Association of random glucose to albumin ratio with post-contrast acute kidney injury and clinical outcomes in patients with ST-elevation myocardial infarction.

Purpose: Both glucose and albumin are associated with chronic inflammation, which plays a vital role in post-contrast acute kidney injury (PC-AKI). To explore the relationship between random glucose to albumin ratio (RAR) and the incidence of PC-AKI after percutaneous coronary intervention (PCI) in patients with ST-elevation myocardial infarction (STEMI). Patients and methods: STEMI patients who underwent PCI were consecutively enrolled from January, 01, 2010 to February, 28, 2020. All patients were categorized into T1, T2, and T3 groups, respectively, based on RAR value (RAR < 3.377; 3.377 ≤ RAR ≤ 4.579; RAR > 4.579). The primary outcome was the incidence of PC-AKI, and the incidence of major adverse clinical events (MACE) was the second endpoint. The association between RAR and PC-AKI was assessed by multivariable logistic regression analysis. Results: A total of 2,924 patients with STEMI undergoing PCI were finally included. The incidence of PC-AKI increased with the increasing tertile of RAR (3.2% vs 4.8% vs 10.6%, P<0.001). Multivariable regression analysis demonstrated that RAR (as a continuous variable) was associated with the incidence of PC-AKI (adjusted odds ratio (OR) =1.10, 95% confidence interval (CI) =1.04 - 1.16, P<0.001) and in-hospital MACE (OR=1.07, 95% CI=1.02 - 1.14, P=0.012); RAR, as a categorical variable, was significantly associated with PC-AKI (T3 vs. T1, OR=1.70, 95% CI=1.08 - 2.67, P=0.021) and in-hospital MACE (T3 vs. T1, OR=1.63, 95% CI=1.02 - 2.60, P=0.041) in multivariable regression analyses. Receiver operating characteristic curve analysis showed that RAR exhibited a predictive value for PC-AKI (area under the curve (AUC)=0.666, 95% CI=0.625 - 0.708), and in-hospital MACE (AUC= 0.662, 95% CI =0.619 - 0.706). Conclusions: The high value of RAR was significantly associated with the increasing risk of PC-AKI and in-hospital MACE after PCI in STEMI patients, and RAR offers a good predictive value for those outcomes.

Acute kidney injury in critical care: complications of hemophagocytic lymphohistiocytosis.

Hemophagocytic lymphohistiocytosis (HLH) is an immune dysfunction characterized by an exaggerated and pathological inflammatory response, potentially leading to systemic inflammatory reactions and multiple-organ failure, including renal involvement. HLH can be classified as primary or secondary, with primary HLH associated with genetic mutations affecting cell degranulation capacity, and secondary HLH often linked to infections, tumors, and autoimmune diseases. The pathogenesis of HLH is not fully understood, but primary HLH is typically driven by genetic defects, whereas secondary HLH involves the activation of CD8+ T cells and macrophages, leading to the release of inflammatory cytokines and systemic inflammatory response syndrome (SIRS). The clinical presentation of HLH includes non-specific manifestations, making it challenging to differentiate from severe sepsis, particularly secondary HLH due to infections. Shared features include prolonged fever, hepatosplenomegaly, hematopenia, hepatic dysfunction, hypertriglyceridemia, and hypofibrinogenemia, along with histiocytosis and hemophagocytosis. However, distinctive markers like dual hemocytopenia, hypertriglyceridemia, hypofibrinogenemia, and elevated sCD25 levels may aid in differentiating HLH from sepsis. Indeed, no singular biomarker effectively distinguishes between hemophagocytic lymphohistiocytosis and infection. However, research on combined biomarkers provides insights into the differential diagnosis. Renal impairment is frequently encountered in both HLH and sepsis. It can result from a systemic inflammatory response triggered by an influx of inflammatory mediators, from direct damage caused by these factors, or as a consequence of the primary disease process. For instance, macrophage infiltration of the kidney can lead to structural damage affecting various renal components, precipitating disease. Presently, tubular necrosis remains the predominant form of renal involvement in HLH-associated acute kidney injury (HLH-AKI). However, histopathological changes may also encompass interstitial inflammation, glomerular abnormalities, microscopic lesions, and thrombotic microangiopathy. Treatment approaches for HLH and sepsis diverge significantly. HLH is primarily managed with repeated chemotherapy to eliminate immune-activating stimuli and suppress hypercellularity. The treatment approach for sepsis primarily focuses on anti-infective therapy and intensive symptomatic supportive care. Renal function significantly influences clinical decision-making, particularly regarding the selection of chemotherapy and antibiotic dosages, which can profoundly impact patient prognosis. Conversely, renal function recovery is a complex process influenced by factors such as disease severity, timely diagnosis, and the intensity of treatment. A crucial aspect in managing HLH-AKI is the timely diagnosis, which plays a pivotal role in reversing renal impairment and creating a therapeutic window for intervention, may have opportunity to improve patient prognosis. Understanding the clinical characteristics, underlying causes, biomarkers, immunopathogenesis, and treatment options for hemophagocytic lymphohistiocytosis associated with acute kidney injury (HLH-AKI) is crucial for improving patient prognosis.

Patient-centered approach to the management of acute kidney injury in the Covid-19 outcomes.

OBJECTIVE: Aim: To identify patients at risk of AKI with severe COVID-19 and to guide management strategies according to national and global scientific data for improving kidney-related outcomes. PATIENTS AND METHODS: Materials and Methods: We conducted retrospective study case-control analysing cases of hospitalisation patients with COVID-19 with or without AKI during hospital stay. RESULTS: Results: In the study, we found that there was a positive correlation between AKI and respiratory insufficiency (0,513 - moderate, p<0,0001), moderate in the case of AKI grade 2 (0.301, <0,001) and mild in the case of AKI grade 1 and 3 correspondingly (0.252, p<0,01; 0.277, <0,001). Lethality (in-hospital death rate) correlated with respiratory insufficiency and AKI (0.733, 0,617; p<0,0001). We found that age had a reverse correlation with AKI and RI (younger patients were more likely to have a higher prevalence of AKI and RI, p<0,001). It was noticed that AKI correlated with the minimal albumin level (-0,35, p=0,016), minimal lymphocyte count (-0.377, p<0,0001), IL-6 (0.201, p=0,035), ferritin (0.34, p <0,0001), maximal CRP (0.439, p<0,0001). There was a mild correlation between Padua Score and AKI (0,232, p<0,01) and PLRI (0,172, p=0,05). CONCLUSION: Conclusions: Early assessment of renal dysfunction could be used as a marker of severe outcomes of COVID-19, especially in the case of comorbidities such as metabolic disorders and cardiovascular events. We suggest using the Padua score, assessment of personal lethality risk index (PLRI), and rise of serum creatinine as additional tools for assessment criteria for hospitalisation.

Association between estimated plasma volume status and acute kidney injury in patients who underwent coronary revascularization: A retrospective cohort study from the MIMIC-IV database.

BACKGROUND: Acute kidney injury (AKI) remains a common complication of coronary revascularization and increases poor outcomes in critically ill surgical patients. Compared to the plasma volume status (PVS), estimated plasma volume status (ePVS) has the advantages of being noninvasive and simple and has been shown to be associated with worse prognosis in patients undergoing coronary revascularization. This study was to evaluate the association of ePVS with the risk of AKI in patients who underwent coronary revascularization. METHODS: In this retrospective cohort study, data of patients who underwent coronary revascularization were extracted from the Medical Information Mart for Intensive Care (MIMIC)-IV database (2008-2019). The outcome was the occurrence of AKI after ICU admission. The covariates were screened via the LASSO regression method. Univariate and multivariate Logistic regression models were performed to assess the association of ePVS and PVS and the odds of AKI in patients who underwent coronary revascularization, with results shown as odds ratios (ORs) and 95% confidence intervals (CIs). Subgroup analyses of age, surgery, and anticoagulation agents and sequential organ failure assessment (SOFA) score were performed to further explore the association of ePVS with AKI. RESULTS: A total of 3,961 patients who underwent coronary revascularization were included in this study, of whom 2,863 (72.28%) had AKI. The high ePVS was associated with the higher odds of AKI in patients who received coronary revascularization (OR = 1.06, 95%CI: 1.02-1.10), after adjusting for the covariates such as age, race, SAPS-II score, SOFA score, CCI, weight, heart rate, WBC, RDW-CV, PT, BUN, glucose, calcium, PH, PaO2, mechanical ventilation, vasopressors, and diuretic. Similar results were found in patients who underwent the CABG (OR = 1.07, 95%CI: 1.02-1.11), without anticoagulation agents use (OR = 1.07, 95%CI: 1.03-1.12) and with high SOFA score (OR = 1.10, 95%CI: 1.04-1.17). No relationship was found between PVS and the odds of AKI in patients who underwent the coronary revascularization. CONCLUSION: The ePVS may be a promising parameter to evaluate the risk of AKI in patients undergoing coronary revascularization, which provides a certain reference for the risk stratification management of ICU patients who underwent coronary revascularization.

Multicentre, retrospective cohort study protocol to identify racial and ethnic differences in acute kidney injuries in children and adolescents with diabetic ketoacidosis.

INTRODUCTION: Approximately 40% of children with diabetic ketoacidosis (DKA) develop acute kidney injury (AKI), which increases the risk of chronic kidney damage. At present, there is limited knowledge of racial or ethnic differences in diabetes-related kidney injury in children with diabetes. Understanding whether such differences exist will provide a foundation for addressing disparities in diabetes care that may continue into adulthood. Further, it is currently unclear which children are at risk to develop worsening or sustained DKA-related AKI. The primary aim is to determine whether race and ethnicity are associated with DKA-related AKI. The secondary aim is to determine factors associated with sustained AKI in children with DKA. METHODS AND ANALYSIS: This retrospective, multicentre, cross-sectional study of children with type 1 or type 2 diabetes with DKA will be conducted through the Paediatric Emergency Medicine Collaborative Research Committee. Children aged 2-18 years who were treated in a participating emergency department between 1 January 2020 and 31 December 2023 will be included. Children with non-ketotic hyperglycaemic-hyperosmolar state or who were transferred from an outside facility will be excluded. The relevant predictor is race and ethnicity. The primary outcome is the presence of AKI, defined by Kidney Disease: Improving Global Outcomes criteria. The secondary outcome is 'sustained' AKI, defined as having AKI ≥48 hours, unresolved AKI at last creatinine measurement or need for renal replacement therapy. Statistical inference of the associations between predictors (ie, race and ethnicity) and outcomes (ie, AKI and sustained AKI) will use random effects regression models, accounting for hospital variation and clustering. ETHICS AND DISSEMINATION: The Institutional Review Board of Children's Minnesota approved this study. 12 additional sites have obtained institutional review board approval, and all sites will obtain local approval prior to participation. Results will be presented at local or national conferences and for publication in peer-reviewed journals.

[Association between onset time of sepsis-associated acute kidney injury and clinical outcome in patients with sepsis].

Objective: To explore the relationship between the onset time of sepsis-associated acute kidney injury (SA-AKI) and adverse clinical outcomes. Methods: Data were derived from Beijing Acute Kidney Injure Trial (BAKIT) which investigated the epidemiology of acute kidney injury (AKI) in critically ill patients at 30 intensive care units (ICU) of 28 tertiary hospitals in Beijing from 1 March to 31 August 2012. Patients who were older than 18 years and diagnosed with sepsis and AKI, and expected to stay in ICU for at least 24 h were included in this study. A total of 653 patients were included in this study, 414 males and 239 females with a mean age of (68.2±17.0) years. According to the onset time of SA-AKI, patients were grouped into early AKI (E-AKI) (AKI occurred within 48 hours after ICU admission) and late AKI (L-AKI) (AKI occurred after 48 hours of ICU admission) group. The primary outcome was major adverse kidney events (MAKE), consisted of all-cause mortality, renal replacement therapy-dependence, and an inability to recover to 1.5 times of the baseline creatinine value up to 30 days. Multivariable logistic regression was used to investigate the association between the onset time of SA-AKI and clinical outcomes. Results: A total of 653 patients with SA-AKI were included, 423 (64.8%) patients developed E-AKI, 230 (35.2%) cases developed L-AKI, MAKE occurred in 405 (62.0%) cases, and 301 (46.1%) patients died in hospital. Compared with E-AKI group, L-AKI patients showed higher AKI 3 level rate [55.7%(128/230) vs 40.2%(170/423), P<0.001], incidence of MAKE [72.6%(167/230) vs 56.3%(238/423,P<0.001)] and hospital mortality [55.2%(127/230) vs 44.1%(174/423), P=0.001]. The risk of MAKE and in-hospital mortality in L-AKI group increased for 2.55-fold times (OR=3.55, 95%CI: 1.94-6.04) and 1.84-fold times (OR=2.84, 95%CI: 1.44-5.60) when compared with those in E-AKI, respectively (both P<0.05). Conclusion: Late timing onset of SA-AKI is associated with poor clinical outcomes.

Postoperative hypoalbuminemia and outcomes of pediatric liver transplantation.

BACKGROUND: Hypoalbuminemia after liver transplantation (LT) is associated with acute kidney injury (AKI) and poor outcomes in adult LT recipients. This study was performed to examine the association between the postoperative serum albumin level and early postoperative outcomes of LT in children. METHODS: This single-center retrospective review involved pediatric LT recipients (0-18 years old) treated from January 2013 to June 2020. All patients were admitted to PICU and received standard post-LT care protocol. We divided patients into low (< 30 g/L) and normal (> 30 g/L) groups based on postoperative albumin day 1 to 3. RESULTS: Among 108 LT recipients, most had biliary atresia. The median age at the time of LT was 1.8 years [interquartile range (IQR), 1.5-5.7]. There were 18 patients in low albumin group [median albumin level, 27.9 g/L (IQR, 25.8-29.6) and 90 patients in normal albumin group [median albumin level, 34.5 g/L (IQR, 32.4-36.9). The low albumin group had significantly higher incidence of AKI, occurring in 20% of patients with a median onset of 2.5 days following LT (IQR, 1-5). Postoperative hypoalbuminemia (OR, 4.94; 95% CI, 1.32-18.47; p = 0.01) and a longer operative time (OR, 1.37; 95% CI, 1.01-1.47; p = 0.02) were independent risk factors for AKI by multivariable analysis. No significant differences between the two groups were found in other early postoperative outcomes. CONCLUSION: Postoperative hypoalbuminemia was associated with early postoperative AKI following LT in children but not with other worsening outcomes.

The REPERFUSE study protocol: The effects of vasopressor therapy on renal perfusion in patients with septic shock-A mechanistically focused randomised control trial.

INTRODUCTION: Acute kidney injury (AKI) is a common complication of septic shock and together these conditions carry a high mortality risk. In septic patients who develop severe AKI, renal cortical perfusion is deficient despite normal macrovascular organ blood flow. This intra-renal perfusion abnormality may be amenable to pharmacological manipulation, which may offer mechanistic insight into the pathophysiology of septic AKI. The aim of the current study is to investigate the effects of vasopressin and angiotensin II on renal microcirculatory perfusion in a cohort of patients with septic shock. METHODS AND ANALYSIS: In this single centre, mechanistically focussed, randomised controlled study, 45 patients with septic shock will be randomly allocated to either of the study vasopressors (vasopressin or angiotensin II) or standard therapy (norepinephrine). Infusions will be titrated to maintain a mean arterial pressure (MAP) target set by the attending clinician. Renal microcirculatory assessment will be performed for the cortex and medulla using contrast-enhanced ultrasound (CEUS) and urinary oxygen tension (pO2), respectively. Renal macrovascular flow will be assessed via renal artery ultrasound. Measurement of systemic macrovascular flow will be performed through transthoracic echocardiography (TTE) and microvascular flow via sublingual incident dark field (IDF) video microscopy. Measures will be taken at baseline, +1 and +24hrs following infusion of the study drug commencing. Blood and urine samples will also be collected at the measurement time points. Longitudinal data will be compared between groups and over time. DISCUSSION: Vasopressors are integral to the management of patients with septic shock. This study aims to further understanding of the relationship between this therapy, renal perfusion and the development of AKI. In addition, using CEUS and urinary pO2, we hope to build a more complete picture of renal perfusion in septic shock by interrogation of the constituent parts of the kidney. Results will be published in peer-reviewed journals and presented at academic meetings. TRIAL REGISTRATION: The REPERFUSE study was registered on Clinical Trials.gov (NCT06234592) on the 30th Jan 24.

Decrease in platelet count in patients with AKI and its association with major adverse kidney events.

INTRODUCTION: A reduction in platelet count in critically ill patients is a marker of severity of the clinical condition. However, whether this association holds true in acute kidney injury (AKI) is unknown. We analyzed the association between platelet reduction in patients with AKI and major adverse kidney events (MAKE). METHODS: In this retrospective cohort, we included AKI patients at the Hospital Civil of Guadalajara, in Jalisco, Mexico. Patients were divided according to whether their platelet count fell >21% during the first 10 days. Our objectives were to analyze the associations between a platelet reduction >21% and MAKE at 10 days (MAKE10) or at 30-90 days (MAKE30-90) and death. RESULTS: From 2017 to 2023, 400 AKI patients were included, 134 of whom had a > 21% reduction in platelet count. The mean age was 54 years, 60% were male, and 44% had sepsis. The mean baseline platelet count was 194 x 103 cells/µL, and 65% of the KDIGO3 patients met these criteria. Those who underwent hemodialysis (HD) had lower platelet counts. After multiple adjustments, a platelet reduction >21% was associated with MAKE10 (OR 4.2, CI 2.1-8.5) but not with MAKE30-90. The mortality risk increased 3-fold (OR 2.9, CI 1.1-7.7, p = 0.02) with a greater decrease in the platelets (<90 x 103 cells/µL). As the platelets decreased, the incidence of MAKE was more likely to increase. These associations lost significance when accounting for starting HD. CONCLUSION: In our retrospective cohort of patients with AKI, a > 21% reduction in platelet count was associated with MAKE. Our results are useful for generating hypotheses and motivating us to continue studying this association with a more robust design.

A reduction in platelet count in critically ill patients has been associated with a worse prognosis, but it is not yet known whether this relationship also exists in patients with acute kidney injury, who are more susceptible to platelet decrease due to the syndrome or due to the onset of hemodialysis. In our study of acute kidney injury patients, we found that those whose platelet count decreased >21% during the first days were more likely to experience a major kidney event. In addition, the greater the decrease in platelet count was, the more likely these events were to occur. The significance of this association was lost in patients who start hemodialysis. Our conclusions could serve to generate hypotheses about this interesting relationship.

AKI-Pro score for predicting progression to severe acute kidney injury or death in patients with early acute kidney injury after cardiac surgery.

BACKGROUND: No reliable clinical tools exist to predict acute kidney injury (AKI) progression. We aim to explore a scoring system for predicting the composite outcome of progression to severe AKI or death within seven days among early AKI patients after cardiac surgery. METHODS: In this study, we used two independent cohorts, and patients who experienced mild/moderate AKI within 48 h after cardiac surgery were enrolled. Eventually, 3188 patients from the MIMIC-IV database were used as the derivation cohort, while 499 patients from the Zhongshan cohort were used as external validation. The primary outcome was defined by the composite outcome of progression to severe AKI or death within seven days after enrollment. The variables identified by LASSO regression analysis were entered into logistic regression models and were used to construct the risk score. RESULTS: The composite outcome accounted for 3.7% (n = 119) and 7.6% (n = 38) of the derivation and validation cohorts, respectively. Six predictors were assembled into a risk score (AKI-Pro score), including female, baseline eGFR, aortic surgery, modified furosemide responsiveness index (mFRI), SOFA, and AKI stage. And we stratified the risk score into four groups: low, moderate, high, and very high risk. The risk score displayed satisfied predictive discrimination and calibration in the derivation and validation cohort. The AKI-Pro score discriminated the composite outcome better than CRATE score, Cleveland score, AKICS score, Simplified renal index, and SRI risk score (all P < 0.05). CONCLUSIONS: The AKI-Pro score is a new clinical tool that could assist clinicians to identify early AKI patients at high risk for AKI progression or death.

[Risk factors for progression to chronic kidney disease in patients with cardiac valve replacement surgery-associated acute kidney injury].

Objective: To explore the risk factors for progression to chronic kidney disease (CKD) in patients with cardiac valve replacement surgery-associated acute kidney injury (AKI). Methods: A retrospective, nested case-control study was conducted at Fuwai Central China Cardiovascular Hospital. The study subjects were patients who underwent cardiac valve replacement surgery from January 1, 2018 to December 31, 2020, with a baseline estimated glomerular filtration rate (eGFR)>60 ml·min-1·(1.73 m2)-1 and postoperative complication of AKI. The patients were followed up for 90 days after discharge from hospital. The endpoint event was defined as progression to CKD 90 days after the occurrence of cardiac valve replacement surgery-associated AKI. The patients were divided into CKD group and non-CKD group based on whether they experienced endpoint event. The baseline clinical data were compared between the two groups. The measurement data with non-normal distribution was represented as M (Q1,Q3). Logistic regression model was used to analyze the risk factors of endpoint event. The receiver-operating characteristic (ROC) curve was drawn to evaluate the performance for predicting CKD in cardiac valve replacement surgery-associated AKI patients. Results: A total of 149 cardiac valve replacement surgery-associated AKI patients (86 males and 63 females) were included in the study, aged (59.0±10.2) years. There were 27 patients (18.1%) who progressed to new-onset CKD 90 days after the occurrence of cardiac valve replacement surgery-associated AKI. Compared with non-CKD group, patients in CKD group had older age [66 (58, 70) vs 59 (53, 64) years], lower baseline eGFR [76.3 (65.8, 98.5) vs 92.7 (78.5, 101.6) ml·min-1·(1.73 m2)-1], higher proportion of preoperative hypertension [51.9% (14/27) vs 27.9% (34/122)] and serum creatinine at discharge [136 (101, 165) vs 86 (65, 104) µmol/L], and the differences were statistically significant (all P<0.05). The multivariate logistic regression analysis results revealed that older age (OR=1.063, 95%CI: 1.001-1.129, P=0.047), preoperative hypertension (OR=3.070, 95%CI: 1.105-8.532, P=0.031) and higher serum creatinine at discharge (OR=1.026, 95%CI:1.013-1.038, P<0.001) were risk factors for progression to CKD in patients with cardiac valve replacement surgery-associated AKI. The clinical risk model including age, preoperative hypertension, preoperative baseline eGFR, and serum creatinine at discharge produced a moderate performance for predicting progression to CKD in patients with cardiac valve replacement surgery-associated AKI [the area under the curve (AUC)=0.865, 95%CI: 0.790-0.940, P<0.001]. Conclusion: Older age, preoperative hypertension and higher serum creatinine at discharge are risk factors for progression to CKD in patients with cardiac valve replacement surgery-associated AKI.

Volume control strategy and patient survival in sepsis-associated acute kidney injury receiving continuous renal replacement therapy: a randomized controlled trial with secondary analysis.

Optimal strategy for volume control and the clinical implication of achieved volume control are unknown in patients with sepsis-associated acute kidney injury (AKI) receiving continuous renal replacement therapy (CRRT). This randomized controlled trial aimed to compare the survival according to conventional or bioelectrical impedance analysis (BIA)-guided volume control strategy in patients with sepsis-associated AKI receiving CRRT. We also compared patient survival according to achieved volume accumulation rate ([cumulative fluid balance during 3 days × 100]/fluid overload measured by BIA at enrollment) as a post-hoc analysis. We randomly assigned patients to conventional volume control strategy (n = 39) or to BIA-guided volume control strategy (n = 34). There were no differences in 28-day mortality (HR, 1.19; 95% CI, 0.63-2.23) or 90-day mortality (HR, 0.99; 95% CI 0.57-1.75) between conventional and BIA-guided volume control group. In the secondary analysis, achieved volume accumulation rate was significantly associated with patient survival. Compared with the achieved volume accumulation rate of ≤ - 50%, the HRs (95% CIs) for the risk of 90-day mortality were 1.21 (0.29-5.01), 0.55 (0.12-2.48), and 7.18 (1.58-32.51) in that of - 50-0%, 1-50%, and > 50%, respectively. Hence, BIA-guided volume control in patients with sepsis-associated AKI receiving CRRT did not improve patient outcomes. In the secondary analysis, achieved volume accumulation rate was associated with patient survival.

Acute Kidney Injury in Sepsis.

Sepsis-associated kidney injury is common in critically ill patients and significantly increases morbidity and mortality rates. Several complex pathophysiological factors contribute to its presentation and perpetuation, including macrocirculatory and microcirculatory changes, mitochondrial dysfunction, and metabolic reprogramming. Recovery from acute kidney injury (AKI) relies on the evolution towards adaptive mechanisms such as endothelial repair and tubular cell regeneration, while maladaptive repair increases the risk of progression to chronic kidney disease. Fundamental management strategies include early sepsis recognition and prompt treatment, through the administration of adequate antimicrobial agents, fluid resuscitation, and vasoactive agents as needed. In septic patients, organ-specific support is often required, particularly renal replacement therapy (RRT) in the setting of severe AKI, although ongoing debates persist regarding the ideal timing of initiation and dosing of RRT. A comprehensive approach integrating early recognition, targeted interventions, and close monitoring is essential to mitigate the burden of SA-AKI and improve patient outcomes in critical care settings.

Renal Complications in Portal Hypertension.

Acute kidney injury (AKI) is a common complication among patients with decompensated cirrhosis and its development is associated with worse prognosis in terms of survival. Patients with decompensated cirrhosis may develop a unique type of AKI, known as hepatorenal syndrome (HRS-AKI), characterized by marked impairment of kidney function due to haemodynamic changes that occur in late stages of liver cirrhosis. Besides, patients with cirrhosis also may develop chronic alterations of kidney function (chronic kidney disease, CKD), the incidence of which is increasing markedly and may be associated with clinical complications. The aim of this review is to provide the reader with an update of the most relevant aspects of alterations of kidney function in patients with cirrhossi that may be useful for theri clinical practice.

Incidence and predictors of acute kidney injury among adults admitted to the medical intensive care unit of a Comprehensive Specialized Hospital in Central Ethiopia.

BACKGROUND: Acute kidney injury is a prevalent complication in the Intensive Care Unit (ICU) and a significant global public health concern. It affects approximately 13 million individuals and contributes to nearly two million deaths worldwide. Acute kidney injury among Intensive Care Unit patients is closely associated with higher rates of morbidity and mortality. This study aims to assess the incidence of acute kidney injury and identify predictors among adult patients admitted to the medical Intensive Care Unit. METHOD: A retrospective follow-up study was conducted by reviewing charts of 317 systematically selected patients admitted to the Intensive Care Unit from September 1, 2018, to August 30, 2022, in Wachemo University Nigist Ellen Mohammed Memorial Comprehensive Specialized Hospital. The extraction tool was used for the data collection, Epi-data version 4.6.0 for data entry, and STATA version 14 for data cleaning and analysis. The Kaplan-Meier, log-rank test, and life table were used to describe the data. The Cox proportional hazard regression model was used for analysis. RESULTS: Among the total study participants, 128 (40.4%) developed Acute Kidney Injury (AKI). The incidence rate of Acute Kidney Injury was 30.1 (95% CI: 25.33, 35.8) per 1000 person-days of observation, with a median survival time of 23 days. It was found that patients with invasive mechanical ventilation (AHR = 2.64; 95% CI: 1.46-4.78), negative fluid balance (AHR = 2.00; 95% CI: 1.30-3.03), hypertension (AHR = 1.6; 95% CI: 1.05-2.38), and a vasopressor (AHR = 1.72; 95% CI: 1.10-2.63) were independent predictors of acute kidney injury. CONCLUSION: The incidence of Acute Kidney Injury was a major concern in the ICU of the study area. In the intensive care unit (ICU), it was found that patients with vasopressors, invasive mechanical ventilation, negative fluid balance, and chronic hypertension were independent predictors of developing AKI. It would be better if clinicians in the ICU provided targeted interventions through close monitoring and evaluation of those patients with invasive ventilation, chronic hypertension, negative fluid balance, and vasopressors.

[The role and mechanism of multifunctional molecule SLPI in regulating ischemia-reperfusion induced acute kidney injury and repair].

The secretory leukocyte protease inhibitor (SLPI) is mainly produced by immune cells and various epithelial cells, and is regulated by a variety of cytokines, such as transforming growth factor ß1, interleukin 1ß and tumor necrosis factor α. In addition to commonly known anti-protease activity, it has been found in recent years that SLPI plays essential roles in anti-apoptosis, regulating cell cycle, cell differentiation and proliferation, and inhibiting inflammatory response. SLPI can also assist the immune system to clear pathogens/damaged cells by enhancing the phagocytic function of phagocytes, so as to ameliorate tissue damage and promote repair. Moreover, recent studies have shown that the change of SLPI level in the serum of patients post cardiovascular surgery has a high diagnostic value in predicting the occurrence of acute kidney injury, suggesting that SLPI is involved in ischemia-reperfusion (IR) induced acute kidney injury. In this review, we summarized the expression, regulation, signaling pathways and associated biological events of SLPI in different organ injury models, and also discussed and evaluated the potential role of SLPI in renoprotection against IR induced acute kidney injury and its potential as a new biomarker.

MicroRNA­17­5p alleviates sepsis­related acute kidney injury in mice by modulating inflammation and apoptosis.

Septic acute kidney injury (AKI) is considered as a severe and frequent complication that occurs during sepsis. Mounting evidence has confirmed the pivotal pathogenetic roles of microRNA (miRNA or miR) in sepsis­induced AKI; however, the role of miRNAs and their underlying mechanisms in sepsis­induced AKI have not been entirely understood. The present study aimed to elucidate the functions of special miRNAs during sepsis­induced AKI and its underlying mechanism. First, a number of differently expressed miRNAs was identified based on the microarray dataset GSE172044. Subsequently, lipopolysaccharide (LPS) was used to induce AKI in mice, and the role of miR­17­5p on AKI was clarified. Finally, the related molecular mechanisms were further examined by western blotting and immunohistochemical analysis. MiR­17­5p was found to be continuously decreased and reached the bottom at h 24 after AKI in mice. Functionally, injection of agomiR­17­5p could observably improve renal injury and survival rate, as well as inhibit inflammatory cytokine production and renal cell apoptosis in mice after AKI. On the contrary, injection of antagomiR­17­5p aggravated LPS­induced renal injury, inflammation and apoptosis in mice after AKI. Moreover, transforming growth factor ß receptor 2 (TGFßR2) was identified as a direct target of miR­17­5p, and its downstream phosphorylated Smad3 was also suppressed by miR­17­5p upregulation. Taken together, these results demonstrated that miR­17­5p overexpression may exhibit a beneficial effect by attenuating LPS­induced inflammation and apoptosis via regulating the TGFßR2/TGF­ß/Smad3 signaling pathway, indicating that miR­17­5p could act as a potential target for sepsis treatment.

Kidney Outcomes and Trajectories of Tubular Injury and Function in Critically Ill Patients With and Without COVID-19.

IMPORTANCE: COVID-19 may injure the kidney tubules via activation of inflammatory host responses and/or direct viral infiltration. Most studies of kidney injury in COVID-19 lacked contemporaneous controls or measured kidney biomarkers at a single time point. OBJECTIVES: To better understand mechanisms of acute kidney injury in COVID-19, we compared kidney outcomes and trajectories of tubular injury, viability, and function in prospectively enrolled critically ill adults with and without COVID-19. DESIGN, SETTING, AND PARTICIPANTS: The COVID-19 Host Response and Outcomes study prospectively enrolled patients admitted to ICUs in Washington State with symptoms of lower respiratory tract infection, determining COVID-19 status by nucleic acid amplification on arrival. MAIN OUTCOMES AND MEASURES: We evaluated major adverse kidney events (MAKE) defined as a doubling of serum creatinine, kidney replacement therapy, or death, in 330 patients after inverse probability weighting. In the 181 patients with available biosamples, we determined trajectories of urine kidney injury molecule-1 (KIM-1) and epithelial growth factor (EGF), and urine:plasma ratios of endogenous markers of tubular secretory clearance. RESULTS: At ICU admission, the mean age was 55 ± 16 years; 45% required mechanical ventilation; and the mean serum creatinine concentration was 1.1 mg/dL. COVID-19 was associated with a 70% greater occurrence of MAKE (relative risk 1.70; 95% CI, 1.05-2.74) and a 741% greater occurrence of KRT (relative risk 7.41; 95% CI, 1.69-32.41). The biomarker cohort had a median of three follow-up measurements. Urine EGF, secretory clearance ratios, and estimated glomerular filtration rate (eGFR) increased over time in the COVID-19 negative group but remained unchanged in the COVID-19 positive group. In contrast, urine KIM-1 concentrations did not significantly change over the course of the study in either group. CONCLUSIONS: Among critically ill adults, COVID-19 is associated with a more protracted course of proximal tubular dysfunction and reduced eGFR despite similar degrees of kidney injury.

Monocytes to lymphocytes multiplying platelets ratio as an early indicator of acute kidney injury in cardiac surgery with cardiopulmonary bypass: a retrospective analysis.

OBJECTIVE: The monocyte-to-lymphocyte multiplying platelets ratio (MLPR) is a novel systemic inflammatory marker, deriving from the monocyte-to-lymphocyte ratio (MLR). However, the link between MLPR and acute kidney injury following cardiac surgery (CSA-AKI) with cardiopulmonary bypass (CPB) has not been investigated yet. We comprehensively explored the potential linear and nonlinear relationship between MLPR or MLR and CSA-AKI. METHODS: Data of patients who underwent cardiac surgery with CPB between December 2018 and April 2021 were retrospectively collected at Fuwai Hospital, Beijing, China. MLPR was defined as monocyte count (×109/L) × 1000/(lymphocyte count (×109/L) × platelets (×109/L)). MLR was defined as monocyte count (×109/L)/lymphocyte count (×109/L). Logistic regression and restricted cubic spline (RCS) were used for linear and nonlinear analysis. The primary outcome was postoperative AKI within 48 h of after cardiac surgery. RESULTS: Of the 2420 patients screened, 2387 eligible patients were enrolled in the final analysis; the mean age was 54.7 years, and 1501 [62.9%] were men. The incidence of AKI was 25.8%. Logistic regression showed that MLPR (odds ratio [OR] = 1.31, 95% confidence interval [CI]: 1.16-1.48, p < .001) and MLR (OR = 3.06, 95% CI: 1.29-7.29, p = .012) were independent risk factors for AKI. Moreover, in the RCS model with adjustment for age (median: 56), female sex, and history of diabetes, a significant statistical difference was detected between preoperative MLPR, MLR, and AKI (p for non-linearity <.001). The subgroup analyses revealed similar results. CONCLUSIONS: The study revealed a nonlinear relationship between MLPR and MLR with AKI. MLPR exhibited a J-shaped curve, and MLR showed a favorable S-shaped curve in relation to AKI. Particularly, MLPR emerges as a promising clinical composite index for early CSA-AKI prediction. These findings emphasize the significance of MLPR as a valuable tool in clinical practice for timely identification and management of CSA-AKI.

Clinical impact of Wnt5a expression on persistence of acute kidney injury in patients with urosepsis.

Abnormal Wnt5a expression is associated with dysregulated inflammation and organ dysfunction. However, the effect of Wnt5a activation on the duration of organ dysfunction remains unclear. This prospective study investigated the association between Wnt5a levels and persistent acute kidney injury (AKI) in patients with urosepsis. Serum creatinine and Wnt5a levels were measured on days 1 and 5 and at discharge in 87 patients diagnosed with urosepsis. Patients with urosepsis were classified into an improving acute kidney injury (AKI) group and a persistent or worsening AKI group according to the AKI stage on days 1 and 5. AKI recovery was defined as a discharge-to-baseline serum creatinine ratio of <1.5. Twenty-eight patients with urosepsis (32.2%) had persistent or worsening AKI, and their Wnt5a levels were higher on days 1 and 5 and at discharge than those with improving AKI. The association between Wnt5a levels and persistent or worsening AKI was maintained after adjusting for age, sex, baseline serum creatinine levels, and disease severity. Moreover, elevated Wnt5a levels were associated with an increased risk of major adverse kidney events. High Wnt5a levels at discharge were associated with unrecovered AKI and participants with AKI recovery had a steeper Wnt5a slope over time than those without recovery, irrespective of age, sex, baseline serum creatinine level, or disease severity. Assessment of Wnt5a expression was helpful in predicting AKI persistence and adverse outcomes in patients with urosepsis. Therefore, Wnt5a may serve as a valuable bio-marker for identifying the risk of persistence of AKI.