Right ventricular (RV) failure accounts for significant morbidity and mortality in critically ill patients. The RV is particularly vulnerable in conditions characterized by elevated pulmonary vascular afterload, which are commonly encountered in the intensive care unit (ICU). Conditions such as acute respiratory distress syndrome, pulmonary embolism, and decompensated pulmonary arterial hypertension are associated with acute and acute-on-chronic RV failure. In the ICU, RV failure may develop or worsen in patients with parenchymal pulmonary disease who acutely experience fluctuations in preload, excessive afterload, and/or insufficient myocardial contractility, often in addition to mechanical ventilation and circulatory compromise. This dynamic clinical scenario demands early recognition and intervention tailored to an individual patient’s physiology. Distinguishing between acute and chronic RV failure in critical illness informs diagnostic workup, hemodynamic monitoring, and resuscitative efforts. This narrative review will provide an overview of common conditions associated with RV failure in critical illness, highlighting a practical, physiology-oriented approach to diagnosis and optimization of ventilator support, fluid resuscitation, vasopressor and inotrope use, and mechanical circulatory support. RV failure due to RV infarction or severe LV failure and decompensated congenital heart disease are distinct pathophysiologic entities. These conditions require distinct treatment approaches and are beyond the scope of this review.

Acute kidney injury (AKI) is a common complication in patients with severe alcohol-associated hepatitis (sAH), yet its risk factors and outcomes remain incompletely defined. Corticosteroids are the only established therapy for sAH, but their impact on renal outcomes is unknown. A post-hoc analysis of the prospective multicenter VTL-308 trial including 151 patients with sAH was conducted to evaluate the incidence and predictors of AKI, the association of corticosteroid therapy with AKI risk, and factors associated with AKI reversal during 90days of follow-up. AKI was independently associated with significantly higher 90-day mortality (subdistribution hazard ratio (sHR) = 8.74; p < 0.001). In multivariate competing risk analysis, higher bilirubin levels (sHR = 1.06; p = 0.003) were linked to increased AKI risk, while corticosteroids were associated with an ameliorated AKI risk (sHR = 0.47; p = 0.01). Time-censored analyses confirmed the protective association of corticosteroids (HR = 0.25; p = 0.001). Once AKI occurred, corticosteroids did not promote renal recovery (HR = 1.15; p = 0.74). Elevated bilirubin levels were linked to a lower probability of AKI reversal. In conclusion, AKI is a devastating complication in sAH. Corticosteroid therapy is independently associated with a significantly lower risk of AKI development but does not influence recovery once AKI has occurred. Future prospective trials are required to provide further validation of these findings.

Pulsed-field ablation (PFA) has emerged as a potentially safer alternative to radiofrequency ablation (RFA). However, recent studies have raised concerns that PFA may induce hemolysis, which could contribute to the development of acute kidney injury (AKI). The PubMed, Embase, Scopus, and Cochrane databases were searched for randomized clinical trials (RCTs) and non-RCTs that reported AKI incidence and hemolysis biomarkers after PFA. Random-effects models were used to calculate pooled odds ratio (OR) and mean differences (MDs) with 95% confidence intervals (CIs). Substantial heterogeneity was defined as I2 > 25%. Ten studies, including one RCT, comprising a total of 3,843 patients, were included, with 1,859 in the PFA group and 1,994 in the RFA group. In the primary endpoint analysis related to AKI and renal function, no significant differences were found between the PFA and RFA groups, with PFA having a total prevalence of 2.1% (95% CI [0.90; 4.84]). The leave-one-out analysis, specifically the exclusion of one outlier study, led to the comparative results having statistical significance statistical significance (OR 3.70, 95% CI [2.49; 5.51], p = 0.0019; I² = 0%), indicating no heterogeneity, and with the total prevalence increasing to 2.4% (95% CI [0.96; 5.93]). Regarding hemolysis, all evaluated biomarkers were significantly elevated in the PFA group, although with high heterogeneity. PFA appears to be associated with a slightly higher risk of AKI than RFA. Renal injury is mostly mild-degree and transient. PFA is associated with significant peri-procedural hemolysis.

Acute kidney injury (AKI) is a clinical syndrome that can be caused by a variety of factors, leading to rapid decline of kidney function and increased morbidity and mortality, whilst also exerting significant economic burden on the affected patient. Salvia miltiorrhiza is a highly valued plant in traditional Chinese medicine (TCM). Tanshinone IIA (Tan IIA) is an important active compound that can be extracted from salvia miltiorrhiza, which has reported anti-inflammatory effects. The objective of the present investigation was to explore the potential effects of Tan IIA on folic acid-induced AKI and elucidate its underlying mechanism. A comprehensive analysis was conducted utilizing the TCM Systematic Pharmacology Database and Analytical Platform database to screen for chemical components and their corresponding targets. Subsequently, by using network pharmacology techniques and Cytoscapes 3.7.2 software, a protein-protein interaction (PPI) network was constructed and analyzed. Through Venn diagram analysis of the DeGeNET, OMIM, PharmGKB, and GeneCards databases using the key word "acute kidney injury," a total of 76 overlapping targets were obtained. Building upon this, a compound-target gene network was constructed and analyzed by Cytoscapes 3.7.2 software, revealing TP53, STAT3, CASP3, VEGFA, and JUN to be pivotal therapeutic targets. Subsequently, an AKI mouse model was established to investigate the renal effects of Tan IIA. By immunohistochemistry, Western blot results showed the Tan IIA ameliorated kidney function by alleviating inflammation, mitigating necrosis of renal tubular cells, promoting their proliferation and attenuating kidney injury. These beneficial effects were found to be achieved by inhibiting the PI3K/AKT signaling pathway and inhibiting the expression of TP53 by Western blot. In conclusion, TP53may be a potential target for folic acid-induced AKI, whilst Tan IIA exerts its renoprotective effects and improves renal function by PI3K/AKT signaling pathways.

Inflammation and ferroptosis play a crucial role in cisplatin (CP)-induced acute kidney injury (AKI). Silybin (SYB), a polyphenolic flavonoid, has shown renal protective effects, but its underlying mechanisms remain unclear. CP-induced HK-2 cell and mouse AKI models were used to explore the role of SYB. CCK-8, lactate dehydrogenase release, flow cytometry, and calcein/PI staining, were performed to evaluate cell viability, proliferation, and apoptosis. Oxidative stress and ferroptosis markers were measured, while renal function was assessed by serum creatinine and urea nitrogen. Mitochondrial ultrastructure was examined, and histological staining was conducted to analyze renal pathology and iron deposition. Western blotting detected HDAC6, NF-κB, NLRP3, and ferroptosis-related proteins expression. SYB treatment alleviated CP-induced mitochondrial damage, reduced lactate dehydrogenase release, inflammatory cytokines, oxidative stress, and ferroptosis, and improved proliferation and viability in HK-2 cells. In mice, 100 mg/kg SYB decreased serum creatinine, urea nitrogen, and cytokine levels, while ameliorating renal tissue injury. Mechanistically, SYB downregulated HDAC6 and inhibited NF-κB/NLRP3 activation, thereby suppressing ferroptosis. Notably, overexpression of HDAC6 restored NF-κB/NLRP3 activity and attenuated the protective effects of SYB. In conclusion, SYB mitigates CP-induced AKI by reducing inflammation and ferroptosis by modulating the HDAC6/NF-κB/NLRP3 pathway.

Patients with a BMI (Body Mass Index) ≥ 60kg/m2 are at high risk for bariatric surgery. They have higher complication rates, longer length of stay and greater technical difficulties with surgery. Surgical robots offer better ergonomics and precision, which facilitate surgery. The role of the robot in patients with obesity class V (BMI ≥ 60kg/m2) surgery has not been adequately evaluated. This study reports data of over 230,000 patients regarding bariatric surgery. We aim to compare the results of laparoscopic and robotic RYGB in patients with BMI ≥ 60kg/m2. MBSAQIP database. Patients aged 18-80 years who underwent Roux-en-Y gastric bypass (RYGB) were included using the 2020-2023 MBSAQIP database. We compared the 30-day outcomes of laparoscopic versus robotic RYGB in patients with BMI < 60kg/m2 versus BMI ≥ 60kg/m2. There are 233,828 patients in this study. Patients with BMI ≥ 60kg/m2, as compared to BMI < 60kg/m2, were more likely to have postoperative complications (5,23% vs. 4,44%, p = 0,039), acute renal failure (0,23% vs. 0,07%, p = 0,007), unplanned admission to ICU (1,08% vs. 0,73%, p = 0,029) and Emergency Department visits after discharge (12,38% vs. 11,02%, p = 0,019). There is no difference in 30-day complication rate between laparoscopic and robotic RYGB in patients with BMI ≥ 60kg/m2. Patients with BMI ≥ 60kg/m2 have higher rates of complications compared to patients with BMI < 60kg/m2. RRYGB seems to be a safe to perform in patients with BMI ≥ 60kg/m2 with no difference in 30-day complication rate, longer average operating time but shorter length of stay. There is still a need for good quality multi-centre prospective research study to define the best approach for patients with obesity class V.

High-dose methotrexate (HDMTX) is an integral component of treatment for multiple malignancies. However, preventive strategies often fail, resulting in renal impairment and delayed methotrexate elimination (DME), which increases the risk of systemic toxicity. This review aims to summarize past, current, and emerging strategies for the management of HDMTX-related toxicity. Recent research has identified host genetic factors, hypoalbuminemia, and larger body surface area as contributors to DME. Animal studies have explored potential nephroprotective agents, including synthetic 1,3,4-oxadiazole (5b) and repurposed drugs such as empagliflozin and amlodipine. The preferred mitigation agent, glucarpidase, continues to demonstrate improved clinical and financial outcomes, with higher odds of renal recovery even at lower doses. Early therapeutic drug monitoring has shown promise as a biomarker for predicting acute kidney injury. In addition, the web-based clinical tool MTXPK.org now integrates population pharmacokinetic models with patient-specific data to guide interpretation and management of DME. Identification of emerging risk factors, advances in pharmacogenomics, and timely methotrexate monitoring, combined with patient-specific pharmacokinetic modeling, underscore the importance of personalized therapeutic strategies to reduce renal toxicity and DME.

Sepsis-associated acute kidney injury (SAKI) is a severe condition associated with high mortality and long-term complications. Currently, there is no effective strategy to halt AKI chronicization. Stress-induced senescence of renal tubular epithelial cells (RTECs) is a pivotal driving mechanism in the AKI-CKD transition. Previous scRNA-seq revealed that the expression of immediate early response gene 3 (IER3) was markedly upregulated in the senescent RTECs of patients with AKI and that the IER3+RTEC subpopulation exhibited diminished differentiation potential and impaired self-renewal capacity. However, the role of IER3 in RTEC stress-induced senescence following AKI remains unclear. In this study, we found that knockout of IER3 reduced mortality rates, alleviated renal injury, mitigated renal maladaptive fibrotic repair, and concurrently inhibited RTEC stress-induced senescence after SAKI. Further RNA-seq of IER3-/- mouse renal tissues revealed significant upregulation of peroxiredoxin 5 (PRDX5) in the absence of IER3. Inhibition of PRDX5 blocked the effects of IER3 knockout on RTEC stress-induced senescence under septic conditions. Intriguingly, we found that IER3 interacted with the presenilin-associated rhomboid-like gene (Parl) and reduced its shear activity. This interaction also inhibited the cleavage and subsequent mitochondrial translocation of cytoplasmic PRDX5, leading to decreased mitochondrial levels in PRDX5 and impaired antioxidant capacity. These changes resulted in oxidative mitochondrial damage and abnormal perinuclear clustering of mitochondria, which promote stress-induced cellular senescence and ultimately facilitates the transition from AKI to CKD. In conclusion, our findings suggest that IER3 might induce RTEC senescence and exacerbate the AKI-CKD transition in sepsis-associated AKI by inhibiting mitochondrial translocation of PRDX5.

The purpose of this study was to determine if prior manipulation under anaesthesia (MUA) and/or lysis of adhesions (LOA) was associated with an increased risk of re-revision following index revision total knee arthroplasty (TKA) in patients that had a diagnosis of arthrofibrosis. The PearlDiver Mariner database was queried by Current Procedural Terminology (CPT) and International Classification of Disease (ICD) codes to identify patients who had a diagnosis of arthrofibrosis at the time of revision TKA. Patients were divided into two groups: those with prior MUA and/or LOA and those without prior MUA and/or LOA. The groups were 1:3 propensity score matched by age, gender, anemia, and Elixhauser Comorbidity Index (ECI). The primary outcome was incidence of re-revision TKA at 5 years. Secondary outcomes included periprosthetic joint infection (PJI) at 6 months and 5 years, 90-day hospital readmission, and the incidence of deep vein thrombosis (DVT), blood transfusion, and acute kidney injury (AKI) at 6 months. Logistic regression was used to determine predictors of re-revision TKA. After propensity matching, 2622 patients with a diagnosis of arthrofibrosis underwent index revision TKA without prior MUA and/or LOA and 874 patients underwent index revision after a prior LOA and/or MUA. The incidence of re-revision TKA at 5 years in patients with prior MUA and/or LOA (20% vs. 14%; OR 1.5, 95% confidence interval [CI] [1.3-1.9], p < 0.001) was significantly higher compared to patients with no prior MUA and/or LOA. Predictors of re-revision were age, ECI, and prior MUA and/or LOA (OR: 1.5, 95% CI [1.2-1.9]) (R2 = 0.21; p < 0.01). No significant differences were observed between groups for PJI at 6 months and 5 years, 90-day hospital readmission, or DVT, blood transfusion, and AKI at 6 months. A history of prior MUA and/or LOA, older age, and ECI are associated with a significantly higher risk of re-revision TKA in patients that have a diagnosis of arthrofibrosis at the time of index revision TKA. Level III, retrospective comparative study.

BACKGROUND Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have become important in the treatment of diabetic kidney disease (DKD). Despite their reno-protective effect, kidney injury from GLP-1 RAs has been rarely reported. The reported kidney injuries varied from mild symptoms to dialysis at presentation and occurred 2 days to 2 years after drug initiation. We report a case of a patient with DKD who developed an episode of interstitial nephritis after dulaglutide administration. CASE REPORT A 63-year-old woman with stage 3b diabetic kidney disease and depressive disorder was prescribed dulaglutide 0.75 mg/week subcutaneously in August 2023 due to persistent albuminuria despite receiving the maximum tolerated dose of azilsartan. Sodium-glucose cotransporter-2 inhibitor was not prescribed in this case due to her frequent urinary tract infections. Serum creatinine at 2-month follow-up increased and then doubled despite reduction in the azilsartan dose. Potentially nephrotoxic medications were discontinued and no other possible causes of kidney injury, including volume depletion, were presented. Kidney biopsy revealed active interstitial nephritis and diabetic nephropathy without accumulation of immune complex. After discontinuing dulaglutide, there was an almost complete recovery of kidney function without steroid therapy. Azilsartan and chlorthalidone could then be successfully rechallenged. CONCLUSIONS Despite the established renoprotective effect of GLP-1 RAs, acute-to-chronic tubulointerstitial nephritis occasionally occurs, requiring vigilant monitoring after drug initiation or titration. Nevertheless, this does not prevent the prescription of GLP-1 RAs to alleviate DKD progression in certain patients. Treatment includes drug discontinuation and steroid therapy in non-responders.

Evaluation of pancreatic stone protein (PSP) plasma levels has been proven effective in predicting unfavourable outcomes in patients with Ventilator-Associated Pneumonia (VAP), infection after cardiothoracic surgery and peritonitis. It is also being studied as a sepsis biomarker with promising results compared to other commonly used biomarkers. We aim to validate PSP in septic patients with community acquired infections. This will help to establish its role in point-of-care settings. Adult patients consecutively admitted to the Emergency Department (ED) of a tertiary medical centre, with the diagnosis of intra-abdominal infection (IAI), urinary tract infection (UTI) and lower respiratory tract infection (LRTI) who met the inclusion criteria were enrolled. PSP was measured in whole blood, within one hour since admission, by spectrophotometry using abioSCOPE device. Statistical analysis was performed, and a cut-off value for PSP to predict the composite outcome of sepsis, readmission, antibiotic treatment escalation and need for invasive treatment was estimated. Patients were followed for 28 days to document their outcomes. A total of one hundred and one (n = 101) patients were included. Forty-five were male. The most common comorbidity was hypertension (33%). Fifty-three (52.5%) had LRTI, thirty-seven (36.6%) had UTI and nineteen (18.8%) had IAI. Thirteen of them had more than one type of infection. Our primary outcome met statistical significance, as PSP predicted the composite outcome of sepsis, readmission, antibiotic treatment escalation and need of invasive treatment with an Area Under Curve (AUC) =0.844 (95% CI 0.767-0.920), in the optimal cut-off of 48.5 ng/ml. PSP predicted sepsis with an AUC = 0.892 (95% CI 0.826-0.956) and was also an independent risk factor for sepsis and mortality after age adjustment. PSP was superior to the common used sepsis biomarkers, C-reactive protein (CRP), ferritin, lactate dehydrogonase (LDH)/albumin ratio, White Blood Cell count (WBC), fibrinogen and lactate both for sepsis and for the composite outcome. It was also correlated with Sequential Organ Failure Assessment (SOFA) day 1 (D1), SOFA peak and qSOFA and its prognostic value was independent of renal function, despite being inversely proportional to estimated Glomerular Filtration Rate (eGFR), reflecting the sepsis-related acute kidney injury (SAKI). PSP is a valuable biomarker that can rule out patients who do not have sepsis and are not in high risk to develop sepsis the following days, giving valuable insights regarding their antimicrobial coverage and management in general. It seems to be superior to other biomarkers in sepsis prediction and adequately compatible with frequently used sepsis assessment scores, such as SOFA. In the Emergency Department setting PSP can distinguish infected patients at high risk for sepsis who have low qSOFA scores.

BACKGROUND Tirzepatide is effective for glycemic control and weight management in type 2 diabetes and obesity. Clinical trials have demonstrated tirzepatide's lower risk of acute kidney injury (AKI) compared with existing glucagon-like peptide-1 receptor agonists, along with benefits including reduced albuminuria and stable estimated glomerular filtration rate. Rare cases of AKI have been reported, potentially associated with dehydration from gastrointestinal side effects, polypharmacy, or comorbidities. We describe AKI in a non-diabetic, multimorbid patient after rapid tirzepatide dose escalation, underscoring the importance of identifying susceptible patient phenotypes. CASE REPORT A 66-year-old man with morbid obesity (body mass index 61.4 kg/m²), hypertension, prediabetes, hypothyroidism, and polypharmacy presented for weight management before bariatric surgery. Tirzepatide was initiated at 2.5 mg weekly and escalated to 12.5 mg over 4 months, resulting in weight loss of 35 kg. Preoperative evaluation revealed AKI, with a serum creatinine level of 2.4 mg/dL, potassium of 6.8 mmol/L, and metabolic acidosis (pH 7.31). Potential contributors included pharmacodynamic interactions with antihypertensive agents or dehydration secondary to gastrointestinal side effects. Management involved intensive care unit admission, antihyperkalemic therapy, intravenous fluids, and tirzepatide discontinuation. Renal function improved (creatinine 1.18 mg/dL) by discharge. CONCLUSIONS The AKI in this case may have resulted from the combination of rapid tirzepatide dose escalation, polypharmacy, and multimorbidity, potentially compounded by subclinical volume depletion or hemodynamic alterations. Clinicians should utilize standard titration schedules, closely monitor blood pressure and renal function, and exercise caution in patients with complex medication regimens to maximize tirzepatide's therapeutic benefits while minimizing renal risk.

Acute kidney injury (AKI) is a life-threatening problem for hospitalized patients, and early detection is crucial to reduce severe outcomes. Traditional predictive methods lack in monitoring complex physiological patterns and ensuring data privacy in decentralized healthcare settings. The study aims to develop and evaluate two distinctly complementary novel graph-based approaches, namely the centralized Graph Attention Network (GAT) and the decentralized model, Gossip Learning with Adaptive Aggregation GAT (GL-AA-GAT), to identify AKI onset between 6 and 12h in advance, using physiological time-series data from the Kaggle Sepsis dataset. Multi-Head Attention is used for modeling feature interactions in centralized GAT, while GL-AA-GAT can further achieve this by decentralized training of five nodes using gossip exchange and adaptive aggregation for privacy and scalability. Through its novel graph structure, centralized GAT predicts the onset of AKI with an accuracy of 94.1%, sensitivity of 94%, AUC-ROC of 95%, and AUPRC of 91%. With decentralized privacy additions, GL-AA-GAT achieves an accuracy of 92.8%, a sensitivity of 93%, an AUC-ROC of 93.8%, and an AUPRC of 90%, with robustness. Sensitivity analyses revealed that the performance was stable with the prediction horizons and correlation thresholds, and external validation on non-sepsis cohorts of the ICU further indicated generalizability. Both models outperform existing models, which means high predictive reliability. The GL-AA-GAT's distributed approach gives privacy and flexibility, making it innovative for distributed clinical environments, with task scheduling enhancing training efficiency.

Despite advancements in artificial enzymes (AEs) for acute kidney injury (AKI) therapy through renal redox homeostasis modulation, the trade-off between organ-specific targeting and high multienzyme-mimicking catalytic efficiency is still a big challenge. Herein, we address this challenge through chirality-engineered Cu2+-phenolic AEs (l-phen@Cu-TA) via incorporation of l-phenylalanine (l-phen) to synergize stereoselective recognition and catalytic activity. Chiral l-phen induces electron density redistribution from phenolic ligands to Cu2+ in the cocatalytic center, significantly enhancing H2O2 adsorption while reducing catalytic energy barriers, thereby amplifying catalase (CAT)-mimicking activity and superoxide dismutase (SOD)-mimetic performance, with concurrent scavenging of secondary radicals (•OH, ONOO-, etc.). Critically, the stereoselective recognition of l-phen@Cu-TA AEs, based on the l-type amino acid transporter 1 (LAT1), enhances the renal tubular cell uptake by 5-fold over pristine Cu-TA AEs, respectively, thereby driving renal pathological-site enrichment and internalization to boost therapeutic bioavailability. In vivo investigation reveals that the l-phen@Cu-TA treatment can restore the physiological homeostasis of AKI via ROS-scavenging by SOD-CAT enzymatic cascades and remodel the renal microenvironmental stability, thereby achieving satisfactory AKI treatment. This work pioneers chirality-modulated AEs for organ-specific antioxidant therapy, establishing a transformative paradigm for precision intervention in oxidative stress-related pathologies.

Advanced non-squamous non-small cell lung cancer has a poor prognosis, and immune checkpoint inhibitors (ICIs) plus platinum-based combination chemotherapy is the first-line treatment. Atezolizumab, an ICI, has three regimens: atezolizumab + carboplatin (CBDCA) + paclitaxel + bevacizumab [ABCP], atezolizumab + CBDCA + nab-paclitaxel (nab-PTX) [A + CnP], and atezolizumab + CBDCA + pemetrexed [A + CbP]. However, clinical trials directly comparing these regimens have not been reported, and the differences in adverse events have not been fully clarified. We calculated the reporting odds ratio (ROR), a measure of adverse drug reaction (ADR) signals, using the FDA Adverse Event Reporting System (FAERS) to compare the major ADRs of ABCP, A + CnP, and A + CbP regimens. The ROR (95% confidence interval [CI]) for rash and hypersensitivity-related adverse events was 2.06 (1.81-2.34) for ABCP, 0.81 (0.42-1.56) for A + CnP, and 0.57 (0.37-0.87) for A + CbP; the signal was only detected for the ABCP regimen. In acute kidney injury (AKI), it was ABCP: 1.24 (0.89-1.73), A + CnP: 1.16 (0.37-3.60), and A + CbP: 1.76 (1.06-2.93), and signal was detected only for the A + CbP regimen. Contrarily, signals were detected for colitis, drug-induced liver injury, and pneumonitis for all regimens. Rash and hypersensitivity-related adverse events and AKI were more frequently reported with the ABCP and A + CbP regimens, respectively. These observations may help generate hypotheses regarding regimen-specific adverse event profiles and support future studies toward individualized chemotherapy.

Aminoglycoside pharmacokinetics is expected to change in premature infant. However, the PK profile of amikacin in Chinese premature infants has not been characterized. The aim of this study was to assess the safety and describe the pharmacokinetics properties of amikacin in Chinese premature infants. This was a two-center, retrospective, pharmacokinetic study. Phoenix NLME was used to construct a pharmacokinetics model. Monte Carlo simulations were performed to screen the optimal dosage regimen. A total of 54 amikacin concentrations from 23 patients were available for population pharmacokinetic analysis. The patients received an amikacin total daily dose (median(range)) of 14.32 (10.34-19.70) mg/kg. The distribution of Cmin (median(range)) was 4.07 (1.01-30.99)µg/mL, and Cmax (median(range)) was 17.45 (4.56-164.72) µg/mL. There were 14 patients achieved target Cmin, and 6 infants achieved Cmax. There were 3 cases occurred acute kidney injury, with Cmax and Cmin all exceeded the recommended range. A one-compartment model with first-order elimination best described the amikacin concentration-time data. The estimated typical values of clearance and volume of distribution for amikacin were 1.43L/h/70kg and 30.97L/70kg, respectively. Covariate analyses revealed that statistically significant relationships between amikacin clearance and weight, postmenstrual age and renal function, while there was a statistically significant relationship between volume of distribution and weight. Based on the model-based simulations, the initial recommend dosage regimens prior to therapeutic drug monitoring were suggested as 13mg/kg q24h, 12mg/kg q36h and q48h for serum creatinine between 15-22µmol/L; 23-36 and 37-60µmol/L, respectively. Weight, postmenstrual age and renal function have significant influence on the PK of amikacin in Chinese premature infants. The optimal dosage regimens might provide an alternative choice for premature infants in China in the therapy of amikacin.

Acute kidney injury (AKI) is highly prevalent during hospital inpatient admissions and is associated with increased length of stay and mortality. This study aimed to outline the incidence, recognition and outcomes of AKI in patients admitted to a tertiary centre. We conducted a retrospective observational study of adult inpatients admitted to medical and surgical units for more than 24 h from 1 March 2023 to 31 August 2023. The outcomes assessed were the incidence of AKI, coding of AKI and the length of stay and mortality in patients with and without AKI. In patients referred for nephrology consult, the medical record was reviewed for best practice AKI care, including repeat serum creatinine, documentation, medication review, urinalysis, imaging and fluid balance review and charting. The incidence of AKI was 22.9% in the 12 543 hospital admissions included. In patients with AKI, the majority had stage 1 (77.4%), followed by stage 2 (15.4%) and stage 3 (7.0%). Mortality was higher in patients with AKI, with 7.4% of patients dying during admission compared with 1.0% of patients without AKI (P < 0.001). Patients with AKI had a longer length of stay, with a median of 6.8 days (interquartile range (IQR), 3.5-13.4 days), compared with those without AKI, with a median of 3.5 days (IQR, 2.0-6.4 days, P < 0.001). There was significant under-recognition of AKI, with <50% of those with AKI having a coded diagnosis. Additionally, in patients referred for nephrology consult, only 16.7% had all aspects of AKI care initiated within a day of meeting the definition for AKI. AKI was present in more than one in five hospital admissions and associated with longer length of stay and mortality. Improving recognition, management and documentation of AKI is an ongoing priority area.

Acute Kidney Injury: Is it a Risk Factor for Long-Term Cognitive Decline.

To investigate the association between endothelial activation and stress index (EASIX) and acute kidney injury (AKI) in heart failure (HF) patients. The study utilized data from the MIMIC-IV database. EASIX was log-transformed to address its right-skewed distribution. The association of log EASIX with AKI and in-hospital mortality was assessed using logistic regression and Kaplan-Meier curves, and its discriminating performance was evaluated by the area under the receiver operating characteristic curve. A competing risk model was further employed, considering AKI occurrence as a primary event and in-hospital mortality as a competing event. Among 4,740 included HF patients, 53.143% were experiencing AKI. Log EASIX was an independent risk factor for AKI across three adjusted regression models (Model 1: OR = 3.398, 95%CI: 2.909-3.980; Model 2: OR = 5.788, 95%CI: 4.965-6.771; Model 3: OR = 2.331, 95%CI: 1.956-2.786), and demonstrated moderate discriminating performance (AUC = 0.704). Additionally, high log EASIX was associated with an increase in in-hospital mortality (p < 0.05). Multivariable competing risk analyses exhibited an independent influence of log EASIX on AKI (p < 0.05). High log EASIX levels are associated with an increased risk of AKI in HF patients. In clinical practice, log EASIX, being simple to operate and readily accessible, may serve as an effective tool for the early identification of high-risk patients and help to develop individualized treatment strategies.

We aimed to evaluate the effect of extracorporeal anticoagulation with nafamostat mesilate (NM) and continuous renal replacement therapy (CRRT) on sepsis complicated with acute kidney injury (AKI). The clinical data of 106 sepsis patients complicated with AKI admitted from January 2023 to December 2024 were retrospectively analyzed. According to different treatment protocols, the patients were assigned into a control group (n=53, regional citrate anticoagulation (RCA) plus CRRT) and a study group (n=53, NM extracorporeal anticoagulation plus CRRT). The use of extracorporeal circulation circuit was compared. After 3 days of treatment, the levels of procalcitonin, interleukin-6, and tumor necrosis factor-α decreased in the two groups compared to those before treatment (p<0.05), and they were lower in the study group than in the control group (p<0.05). After 3 days of treatment, both groups had lowered levels of serum creatinine (Scr), cystatin C (Cys-C), and blood urea nitrogen (BUN), together with increased mean transit time (MTT), peak intensity (PI), and area under the curve (AUC) compared with those before treatment. In the study group, the levels of Scr, Cys-C, and BUN declined, while MTT, PI, and AUC rose compared with those in the control group (p<0.05). The incidence of adverse reactions in the study group was lower than that in the control group (3.77 vs. 16.98%) (p<0.05). NM outperforms RCA in prolonging the hemofilter lifespan, reducing hemofilter replacement frequency, improving renal perfusion and renal function, and eliminating inflammatory mediators.