Definition Of Acute Kidney Injury Research Articles

Reframing acute kidney injury as a pathophysiological continuum of disrupted renal excretory function.

Surrogate measures of glomerular filtration rate (GFR) continue to serve as pivotal determinants of the incidence, severity, and management of acute kidney injury (AKI), as well as the primary reference point underpinning knowledge of its pathophysiology. However, several clinically important deficits in aspects of renal excretory function during AKI other than GFR decline, including acid-base regulation, electrolyte and water balance, and urinary concentrating capacity, can evade detection when diagnostic criteria are built around purely GFR-based assessments. The use of putative markers of tubular injury to detect "sub-clinical" AKI has been proposed to expand the definition and diagnostic criteria for AKI, but their diagnostic performance is curtailed by ambiguity with respect to their biological meaning and context specificity. Efforts to devise new holistic assessments of overall renal functional compromise in AKI would foster the capacity to better personalize patient care by replacing biomarker threshold-based diagnostic criteria with a shift to assessment of compromise along a pathophysiological continuum. The term AKI refers to a syndrome of sudden renal deterioration, the severity of which is classified by precise diagnostic criteria that have unquestionable utility in patient management as well as blatant limitations. Particularly, the absence of an explicit pathophysiological definition of AKI curtails further scientific development and clinical handling, entrapping the field within its present narrow GFR-based view. A refreshed approach based on a more holistic consideration of renal functional impairment in AKI as the basis for a new diagnostic concept that reaches beyond the boundaries imposed by the current GFR threshold-based classification of AKI, capturing broader aspects of pathogenesis, could enhance AKI prevention strategies and improve AKI patient outcome and prognosis.

#462 Initiation of SGLT2i vs GLP1-RA and incidence of AKI in persons with type 2 diabetes mellitus

Abstract Background and Aims Adverse kidney outcomes, including acute kidney injury (AKI), are frequent complications in people with diabetes mellitus type 2. In large placebo-controlled randomized trials, both sodium-glucose cotransporter-2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor agonists (GLP1-RA) have shown efficacy in reducing the risk of kidney outcomes; however, no trial has compared the kidney protective effects of these drug classes head-to-head. We therefore conducted an emulated target trial to compare the effect of SGLT2i to that of GLP1-RA on the incidence of AKI. Method Using routinely collected data from nationwide Danish population-based registries, we included all adults with diabetes mellitus type 2 initiating SGLT2i or GLP1-RA in 2015-2020. Patients with prevalent kidney failure (defined as eGFR < 15 mL/min/1.73m2, dialysis, or kidney transplant), and patients initiating GLP1-RA marketed specifically for treatment of obesity were excluded. We assessed demographic and diabetes-related baseline characteristics along with comorbidities and comedication. We used propensity scores, estimated by logistic regression, to compute stabilized inverse probability of treatment weights, which were applied in all analyses to reduce confounding. Using an intention to treat approach, we followed patients from treatment initiation until the first of death, emigration, or end of follow-up (31 December 2021). Using creatinine measurements from in- and outpatient settings, we applied the KDIGO definition of AKI to record each episode of AKI during follow-up. We estimated the risk of a first AKI episode over time using the Aalen-Johansen estimator. Furthermore, to estimate the mean number of AKIs over time, i.e., including recurrent AKIs, we used the mean cumulative count estimator. Both estimators account for the competing risk of death. Comparing SGLT2i to GLP1-RA, we reported differences in risks and counts at 1, 3 and 5 years of follow-up. Finally, we estimated all-cause mortality using the Kaplan-Meier estimator. We used bootstrapping to obtain 95% confidence intervals (95% CI). Results We included 68 010 individuals, of which 44 034 (65%) initiated SGLT2i, and 23 976 (35%) initiated GLP1-RA. Initiators of SGLT2i were slightly older (median age 63 vs 62 years) and more often male (63% vs 56%) than initiators of GLP1-RA, but with similar diabetes duration (7 vs 7 years). The annual number of initiators of each drug in Denmark increased over the study period. Compared to GLP1-RA, initiators of SGLT2i generally had better estimated glomerular filtration rate (eGFR) at baseline (9% vs 18% had eGFR < 60 mL/min/1.73m2), more frequently used metformin (91% vs 84%), but less frequently insulin (11% vs 28%). Initiators of SGLT2i had a lower prevalence of hospital-diagnosed retinopathy (7% vs 9%), neuropathy (5% vs 6%), and obesity (13% vs 23%) than initiators of GLP1-RA. After inverse probability of treatment weighting, each variable was well balanced with absolute standardized mean differences below 0.02. During a median follow-up of 2.8 years, the weighted absolute risks of first time AKI at 1, 3, and 5 years were 4.8%, 11.2%, and 17.0% for initiators of SGLT2i, and 5.4%, 12.3%, and 19.1% for initiators of GLP1-RA, resulting in AKI risk differences of −0.6% (95% CI: −1.0% to −0.3%), −1.0% (95% CI: −1.7% to −0.5%), and −2.0% (95% CI: −3.0% to −1.1%). The mean cumulative counts showed a similar pattern, with SGLT2i initiators experiencing slightly fewer AKI episodes than GLP1-RA initiators on average (Fig. 1). After 5 years, an estimated 10.3% of SGLT2i initiators and 9.6% of GLP1-RA initiators had died, resulting in a risk difference of 0.7% (95% CI: -0.1% to 1.5%). Conclusion People with diabetes mellitus type 2 who initiated SGLT2i had slightly lower weighted incidence of AKI over 5 years than those initiating GLP1-RA.

Cardiac Surgery Associated Acute Kidney Injury (CSA-AKI).

Acute kidney injury (AKI) is a common and serious complication of cardiac surgery that has a significant impact on patient morbidity and mortality. The Kidney Disease Improving Global Outcomes (KDIGO) definition of AKI is widely used to classify and identify AKI associated with cardiac surgery (CSA-AKI) based on changes in serum creatinine and/or urine output. There are various pre-, intra-, and postoperative risk factors for the development of CSA-AKI which should be recognized and addressed as early as possible to expedite its diagnosis, reduce its occurrence and prevent or ameliorate its devastating complications. Crucial issues are the inaccuracy of serum creatinine as a surrogate parameter of kidney function in the perioperative setting of cardiothoracic surgery and the necessity to discover more representative markers of the pathophysiology of AKI. However, except for the tissue inhibitor of metalloproteinase-2 and insulin-like growth factor binding protein 7 ratio (TIMP2/IGFBP7), other diagnostic biomarkers with an acceptable sensitivity and specificity are still lacking. This article provides a comprehensive review of various aspects of CSA-AKI, including pathogenesis, risk factors, diagnosis, biomarkers, classification, prevention and treatment management.

Updates on new eGFR equations and acute kidney injury definitions

Updates on new eGFR equations and acute kidney injury definitions

Uric acid and acute kidney injury in high-risk patients for developing acute kidney injury undergoing cardiac surgery: A prospective multicenter study

PurposeIt is unclear whether preoperative serum uric acid (SUA) elevation may play a role in the development of acute kidney injury (AKI) associated with cardiac surgery (CSA-AKI). We conducted a cohort study to evaluate the influence of preoperative hyperuricemia on AKI in patients at high risk for developing SC-AKI. DesignMulticenter prospective international cohort study. SettingFourteen university hospitals in Spain and the United Kingdom. ParticipantsWe studied 261 consecutive patients at high risk of developing CSA-AKI, according to a Cleveland score ≥ 4 points, from July to December 2017. InterventionsNone. Measurements and main resultsAKIN criteria were used for the definition of AKI. Multivariable logistic regression models and propensity score-matched pairwise analysis were used to determine the adjusted association between preoperative hyperuricemia (≥7 mg/dL) and AKI. Elevated preoperative AUS (≥7 mg/dL) was present in 190 patients (72.8%), whereas CSA-AKI occurred in 145 patients (55.5%). In multivariable logistic regression models, hyperuricemia was not associated with a significantly increased risk of AKI (adjusted Odds Ratio [OR]: 1.58; 95% confidence interval [CI]: 0.81–3; P = .17). In propensity score-matched analysis of 140 patients, the hyperuricemia group experienced similar adjusted odds of AKI (OR 1.05, 95%CI 0.93–1.19, P = .37). ConclusionsHyperuricemia was not associated with an increased risk of AKI in this cohort of patients undergoing cardiac surgery at high risk of developing CSA-AKI.

Short-, Mid-, and Long-term Outcomes after Deceased Donor Kidney Transplantation in Patients with Acute Kidney Injury.

Acute kidney injury (AKI) is a common complication in hospitalized patients and may occur in potential kidney donors. Observational studies have suggested that kidney transplantation in patients with AKI is feasible and safe, but no systematic evaluation has been performed. We performed a systematic review and meta-analysis to evaluate the outcomes of kidney transplantation in patients with AKI. We searched MEDLINE, EMBASE, Cochrane, Google Scholar, and other databases for studies reporting outcomes of donor kidneys with AKI. We included single-center, multicenter, and registry-based studies and analyzed them according to the definition and severity of AKI. Endpoints were primary and delayed graft function (PNF, DGF), length of hospital stay, rejection, graft function, patient and graft survival at one, three, five, and eight to ten years after transplantation. This study was registered in PROSPERO, number CRD42021260088. We identified 33 single-center, 4 multicenter, and 7 registry studies with more than 100,000 patients published between 2005 and 2022. Recipients from donors with AKI had a higher risk of delayed graft function (RR 1.51, 95% CI 1.35-1.68). Graft function at discharge was worse in the AKI group (MDCrea (95%CI): 0.96 mg/dl (0.36-1.56 I2=96%), MDGFR (95%CI): -8.88 ml/min1.73 m2 (-15.32 - -2.44 I2=93%)), but improved thereafter and was similar in both groups at 3 months after transplantation (MDCrea (95%CI): -0.05 mg/dl (-0.18-0.07 I2=0%), MDGFR (95%CI): -1.83 ml/min1.73 m2 (-5.29 - 1.63 I2=91%)). PNF and patient and graft survival were simila at one, three, five, and eight to ten years after transplantation. There were no differences in rejections regardless of AKI definition and severity. Transplantation of kidneys with AKI is associated with satisfactory short- and long-term outcomes and should be pursued to increase the donor pool.

Acute kidney injury in acute liver failure: A narrative review.

Acute kidney injury (AKI) is a frequent complication of acute liver failure (ALF) and it worsens the already worse prognoses of ALF. ALF is an uncommon disease, with varying etiologies and varying definitions in different parts of the world. There is limited literature on the impact of AKI on the outcome of ALF with or without transplantation. The multifaceted etiology of AKI in ALF encompasses factors such as hemodynamic instability, systemic inflammation, sepsis and direct nephrotoxicity. Indications of renal replacement therapy (RRT) for AKI in ALF patients extend beyond the conventional criteria for dialysis and continuous renal replacement therapy (CRRT) may have a role in transplant-free survival or bridge to liver transplantation (LT). LT is a life-saving option for ALF, so despite somewhat lower survival rates of LT in ALF patients with AKI, LT is not usually deferred. In this review, we will discuss the guidelines' recommended definition and classification of AKI in ALF, the impact of AKI in ALF, the pathophysiology of AKI and the role of CRRT and LT in ALF patients with AKI.

Sepsis-Associated Acute Kidney Injury: Where Are We Now?

Worldwide, sepsis is a well-recognized cause of death. Acute kidney injury (AKI) may be related to sepsis in up to 70% of AKI cases. Sepsis-associated AKI (SA-AKI) is defined as the presence of AKI according to the Kidney Disease: Improving Global Outcomes criteria in the context of sepsis. SA-AKI is categorized into early, which presents during the first 48 h of sepsis, and late, presenting between 48 h and 7 days of sepsis. SA-AKI is associated with a worse prognosis among patients with sepsis. However, there are different SA-AKI phenotypes as well as different pathophysiological pathways of SA-AKI. The aim of this review is to provide an updated synopsis of the pathogenetic mechanisms underlying the development of SA-AKI as well as to analyze its different phenotypes and prognosis. In addition, potential novel diagnostic and prognostic biomarkers as well as therapeutic approaches are discussed. A plethora of mechanisms are implicated in the pathogenesis of SA-AKI, including inflammation and metabolic reprogramming during sepsis; various types of cell death such as apoptosis, necroptosis, pyroptosis and ferroptosis; autophagy and efferocytosis; and hemodynamic changes (macrovascular and microvascular dysfunction). Apart from urine output and serum creatinine levels, which have been incorporated in the definition of AKI, several serum and urinary diagnostic and prognostic biomarkers have also been developed, comprising, among others, interleukins 6, 8 and 18, osteoprotegerin, galectin-3, presepsin, cystatin C, NGAL, proenkephalin A, CCL-14, TIMP-2 and L-FABP as well as biomarkers stemming from multi-omics technologies and machine learning algorithms. Interestingly, the presence of long non-coding RNAs (lncRNAs) as well as microRNAs (miRNAs), such as PlncRNA-1, miR-22-3p, miR-526b, LncRNA NKILA, miR-140-5p and miR-214, which are implicated in the pathogenesis of SA-AKI, may also serve as potential therapeutic targets. The combination of omics technologies represents an innovative holistic approach toward providing a more integrated view of the molecular and physiological events underlying SA-AKI as well as for deciphering unique and specific phenotypes. Although more evidence is still necessary, it is expected that the incorporation of integrative omics may be useful not only for the early diagnosis and risk prognosis of SA-AKI, but also for the development of potential therapeutic targets that could revolutionize the management of SA-AKI in a personalized manner.

Artificial intelligence and acute kidney injury

Digitalization is increasingly finding its way into intensive care units and with it artificial intelligence (AI) for critically ill patients. One promising area for the use of AI is in the field of acute kidney injury (AKI). The use of AI is primarily focused on the prediction of AKI, but further approaches are also being used to classify existing AKI into different phenotypes. Different AI models are used for prediction. The area under the receiver operating characteristic curve values (AUROC) achieved with these models vary and are influenced by several factors, such as the prediction time and the definition of AKI. Most models have an AUROC between 0.650 and 0.900, with lower values for predictions further into the future and when applying Acute Kidney Injury Network (AKIN) instead of KDIGO criteria. Classification into phenotypes already makes it possible to categorize patients into groups with different risks of mortality or requirement of renal replacement therapy (RRT), but the etiologies or therapeutic consequences derived from this are still lacking. However, all the models suffer from AI-specific shortcomings. The use of large databases does not make it possible to promptly include recent changes in therapy and the implementation of new biomarkers in arelevant proportion. For this reason, serum creatinine and urinary output, with their known limitations, dominate current AI models for prediction impairing the performance of the current models. On the other hand, the increasingly complex models no longer allow physicians to understand the basis on which the warning of athreatening AKI is calculated and subsequent initiation of therapy should take place. The successful use of AIs in routine clinical practice will be highly determined by the trust of the physicians in the systems and overcoming the aforementioned weaknesses. However, the clinician will remain irreplaceable as the decisive authority for critically ill patients by combining measurable and nonmeasurable parameters.

Acute kidney injury in neonates with hypoxic ischemic encephalopathy based on serum creatinine decline compared to KDIGO criteria.

Neonates with hypoxic ischemic encephalopathy receiving therapeutic hypothermia (HIE + TH) are at risk for acute kidney injury (AKI). The standardized Kidney Disease Improving Global Outcomes (KDIGO) criteria identifies AKI based on a rise in serum creatinine (SCr) or reduced urine output. This definition is challenging to apply in neonates given the physiologic decline in SCr during the first week of life. Gupta et al. proposed alternative neonatal criteria centered on rate of SCr decline. This study aimed to compare the rate of AKI based on KDIGO and Gupta in neonates with HIE and to examine associations with mortality and morbidity. A retrospective review was performed of neonates with moderate to severe HIE + TH from 2008 to 2020 at a single center. AKI was assessed in the first 7days after birth by KDIGO and Gupta criteria. Mortality, brain MRI severity of injury, length of stay, and duration of respiratory support were compared between AKI groups. Among 225 neonates, 64 (28%) met KDIGO, 69 (31%) neonates met Gupta but not KDIGO, and 92 (41%) did not meet either definition. Both KDIGO-AKI and GuptaOnly-AKI groups had an increased risk of the composite mortality and/or moderate/severe brain MRI injury along with longer length of stay and prolonged duration of respiratory support compared to those without AKI. AKI in neonates with HIE + TH was common and varied by definition. The Gupta definition based on rate of SCr decline identified additional neonates not captured by KDIGO criteria who are at increased risk for adverse outcomes. Incorporating the rate of SCr decline into the neonatal AKI definition may increase identification of clinically relevant kidney injury in neonates with HIE + TH.

Ácido úrico y daño renal agudo en pacientes con alto riesgo de desarrollar daño renal agudo sometidos a cirugía cardiaca: cohorte prospectiva multicéntrica

PurposeIt is unclear whether preoperative serum uric acid (SUA) elevation may play a role in the development of acute kidney injury (AKI) associated with cardiac surgery (CSA-AKI). We conducted a cohort study to evaluate the influence of preoperative hyperuricemia on AKI in patients at high risk for developing SC-AKI. DesignMulticenter prospective international cohort study. SettingFourteen university hospitals in Spain and the United Kingdom. ParticipantsWe studied 261 consecutive patients at high risk of developing CSA-AKI, according to a Cleveland score ≥4 points, from July to December 2017. InterventionsNone. Measurements and Main ResultsAKIN criteria were used for the definition of AKI. Multivariable logistic regression models and propensity score-matched pairwise analysis were used to determine the adjusted association between preoperative hyperuricemia (> = 7 mg/dL) and AKI. Elevated preoperative AUS (> = 7 mg/dL) was present in 190 patients (72.8%), whereas CSA-AKI occurred in 145 patients (55.5%). In multivariable logistic regression models, hyperuricemia was not associated with a significantly increased risk of AKI (adjusted Odds Ratio [OR]: 1.58; 95% confidence interval [CI]: 0.81-3; p = 0.17). In propensity score-matched analysis of 140 patients, the hyperuricemia group experienced similar adjusted odds of AKI (OR 1.05, 95% CI 0.93-1.19, p = 0.37). ConclusionsHyperuricemia was not associated with an increased risk of AKI in this cohort of patients undergoing cardiac surgery at high risk of developing CSA-AKI.

Assessing Discharge Communication and Follow-up of Acute Kidney Injury in British Columbia: A Retrospective Chart Review.

Acute kidney injury (AKI) affects up to 20% of hospitalizations and is associated with chronic kidney disease, cardiovascular disease, increased mortality, and increased health care costs. Proper documentation of AKI in discharge summaries is critical for optimal monitoring and treatment of these patients once discharged. Currently, there is limited literature evaluating the quality of discharge communication after AKI. This study aimed to evaluate the accuracy and quality of documentation of episodes of AKI at a tertiary care center in British Columbia, Canada. This was a retrospective chart review study of adult patients who experienced AKI during hospital admission between January 1, 2018, and December 31, 2018. Laboratory data were used to identify all admissions to the cardiac and general medicine ward complicated by AKI defined by the Kidney Disease Improving Global Outcomes (KDIGO) criteria. A random sample of 300 AKI admissions stratified by AKI severity (eg, stages 1, 2, and 3) were identified for chart review. Patients were excluded if they required ongoing renal replacement therapy after admission, had a history of kidney transplant, died during their admission, or did not have a discharge summary available. Discharge summaries were reviewed for documentation of the following: presence of AKI, severity of AKI, AKI status at discharge, practitioner and laboratory follow-up plans, and medication changes. A total of 1076 patients with 1237 AKI admissions were identified. Of the 300 patients selected for discharge summary review, 38 met exclusion criteria. In addition, AKI was documented in 140 (53%) discharge summaries and was more likely to be documented in more severe AKI: stage 1, 38%; stage 2, 51%; and stage 3, 75%. Of those with their AKI documented, 94 (67%) documented AKI severity, and 116 (83%) mentioned the AKI status or trajectory at the time of discharge. A total of 239 (91%) of discharge summaries mentioned a follow-up plan with a practitioner, but only 23 (10%) had documented follow-up with nephrology. Patients with their AKI documented were more likely to have nephrology follow-up than those without AKI documented (17% vs 1%). Regarding laboratory investigations, 92 (35%) of the summaries had documented recommendations. In summaries that included medications typically held during AKI, only about half made specific reference to those medications being held, adjusted, or documented a post-discharge plan for that medication. For those with nonsteroidal anti-inflammatory drugs (NSAIDs) listing, 64% of discharge summaries mentioned holding, and 9% mentioned a discharge plan. For those with angiotensin converting enzyme inhibitor (ACEi)/angiotensin II receptor blocker (ARB) listing, 38% mentioned holding these medications, and 46% mentioned a discharge plan. In summaries with diuretics listed, 35% mentioned holding, and 51% included a discharge plan. We found suboptimal quality and completeness of discharge reporting in patients hospitalized with AKI. This may contribute to inadequate follow-up and post-hospitalization care for this patient population. Strategies are required for increasing the presence and quality of AKI reporting in discharge summaries. Limitations include our definition of AKI based on lab criteria, which may have missed some of the injuries that met the criteria based on urine output. Another limitation is that our definition of AKI based on the highest and lowest creatinine during admission may have led to some overclassification. In addition, without outpatient laboratories, it is possible that we have not captured the true baseline creatinine in some patients.

Review of the limitations of current biomarkers in acute kidney injury clinical practices.

Acute kidney injury is a prevalent disease in hospitalized patients and is continuously increasing worldwide. Various efforts have been made to define and classify acute kidney injury to understand the progression of this disease. Furthermore, deviations from structure and kidney function and the current diagnostic guidelines are not adequately placed due to baseline serum creatinine values, which are rarely known and estimated based on glomerular function rate, resulting in misclassification of acute kidney injury staging. Hence, the current guidelines are still developing to improve and understand the clinical implications of risk factors and earlier predictive biomarkers of acute kidney injury. Yet, studies have indicated disadvantages and limitations with the current acute kidney injury biomarkers, including lack of sensitivity and specificity. Therefore, the present narrative review brings together the most current evidenced-based practice and literature associated with the limitations of the gold standard for acute kidney injury diagnoses, the need for novel acute kidney injury biomarkers, and the process for biomarkers to be qualified for diagnostic use under the following sections and themes. The introduction section situates the anatomy and normal and abnormal kidney functions related to acute kidney injury disorders. Guidelines in providing acute kidney injury definitions and classification are then considered, followed by a discussion of the disadvantages of standard markers used to diagnose acute kidney injury. Characteristics of an ideal acute kidney injury biomarker are discussed concerning sensitivity, specificity, and anatomic location of injury. A particular focus on the role and function of emerging biomarkers is discussed in relation to their applications and significance to the prognosis and severity of acute kidney injury. Findings show emerging markers are early indicators of acute kidney injury prediction in different clinical settings. Finally, the process required for a biomarker to be applied for diagnostic use is explained.

Acute Kidney Injury and Hepatorenal Syndrome in Patients with Cirrhosis.

Acute kidney injury (AKI) is common in hospitalized patients with cirrhosis. Hepatorenal syndrome (HRS) is a type of AKI known as HRS-AKI. It is a severe complication of cirrhosis with high morbidity and mortality. While certain vasoconstrictor medications have been shown to improve HRS-AKI, no clear transplant-free survival benefit has been reported with medical therapies. Patients with HRS-AKI should be considered for urgent liver transplantation evaluation. In this review, we discuss the most recent updates on the definition, diagnosis, and management of AKI in cirrhosis, with special a emphasis on HRS.

Incidence of Antimicrobial-Associated Acute Kidney Injury in Children: A Structured Review.

Acute kidney injury (AKI) is a commonly reported adverse effect of administration of antimicrobials. While AKI can be associated with poorer outcomes, there is little information available to understand rates of AKI in children exposed to various antimicrobials. We performed a structured review using the PubMed and Embase databases. Articles were included if they provided an AKI definition in patients who were <19 years of age receiving an antimicrobial and reported the frequency of AKI. Author-defined AKI rates were calculated for each study and mean pooled estimates for each antimicrobial were derived from among all study participants. Pooled estimates were also derived for those studies that reported AKI according to pRIFLE(pediatric risk, injury, failure, loss, end stage criteria), AKIN(acute kidney injury network), or KDIGO (kidney disease improving global outcomes)creatinine criteria. A total of 122 studies evaluating 28 antimicrobials met the inclusion criteria. Vancomycin was the most commonly studied drug: 11,514 courses across 44 included studies. Among the 27,285 antimicrobial exposures, the overall AKI rate was 13.2% (range 0-42.1% by drug), but the rate of AKI varied widely across studies (range 0-68.8%). Cidofovir (42.1%) and conventional amphotericin B (37.0%) had the highest pooled rates of author-defined AKI. Eighty-one studies used pRIFLE, AKIN, or KDIGO AKI criteria and the pooled rates of AKI were similar to author-defined AKI rates. In conclusion, antimicrobial-associated AKI is reported to occur frequently in children, but the rates of AKI varies widely across studies and drugs. Most published studies examined hospitalized patients and heterogeneity in study populations and in author definitions of AKI are barriers to a comparison of nephrotoxicity risk among antimicrobials in children.

Association of cardiopulmonary bypass with acute kidney injury in patients undergoing coronary artery bypass grafting: a retrospective cohort study.

Association of cardiopulmonary bypass with acute kidney injury in patients undergoing coronary artery bypass grafting: a retrospective cohort study.

Abstract 14823: Assessment of the Appropriateness and Prognostic Significance of the Current Universal Diagnostic Definition for Acute Kidney Injury in Patients After Cardiac Surgery and Exploration of Tailored Criteria

Background: Cardiac surgery-associated AKI (CSA-AKI) is prevalent and its diagnosis currently adheres to the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines, commonly used criteria developed for general populations. Limited evidence exists on their appropriateness and prognostic value for CSA-AKI, which exhibits unique mechanisms and clinical courses. Aims: We aimed to assess the prognostic value of the KDIGO diagnostic criteria for CSA-AKI and explore potentially more prognostically relevant criteria for cardiac surgery. Methods: Patients undergoing coronary artery bypass grafting surgery at a single institution were included and categorized into four groups: no AKI, AKI stage-1, AKI stage-2, and AKI stage-3, based on KDIGO guidelines. Patients of AKI-1 were further divided based on specific criteria met: absolute criteria (0.3mg/dL serum creatinine (SCr) increase over 48-hour intervals), ratio criteria (1.5-1.9 times baseline SCr), and dual criteria (meeting both criteria) AKI-1. The primary outcome was 30-day all-cause mortality. Results: Among 20626 patients, the overall incidence of CSA-AKI was 47.4%, with rates of 44.2% for AKI-1, 2.2% for AKI-2, and 0.9% for AKI-3. The overall 30-day mortality was 0.6%. Among AKI-1, 72.4%, 3.2%, and 24.2% met the absolute criteria, ratio criteria, and dual criteria, respectively. After multivariate adjustment, AKI-2 and AKI-3 were significantly associated with increased 30-day mortality. However, neither AKI-1 nor its subcategories showed prognostic significance. Subsequent restricted cubic spline analysis identified more prognostically relevant cut-off values for AKI-1 criteria as &gt;0.7 mg/dL SCr increase over 48-hour intervals and &gt;1.3 times baseline SCr, respectively. Conclusions: The current universal KDIGO diagnostic criteria may not be suitable for CSA-AKI, especially regarding cut-off values for AKI stage-1, highlighting the necessity of tailored criteria for cardiac surgery.

Acute Kidney Injury in Critically Ill Cirrhotic Patients with Spontaneous Bacterial Peritonitis

Acute kidney injury (AKI) is an important independent predictor of mortality in cirrhotic patients with spontaneous bacterial peritonitis (SBP). However, the definition of AKI in cirrhosis has been debated for many years. This study aims to compare the prediction accuracy of Kidney Disease: Improving Global Outcomes (KDIGO) and International Club of Ascites (ICA) criteria for hospital mortality in cirrhotic patients with SBP admitted to the intensive care unit (ICU).

Nouveaux marqueurs biologiques de l’insuffisance rénale aiguë

AbstractDespite a great heterogeneity of clinical situations, the definition of acute kidney injury (AKI) is unique and its diagnosis includes an increase in serum creatinine and/or a decrease in diuresis. Contrary to the evolution of the biological markers of myocardial infarction observed for more than 50 years, it is always the “functional marker” creatinine which serves as the biological gold standard for the diagnosis of AKI. However, under the term of acute renal failure, very heterogeneous clinical situations are grouped together from an etiological, pathophysiological mechanisms, duration, evolution and associated complications. For fifteen/twenty years, new potential biomarkers have been studied and seem promising. Unlike troponin, which is increased in all types of myocardial infarction, these new biomarkers have different sensitivities and specificities depending on the type of AKI, which possibly explains their under-use in current practice.

Early recognition and prevention of acute kidney injury in hospitalised children.

Acute kidney injury is common in hospitalised children and is associated with poor patient outcomes. Once acute kidney injury occurs, effective therapies to improve patient outcomes or kidney recovery are scarce. Early identification of children at risk of acute kidney injury or at an early injury stage is essential to prevent progression and mitigate complications. Paediatric acute kidney injury is under-recognised by clinicians, which is a barrier to optimisation of inpatient care and follow-up. Acute kidney injury definitions rely on functional biomarkers (ie, serum creatinine and urine output) that are inadequate, since they do not account for biological variability, analytical issues, or physiological responses to volume depletion. Improved predictive tools and diagnostic biomarkers of kidney injury are needed for earlier detection. Novel strategies, including biomarker-guided care algorithms, machine-learning methods, and electronic alerts tied to clinical decision support tools, could improve paediatric acute kidney injury care. Clinical prediction models should be studied in different paediatric populations and acute kidney injury phenotypes. Research is needed to develop and test prevention strategies for acute kidney injury in hospitalised children, including care bundles and therapeutics.