Development Of AKI Research Articles

Impact of Development and Severity of AKI on In-Hospital Outcomes Among Patients With COVID-19

Impact of Development and Severity of AKI on In-Hospital Outcomes Among Patients With COVID-19

Trough anti-Xa activity after intermediate dose nadroparin for thrombosis prophylaxis in critically ill patients with COVID-19 and acute kidney injury

Our objective was to assess the incidence of drug bioaccumulation in critically ill COVID-19 patients with AKI receiving intermediate dose nadroparin for thrombosis prophylaxis. We conducted a Prospective cohort study of critically ill COVID-19 patients. In patients on intermediate dose nadroparin (5700 IU once daily) we assessed the incidence of bioaccumulation (trough anti-Xa level > 0.2 IU/mL) stratified according to presence of AKI. We quantified this association using multilevel analyses. To assess robustness of our observations, we explored the association between AKI and anti-Xa activity in patients receiving high dose nadroparin (> 5700 IU). 108 patients received intermediate dose nadroparin, of whom 24 had AKI during 36 anti-Xa measurements. One patient with AKI (4.2% [95%CI 0.1–21%]) and 1 without (1.2% [95%CI 0.03–6.5%]) developed bioaccumulation (p = 0.39). Development of AKI was associated with a mean increase of 0.04 (95%CI 0.02–0.05) IU/ml anti-Xa activity. There was no statistically significant association between anti-Xa activity and AKI in 51 patients on high dose nadroparin. There were four major bleeding events, all in patients on high dose nadroparin. In conclusion, Bioaccumulation of an intermediate dose nadroparin did not occur to a significant extent in critically ill patients with COVID-19 complicated by AKI. Dose adjustment in AKI may be unnecessary.

Predictors of poor outcome in critically ill patients with COVID-19 pneumonia treated with extracorporeal membrane oxygenation.

IntroductionWe aimed to identify risk factors associated with ICU mortality in critically ill patients with COVID-19 pneumonia treated with Extracorporeal membrane oxygenation (ECMO). We also aimed to assess protocol violations of the local eligibility criteria of ECMO initiation.MethodsAll 31 consecutive adult patients with confirmed COVID-19 pneumonia admitted to ICU and treated with ECMO from March 13th 2020 to 8 December 2021 were enrolled. Eligibility criteria for ECMO initiation were: P/F-ratio<50 mmHg >3 hours, P/F-ratio<80 mmHg >6 hours or pH<7.25 + PaCO2>60 mmHg >6 hours, despite maximal protective invasive ventilation. Primary outcome was ICU mortality. Univariate logistic regression analyses were performed to identify predictors of ICU mortality.Results12 out of 31 patients (38.7%) did not survive ECMO treatment in ICU. Half of the non-survivors suffered from acute kidney failure compared to 3 out of 19 survivors (15.79%) (p = .04). Half of the non-survivors required CRRT treatment versus 1 patient in the survivor group (5.3%) (p < .01). Higher age (2.45 (0.97–6.18), p = .05), the development of AKI (5.33 (1.00–28.43), p = .05), need of CRRT during ICU stay (18.00 (1.79–181.31), p = .01) and major bleeding during ECMO therapy (0.51 (0.19–0.89), p < .01) were identified to be predictors of ICU mortality.ConclusionAlmost 60% of patients could be treated successfully with ECMO with sustained results at 3 months. Predictors for ICU mortality were development of AKI and need of CRRT during ICU stay, higher age category and major bleeding. Inadvertent ECMO allocation was noted in almost one in five patients.

Unsupervised clustering reveals phenotypes of AKI in ICU COVID-19 patients.

BackgroundAcute Kidney Injury (AKI) is a very frequent condition, occurring in about one in three patients admitted to an intensive care unit (ICU). AKI is a syndrome defined as a sudden decrease in glomerular filtration rate. However, this unified definition does not reflect the various mechanisms involved in AKI pathophysiology, each with its own characteristics and sensitivity to therapy. In this study, we aimed at developing an innovative machine learning based method able to subphenotype AKI according to its pattern of risk factors.MethodsWe adopted a three-step pipeline of analyses. First, we looked for factors associated with AKI using a generalized additive model. Second, we calculated the importance of each identified AKI related factor in the estimated AKI risk to find the main risk factor for AKI, at the single patient level. Lastly, we clusterized AKI patients according to their profile of risk factors and compared the clinical characteristics and outcome of every cluster. We applied this method to a cohort of severe COVID-19 patients hospitalized in the ICU of the Geneva University Hospitals.ResultsAmong the 248 patients analyzed, we found 7 factors associated with AKI development. Using the individual expression of these factors, we identified three groups of AKI patients, based on the use of Lopinavir/Ritonavir, baseline eGFR, use of dexamethasone and AKI severity. The three clusters expressed distinct characteristics in terms of AKI severity and recovery, metabolic patterns and hospital mortality.ConclusionWe propose here a new method to phenotype AKI patients according to their most important individual risk factors for AKI development. When applied to an ICU cohort of COVID-19 patients, we were able to differentiate three groups of patients. Each expressed specific AKI characteristics and outcomes, which probably reflect a distinct pathophysiology.

Impact of mean perfusion pressure and vasoactive drugs on occurrence and reversal of cardiac surgery-associate acute kidney injury: A cohort study.

Low cardiac output and kidney congestion are associated with acute kidney injury after cardiac surgery (CSA-AKI). This study investigates hemodynamics on CSA-AKI development and reversal. Adult patients undergoing cardiac surgery were retrospectively included. Hemodynamic support was quantified using a new time-weighted vaso-inotropic score (VISAUC), and hemodynamic variables expressed by mean perfusion pressure and its components. The primary outcome was AKI stage ≥2 (CSA-AKI ≥2) and secondary outcome full AKI reversal before ICU discharge. 3415 patients were included. CSA-AKI ≥2 occurred in 37.4%. Mean perfusion pressure (MPP) (OR 0.95,95%CI 0.94-0.96, p < 0.001); and central venous pressure (CVP) (OR 1.17, 95%CI 1.13-1.22, p < 0.001) are associated with CSA-AKI ≥2 development, while VISAUC/h was not (p = 0.104). Out of 1085 CSA-AKI ≥2 patients not requiring kidney replacement therapy, 76.3% fully recovered of AKI. Full CSA-AKI reversal was associated with MPP (OR 1.02 per mmHg (95%CI 1.01-1.03, p = 0.003), and MAP (OR = 1.01 per mmHg (95%CI 1.00-1.02), p = 0.047), but not with VISAUC/h (p = 0.461). Development and full recovery of CSA-AKI ≥2 are affected by mean perfusion pressure, independent of vaso-inotropic use. CVP had a significant effect on AKI development, while MAP on full AKI reversal.

Postoperative Acute Kidney Injury.

Postoperative AKI is a common complication of major surgery and is associated with significant morbidity and mortality. The Kidney Disease Improving Global Outcomes AKI definition allows consensus classification and identification of postoperative AKI through changes in serum creatinine and/or urine output. However, such conventional diagnostic criteria may be inaccurate in the postoperative period, suggesting a potential to refine diagnosis by application of novel diagnostic biomarkers. Risk factors for the development of postoperative AKI can be thought of in terms of preoperative, intraoperative, and postoperative factors and, as such, represent areas that may be targeted perioperatively to minimize the risk of AKI. The treatment of postoperative AKI remains predominantly supportive, although application of management bundles may translate into improved outcomes.

Extracellular CIRP induces acute kidney injury via endothelial TREM-1.

Introduction: Acute kidney injury is associated with elevated serum levels of extracellular cold-inducible RNA-binding protein (eCIRP), a damage-associated molecular pattern released during ischemia/reperfusion injury, hemorrhagic shock, and sepsis. It is unknown if circulating eCIRP and eCIRP-induced activation of receptor triggering receptor expressed on myeloid cells-1 (TREM-1), expressed on endothelial cells, play an important role in the pathogenesis of AKI. Methods: Male B6 wild-type (WT) and TREM-1−/− mice were subjected to intravenous injection of recombinant murine (rm) CIRP. Serum, urine, and renal tissue were collected 6 h later for analysis. Additionally, primary human renal glomerular endothelial cells (HRGEC) were stimulated in vitro with rmCIRP after pretreatment with M3, a novel inhibitory peptide of TREM-1, or vehicle. Supernatants and cells were collected 20 h after stimulation. Results: After injection with rmCIRP, WT mice had a significant increase in serum levels of BUN, creatinine, and NGAL compared to control. Additionally, NGAL was significantly increased in the urine of rmCIRP-injected mice, suggesting that circulating eCIRP can directly induce AKI. The levels of TREM-1 mRNA in the kidneys, as well as soluble (s) TREM-1 released into the serum and urine, were significantly increased in rmCIRP-injected mice. TREM-1−/− mice injected with rmCIRP had attenuated AKI, indicated by significantly decreased serum BUN, creatinine, and NGAL, and renal mRNA expression of NGAL and KIM-1 compared to WT mice. TREM-1−/− mice also had attenuated endothelial activation, with decreased mRNA and protein expression of ICAM-1 in renal tissue. HRGEC stimulated with rmCIRP in vitro had significant increases in cytokine production and sTREM-1 release, which was attenuated in cells treated with M3. Conclusion: Activation of renal TREM-1 with circulating eCIRP is sufficient to cause AKI. Elevated levels of eCIRP may be critical for the development of AKI under conditions such as ischemia/reperfusion injury, hemorrhagic shock, and sepsis. Mice deficient in the TREM-1 receptor have attenuated AKI and reduced endothelial cell activation after injection of rmCIRP. TREM-1 inhibition with M3 attenuates HRGEC activation after eCIRP stimulation. Targeting eCIRP activation of TREM-1 may provide a novel and effective treatment for AKI.

Can the Development of AKI be Predicted in COVID-19 Patients with Severe Pneumonia?

Can the Development of AKI be Predicted in COVID-19 Patients with Severe Pneumonia?

Neonatal acute kidney injury and serum cystatin C as its early predictor

Aim: To assess cystatin-C as an early biomarker for identifying AKI in newborns at risk for the condition. Methodology: Prospective cohort study in neonates with preterm and term admitted to NICU. The study group comprised of 24 Neonates with risk of AKI &amp; 24 Neonates with no risk of AKI. The Biochemical investigations were done. Collected data was subjected to statistical analysis using SPSS. Results: In this study, there is no significant correlation between gestational age and Creatinine &amp; Cystatin C levels of day 1 &amp; day 5/ death.There is no significant correlation between birth weight and Creatinine day 1, Creatinine &amp; Cystatin C levels of day 5/ death. But positive correlation between birth weight and Cystatin C levels of day 1. Serum Cystatin C can predict development of AKI in at cutoff point of &gt;1.41 mg/l, AUC= 1.000 with sensitivity of 93.3 % and specificity of 97.4 %. Conclusion : The rate of rise of serum cystatin C was earlier and the absolute number was also higher than serum creatinine. Cystatin C levels can predict AKI earlier than serum creatinine value. It can predict AKI atleast 1 or 2 days earlier than serum creatinine.

Decreased renal cortical perfusion, independent of changes in renal blood flow and sublingual microcirculatory impairment, is associated with the severity of acute kidney injury in patients with septic shock

BackgroundReduced renal perfusion has been implicated in the development of septic AKI. However, the relative contributions of macro- and microcirculatory blood flow and the extent to which impaired perfusion is an intrinsic renal phenomenon or part of a wider systemic shock state remains unclear.MethodsSingle-centre prospective longitudinal observational study was carried out. Assessments were made at Day 0, 1, 2 and 4 after ICU admission of renal cortical perfusion in 50 patients with septic shock and ten healthy volunteers using contrast-enhanced ultrasound (CEUS). Contemporaneous measurements were made using transthoracic echocardiography of cardiac output. Renal artery blood flow was calculated using velocity time integral and vessel diameter. Assessment of the sublingual microcirculation was made using handheld video microscopy. Patients were classified based on the degree of AKI: severe = KDIGO 3 v non-severe = KDIGO 0–2.ResultsAt study enrolment, patients with severe AKI (37/50) had prolonged CEUS mean transit time (mTT) (10.2 vs. 5.5 s, p < 0.05), and reduced wash-in rate (WiR) (409 vs. 1203 au, p < 0.05) and perfusion index (PI) (485 vs. 1758 au, p < 0.05); differences persisted throughout the entire study. Conversely, there were no differences in either cardiac index, renal blood flow or renal resistive index. Sublingual microcirculatory variables were not significantly different between groups at study enrolment or at any subsequent time point. Although lactate was higher in the severe AKI group at study enrolment, these differences did not persist, and there were no differences in either ScvO2 or ScvCO2-SaCO2 between groups. Patients with severe AKI received higher doses of noradrenaline (0.34 vs. 0.21mcg/kg/min, p < 0.05). Linear regression analysis showed no correlation between mTT and cardiac index (R-0.18) or microcirculatory flow index (R-0.16).ConclusionRenal cortical hypoperfusion is a persistent feature in critically ill septic patients who develop AKI and does not appear to be caused by reductions in macrovascular renal blood flow or cardiac output. Cortical hypoperfusion appears not be associated with changes in the sublingual microcirculation, raising the possibility of a specific renal pathogenesis that may be amenable to therapeutic intervention.Trial Registration Clinical Trials.gov NCT03713307, 19 Oct 2018.

Deoxycholate amphotericin for management of mucormycosis: a retrospective cohort study from South India.

Liposomal amphotericin use is limited in developing countries due to its extremely high cost and availability. Therefore, the study aimed to evaluate deoxycholate amphotericin B's utility and adverse effect profile in patients with mucormycosis. This retrospective cohort study from 2019 to 2021 included patients with proven mucormycosis who received deoxycholate amphotericin B for more than or equal to five days and had at least three creatinine values on treatment. Baseline demographic details, risk factors and treatment details of all the patients were recorded. In addition, the details of treatment-related adverse effects and outcomes were ascertained. Of the 57 included patients, a history of diabetes, COVID-19 and steroid use was present in 49 (86%), 43 (75.4%) and 33 (57.9%) patients, respectively. Isolated rhino-orbital mucormycosis was the most common presentation (n=49, 86%). The median time of follow-up was 48 (30.5-90) days. A total of 8 (14%) patients died during the hospital stay. The median duration of amphotericin treatment was 21 (14-40) days. Thirty-nine patients (68.4%) developed hypokalaemia on treatment, while 27 (47.4%) patients developed hypomagnesaemia. A total of 34 (59.6%) patients developed AKI on treatment. The median day of development of AKI was 6 (4-10) days. The median baseline, highest and final creatinine values were 0.78 (0.59-0.94) mg/dl, 1.27 (0.89-2.16) mg/dl and 0.93 (0.74-1.59) mg/ dl respectively. The median percentage change from baseline to highest value and last follow-up value was 45% (0.43%-161%) and 25% (-4.8%-90.1%) respectively. The final creatinine was less than 150% of the baseline in 36 (63.2%) patients. Deoxycholate amphotericin is an acceptable alternative for treating mucormycosis in resource-constrained settings.

Monitoring of intraoperative femoral oxygenation predicts acute kidney injury after pediatric cardiac surgery.

Cardiopulmonary bypass-associated acute kidney injury (CPB-AKI) is a pediatric cardiac surgery postoperative complication that is associated with a longer duration of mechanical ventilation and length of hospital stay. Identifying an early predictor of CPB-AKI is critical. Near infrared spectroscopy (NIRS), which can provide real-time monitoring of regional tissue oxygen saturation (rSO2) during CPB, may predict CPB-AKI in an early phase of surgical treatment. This study analyzed clinical data from 87 children who underwent an elective surgical repair of ventricular septal defect (VSD) from January 2013 to March 2019. NIRS sensors were placed on the patients' forehead, abdomen, and thighs. The pediatric modified risk, injury, failure, loss, and end-stage (p-RIFLE) score was determined for each patient postoperatively. The incidence of AKI based on the p-RIFLE classification was 11.5% at the end of surgery, 23.0% at 24 h after surgery, and 5.7% at 48 h after surgery. The AKI incidence rate was highest at 24 h after surgery. Multiple regression analysis revealed that femoral oxygenation (rSO2) during CPB, CPB time, oxygen delivery index (DO2i), and lactate at the end of CPB were independent risk factors for AKI. Receiver-operating characteristic curve analysis indicated that femoral oxygenation of 74% or less predicted AKI development within 24 h after surgery. In conclusion, rSO2 measured at the thigh during CPB is highly predictive of CPB-AKI.

COVID-19 impact on kidneys

Introduction and purposeThe COVID-19 pandemic, which has been ongoing since early 2020, has significantly affected the health care system worldwide. SARS-CoV-2 virus being the etiological factor of the disease has a high affinity for the renal organ. The purpose of this study was to provide an overview of the current knowledge of the problem of frequent AKI in the course of coronavirus infection, the impact of COVID-19 disease in patients with chronic kidney disease and on renal replacement therapy or dialysis.Review methodIn the process of writing, we used available articles and scientific papers in Pubmed and Google Scholar databases based on keywords: COVID-19, SARS-CoV-2, AcuteKidneyInjury, ChronicKidneyDisease.State of knowledgeSARS-CoV-2 virus enters target cells through the ACE2 receptor. In the pathophysiology of AKI in the course of COVID-19, a key role is attributed to secondary damage mechanisms such as cytokine storm, hypoperfusion with hypoxia, endothelial dysfunction. The incidence of acute kidney injury ranges from 5.1% to 36.6%. The development of AKI, renal transplant status, the presence of chronic kidney disease or renal replacement therapy is associated with an increased risk of severe course and higher mortality on COVID-19. SummaryThe COVID-19 pandemic has posed new logistical and therapeutic challenges to the health care system. Due to the high tropism of SARS-CoV-2 to the kidneys and the frequent occurrence of AKI during the course of the infection, nephrology patients, those on renal replacement therapy and those awaiting transplantation should be placed under special surveillance. Patients in these groups are at particular risk for a severe course of COVID-19.

A novel animal model to study delayed resuscitation following traumatic hemorrhage.

A focus of combat casualty care research is to develop treatments for when full resuscitation after hemorrhage is delayed. However, few animal models exist to investigate such treatments. Given the kidney's susceptibility to ischemia, we determined how delayed resuscitation affects renal function in a model of traumatic shock. Rats were randomized into three groups: resuscitation after 1 h (ETH-1) or 2 h (ETH-2) of extremity trauma and hemorrhagic shock, and sham control. ETH was induced in anesthetized rats with muscle injury and fibula fracture, followed by pressure-controlled hemorrhage [mean arterial pressure (MAP) = 55 mmHg] for 1 or 2 h. Rats were then resuscitated with whole blood until MAP stabilized between 90 and 100 mmHg for 30 min. MAP, glomerular filtration rate (GFR), creatinine, blood gases, and fractional excretion of sodium (nFENa+) were measured for 3 days. Compared with control, ETH-1 and ETH-2 exhibited decreases in GFR and nFENa+, and increases in circulating lactate, creatinine, and blood urea nitrogen (BUN) before and within 30 min after resuscitation. The increases in creatinine, BUN, and potassium were greater in ETH-2 than in ETH-1, whereas lactate levels were similar between ETH-1 and ETH-2 before and after resuscitation. All measurements were normalized in ETH-1 within 2 days after resuscitation, with 22% mortality. However, ETH-2 exhibited a prolonged impairment of GFR, increased nFENa+, and a 66% mortality. Resuscitation 1 h after injury therefore preserves renal function, whereas further delay of resuscitation irreversibly impairs renal function and increases mortality. This animal model can be used to explore treatments for prolonged prehospital care following traumatic hemorrhage.NEW & NOTEWORTHY A focus of combat casualty care research is to develop treatment where full resuscitation after hemorrhage is delayed. However, animal models of combat-related hemorrhagic shock in which to determine physiological outcomes of such delays and explore potential treatment for golden hour extension are lacking. In this study, we filled this knowledge gap by establishing a traumatic shock model with reproducible development of AKI and shock-related complications determined by the time of resuscitation.

Acute Kidney Injury After Pulmonary Thromboendarterectomy: Associated Factors and Impact

BackgroundAcute kidney injury (AKI) is a common complication after pulmonary thromboendarterectomy (PTE) that has been shown to be associated with worse outcomes. Our study assesses factors associated with the development of postoperative AKI after PTE and its impact on clinical outcomes. MethodsWe retrospectively analyzed 247 patients who underwent PTE at our institution between June 2009 and December 2020. Baseline characteristics, risk factors, and outcomes were compared between patients with and without postoperative AKI. The primary endpoint was development of postoperative AKI using the Kidney Disease Improving Global Outcomes definition, and secondary endpoints were length of hospital stay, hospital mortality, and 5-year mortality. ResultsThe overall incidence of postoperative AKI in our study population was 49%. One hundred twenty-three patients (50.8%) did not develop AKI postoperatively, 87 patients (35.9%) developed stage 1 AKI postoperatively, 21 patients (8.7%) developed stage 2 AKI postoperatively, and 11 (4.5%) developed stage 3 AKI postoperatively. Patients who developed AKI postoperatively had longer hospital stays, higher in-hospital mortality rates, and higher 5-year mortality rates than patients who did not develop postoperative AKI. Higher body mass index, older age, low preoperative hemoglobin, low ejection fraction, and low creatinine were shown to be associated with postoperative AKI development. ConclusionsPatients who developed AKI after PTE had worse mortality and morbidity. Clinicians should have a lower threshold for suspecting AKI and consider implementing Kidney Disease Improving Global Outcomes–based AKI prevention bundles for patients with factors associated with development of AKI.

Is AKI a menace in COVID pregnancy?

COVID-19 is primarily thought to be a respiratory sickness, however because SARS-CoV-2 targets human cells, it can also damage the kidney. The most concerning complication in COVID-19 patients is acute kidney damage (AKI). Hypovolemia, cytokine storm, and collapsing glomerulopathy are all factors to consider. Our interest in the topic stems from an increasing number of articles that demonstrate a strong link between AKI development and greater mortality in COVID-19 patients. Although our understanding of the role of the kidneys especially in pregnancy with SARS-CoV-2 infection is constantly evolving and remains unexplored. We have studied 66 pregnant women with COVID 19 infection and AKI and we present an overview of the possible patho mechanisms of AKI in COVID-19, its clinical features, risk factors, impact on hospitalization, and management with renal replacement therapy in relation to pregnancy.

Performance of a Standardized Clinical Assay for Urinary C-C Motif Chemokine Ligand 14 (CCL14) for Persistent Severe Acute Kidney Injury.

Clinical use of biomarkers requires the development of standardized assays and establishment of cutoffs. Urinary C-C motif chemokine ligand 14 (CCL14) has been validated to predict persistent severe AKI in critically ill patients with established AKI. We now report on the performance of standardized cutoffs using a clinical assay. A second aim of the multicenter RUBY Study was to establish two cutoffs for the prediction of persistent severe AKI (defined as KDIGO stage 3 AKI for at least 72 consecutive hours). Patients who received renal replacement therapy (RRT) or died before achieving 72 hours in stage 3 AKI were also considered to have reached the end point. A cutoff value for urinary CCL14 of 1.3 ng/ml was determined to achieve high sensitivity (91%; 95% CI, 84% to 96%), and 13 ng/ml achieved high specificity (93%; 95% CI, 89% to 96%). The cutoff of 1.3 ng/ml identifies the majority (91%) of patients who developed persistent severe AKI with a negative predictive value of 92%. The cutoff at 13 ng/ml had a positive predictive value of 72% (with a negative predictive value of 75%). In multivariable adjusted analyses, a CCL14 concentration between 1.3 and 13 ng/ml had an adjusted odds ratio (aOR) of 3.82 (95% CI, 1.73 to 9.12; P=0.001) for the development of persistent severe AKI compared with those with a CCL14 ≤1.3 ng/ml, whereas a CCL14 >13 ng/ml had an aOR of 10.4 (95% CI, 3.89 to 29.9; P<0.001). Using a clinical assay, these standardized cutoffs (1.3 and 13 ng/ml) allow for the identification of patients at high risk for the development of persistent severe AKI. These results have immediate utility in helping to guide AKI patient care and may facilitate future clinical trials.Clinical Trial registry name and registration number: Identification and Validation of Biomarkers of Acute Kidney Injury Recovery, NCT01868724.

Prediction of acute kidney injury in patients with femoral neck fracture utilizing machine learning.

BackgroundAcute kidney injury (AKI) is a common complication associated with significant morbidity and mortality in high-energy trauma patients. Given the poor efficacy of interventions after AKI development, it is important to predict AKI before its diagnosis. Therefore, this study aimed to develop models using machine learning algorithms to predict the risk of AKI in patients with femoral neck fractures.MethodsWe developed machine-learning models using the Medical Information Mart from Intensive Care (MIMIC)-IV database. AKI was predicted using 10 predictive models in three-time windows, 24, 48, and 72 h. Three optimal models were selected according to the accuracy and area under the receiver operating characteristic curve (AUROC), and the hyperparameters were adjusted using a random search algorithm. The Shapley additive explanation (SHAP) analysis was used to determine the impact and importance of each feature on the prediction. Compact models were developed using important features chosen based on their SHAP values and clinical availability. Finally, we evaluated the models using metrics such as accuracy, precision, AUROC, recall, F1 scores, and kappa values on the test set after hyperparameter tuning.ResultsA total of 1,596 patients in MIMIC-IV were included in the final cohort, and 402 (25%) patients developed AKI after surgery. The light gradient boosting machine (LightGBM) model showed the best overall performance for predicting AKI before 24, 48, and 72 h. AUROCs were 0.929, 0.862, and 0.904. The SHAP value was used to interpret the prediction models. Renal function markers and perioperative blood transfusions are the most critical features for predicting AKI. In compact models, LightGBM still performs the best. AUROCs were 0.930, 0.859, and 0.901.ConclusionsIn our analysis, we discovered that LightGBM had the best metrics among all algorithms used. Our study identified the LightGBM as a solid first-choice algorithm for early AKI prediction in patients after femoral neck fracture surgery.

Influence of the Initial Neutrophils to Lymphocytes and Platelets Ratio on the Incidence and Severity of Sepsis-Associated Acute Kidney Injury: A Double Robust Estimation Based on a Large Public Database.

BackgroundAcute kidney injury (AKI) is a frequent consequence of sepsis and has been linked to poor prognosis. In critically ill patients, the ratio of neutrophils to lymphocytes and platelets (N/LP) has been confirmed as an inflammation-related marker connected with the development of renal dysfunction. However, the effect of the N/LP ratio on the initiation and development of AKI in patients with sepsis remained unclear. The purpose of this study was to determine if the N/LP ratio on intensive care unit (ICU) admission was associated with the occurrence of sepsis-associated AKI (S-AKI) and severe AKI.MethodsAdult septic patients from the Medical Information Mart for Intensive Care-IV database were screened and classified into three categories (low, middle, or high) based on their N/LP ratio quartiles. The Cox proportional hazard and competing risk models were used to determine the risk of S-AKI in various N/LP groups, whilst the logistic regression model and restricted cubic splines (RCS) analysis were employed to investigate the link between N/LP ratios and the occurrence of severe AKI. Finally, we did a doubly robust estimation, a subgroup analysis, and a sensitivity analysis to determine the findings’ robustness.ResultsWe categorized 485, 968, and 485 septic patients into three groups based on their N/LP ratios: low, intermediate, and high. According the Cox proportional hazard model, the hazard rate (95% CI) for those in the middle and high N/LP groups on the incidence of S-AKI were 1.30(1.07, 1.58) and 1.27(1.02, 1.59), respectively, as compared to those in the low N/LP group. And the Fine-Gray proportional subdistribution hazards model indicated that mortality was not a substantial competing risk for S-AKI. Additionally, multivariate logistic regression revealed that the risk of severe AKI increased 1.83 fold in the high group compared to the low group. The RCS result also suggested that the probability of severe AKI rose significantly when N/LP > 9.5. The consistency of these findings was confirmed using doubly robust estimation. However, subgroup and sensitivity analyses revealed that the association between N/LP and the incidence of S-AKI, severe AKI varied considerably between different populations and diagnostic criteria.ConclusionA raised initial N/LP level may induce the development of S-AKI and severe AKI within 7 days after ICU admission in septic patients. These influences were enhanced in elder, male, septic shock, and those with poor health condition. Furthermore, high NLP was more strongly connected to the risk of S-AKI and severe AKI in sepsis patients on the urine output-based AKI criteria than on the serum creatinine-based criteria.

Effect of diabetes on various outcomes in intensive care settings: A case–control study

Abstract: BACKGROUND: There are conflicting data in the literature about the influence of diabetes on clinical outcomes and death in critically ill patients. Thus, we assessed the effect of diabetes on mortality rate and other outcomes in critically ill patients admitted to the intensive care unit (ICU). MATERIALS AND METHODS: This prospective case–control was conducted in the ICU of a tertiary care institute. Adult critically ill diabetics (cases, n = 46) and nondiabetic patients (controls, n = 85) were included in this study. Both the groups were compared regarding mortality rate, length of ICU stay, as well as the need for mechanical ventilation (MV) and inotropic/vasopressor supports. RESULTS: The groups did not differ significantly regarding age (P = 0.087), sex (P = 0.568), and vital parameters (P &gt; 0.05). The groups were comparable regarding Glasgow Coma Scale (P = 0.882), Acute Physiology and Chronic Health Evaluation II (APACHE II) score (P = 0.774), and laboratory parameters (P &gt; 0.05), except significantly greater proportion of diabetic patients had plasma glucose &gt;200 mg/dL (P &lt; 0.0001) and serum HCO3 &lt;18 mEq/L (P = 0.038) relative to nondiabetic patients. The groups did not differ significantly in need of MV (P = 0.413), or vasopressor support (P = 0.590), development of AKI (P = 0.424), and length of ICU stay of 0–3 days (P = 0.300). Around a quarter of diabetic (26.09%) and nondiabetic patients (23.53%) were nonsurvivors (P = 0.745). Assessment of mortality according to the age groups, indication of admission, plasma glucose levels, and APACHE II score suggested no significant difference between the groups (all P &gt; 0.05). CONCLUSION: In critically ill patients, the presence of diabetes does not affect outcomes, including the need for MV or vasopressor support, development of AKI, length of ICU stay, and mortality.