration of furosemide (adjusted OR 2.42 [1.39 – 4.29]). Death during follow-up occurred in 35% of patients in the AKI group compared to 21% in the non-AKI group (p &lt; 0.001). In multivariate analysis, persistent AKI was independently associated with increased mortality in a period of 100 days following furosemide initiation (adjusted HR 2.31 [1.07 – 4.99]). Transient AKI was not significantly associated with mortality (adjusted HR 0.64 [0.34 – 1.19]). Hemoconcentration was independently associated with decreased mortality (adjusted HR 0.46 [0.27 – 0.79]). Conclusion After furosemide initiation during hospitalization for AHF, persistent AKI (≥ 14 days) was independently associated with increased 100 days mortality. Hemoconcentration, using a definition suited for clinical practice (≥ 5 g/l increase in serum proteins), was independently associated with decreased 100 days mortality. No significant association was found between mortality and transient AKI (&lt; 14 days). Those findings show that laboratory tests at a limited cost – serum proteins and creatinine – are helpful to evaluate treatment response and mortality risk during AHF. Prospective randomized controlled trials are needed to establish diuretic strategies based on both AKI and hemoconcentration.

Risk factors and in-hospital outcomes of acute kidney injury that developed after coronary artery bypass grafting in patients with stable angina

The aim of the study is to assess frequency, risk factors and in-hospital outcomes of acute kidney injury after coronary artery bypass grafting in patients with stable angina. Materials and methods. The study included patients with stable angina pectoris and indications for coronary artery bypass grafting. We examined 93 patients aged 58±7.6 years, with duration of coronary heart disease 6±6.0 years. Previous myocardial infarction had 79.6% of patients. Arterial hypertension was present in 92.5% of patients. Multi-vessel coronary disease was registered in 94.6%, stenosis of the left main coronary artery > 50% was in 16.1% of patients. Coronary artery bypass grafting in conditions of artificial circulation was performed in 89.2% of patients, coronary grafting on working heart was held in 10.8% of patients. At initial stage, on the first and second days after coronary grafting the level of creatinine was determined by the method of Jaffe. The presence, the severity of acute kidney injury after (AKI) coronary artery bypass grafting was evaluated according to the criteria KDIGO (2012). We took into account in-hospital complications: cardiac death, intraoperative myocardial infarction (iMI), stroke, atrial fibrillation (AF), acute heart failure (AHF) according to requirement in intraaortic balloon pump, and the use of adrenaline. Results. The proportion of persons with transient AKI stage 1 after coronary artery bypass grafting was 31.2%, those of 2 stage was 3.2%. The development of AKI was associated with cases of AHF. The increase in the duration of therapy with adrenaline - more than 1±1.8 days (median) - was connected with increase of the relative risk of AKI developing in 1.9 times. The incidence of cardiac death, iMI, strokes, paroxysmal AF did not differ among patients with AKI and without it. Conclusion. The frequency of transient AKI after coronary artery bypass grafting was 34.4%. The development of AKI is associated with AHF that occurred during coronary artery bypass grafting. The frequency of hospital complications did not differ among patients with AKI after coronary artery bypass grafting and without it.

The role of novel biomarkers in acute kidney injury

Although there is a growing literature on the performance of various biomarkers in clinical studies, there is limited information on how these biomarkers would be utilized by clinicians to manage patients with acute kidney injury (AKI). The majority of investigations have focused on the ability of biomarkers to detect early either incipient or established AKI. Other studies have prospectively explored their prognostic performance in predicting either need for renal replacement therapy or intensive care unit (ICU) or hospital mortality or duration of either ICU or hospital stay. A few studies have also investigated their potential in the differential diagnosis between ‘transient AKI’, ‘prerenal AKI’, and established intrinsic AKI, mostly acute tubular necrosis.