Kidney function abnormalities is a common complication following ischemic stroke. Lipocalin 2 (LCN2) is currently a well-recognized specific biomarker of tubular injury. However, the role of LCN2 in kidney function abnormalities following stroke remains elusive. The sympathetic nervous system plays a crucial role in linking the brain and kidney. However, whether the kidney sympathetic nervous system regulates the expression of LCN2 following ischemic stroke has not been identified.

In this study, we established a middle cerebral artery occlusion (MCAO) model to induce ischemic stroke in mice. Renal function was assessed 24 h after cerebral ischemia-reperfusion injury. Transcriptomic sequencing of kidney tissue was performed to identify potential pathological mechanisms. The role of LCN2 in post-stroke renal injury was investigated using renal tubule-specific LCN2 knockout mice and a combination of qPCR, western blotting, immunofluorescence, and transmission electron microscopy. In addition, renal denervation (RDN) was used to explore the relationship between sympathetic nerves and the expression of renal LCN2.

Ischemic stroke significantly exhibits renal functional impairment 24 h after reperfusion. Notably, RNA sequencing and Western blotting revealed a markedly increased expression of renal LCN2 following ischemic stroke. Renal tubular Lcn2-specific knockout significantly ameliorated the occurrence of kidney function abnormalities after stroke. Subsequently, we observed that the activation of renal sympathetic nerves upregulates LCN2 and induces kidney function abnormalities after stroke.

These findings reveal a neural pathway in which the sympathetic nervous system upregulates LCN2, providing potential therapeutic strategies for renal protection following ischemic stroke.

This was a prospective, longitudinal study, of 40 children who had open heart surgery, on account of congenital heart diseases, at our study center, between April 2020 and June 2022. Plasma samples were assayed for cystatin-C using the enzyme-linked immunosorbent assay method, while quantification of creatinine was done using a Roche automated analyzer (Cobas C311).

Mean plasma concentrations of cystatin-C at 0, 4, 8, 12, 24 and 48 hours were 0.49±0.11 ng/dL, 0.75 ± 0.19 ng/dL, 0.96 ± 0.23 ng/dL, 0.79 ± 0.20 ng/dL, 0.66 ± 0.15 ng/dL, and 0.60 ± 0.14 ng/dL, respectively, versus 48.98 ± 11.6 μmol/L, 59.65 ± 13.06 μmol/L, 63.00 ± 16.53 μmol/L, 64.90 ± 17.65 μmol/L, 68.50 ± 19.99 μmol/L, and 70.78 ± 21.86 μmol/L, respectively, of creatinine. Plasma cystatin-C peaked earlier at 8 hours compared to creatinine, which peaked at 48 hours. The ROC curve showed that cystatin-C had an AUC of 0.983.

This study showed that cystatin-C has a better sensitivity and specificity than creatinine in predicting CSA-AKI in children who had open heart surgery for congenital heart diseases.

ObjectiveThe potential benefit of measures to prevent contrast-induced acute kidney injury (CIAKI) remains uncertain. This uncertainty is partly due to the reliance on serum creatinine, a biomarker influenced by non-renal factors such as muscle mass, hydration status, and age. Therefore, this study aims to evaluate CIAKI prevention based on cystatin C levels-a more stable and earlier biomarker of renal dysfunction, which may improve diagnostic precision and the assessment of therapeutic efficacy.MethodsWe performed a systematic review and meta-analysis of all randomized clinical trials (RCTs) on preventive measures of contrast-induced acute kidney injury, based on cystatin C levels, in patients who underwent percutaneous procedures. We searched PubMed, Scopus, and Cochrane Central for studies comparing the use of high-dose statins in prevention. The outcome of interest was an acute kidney injury based on increased serum cystatin C after the procedure. Statistical analysis was performed using RevMan 5.4. This systematic review with meta-analysis was registered in the International Prospective Register of Systematic Reviews (PROSPERO) under protocol (CRD42023441815).ResultsWe included four studies with a total of 1167 patients, of whom 594 (50.8%) received high-dose statins (atorvastatin or rosuvastatin). On the baseline characteristics of the study population, 65% were male; 79.2% had hypertension; 44.3% had diabetes; 35.7% had dyslipidemia, and 35.4% were currently smokers. Overall, high doses of statins were associated with a lower incidence the CIAKI (OR 0.31; 95% CI [0.19,0.53]; P < .0001).ConclusionOur findings suggest that high doses of statins may play an important role as a measure to prevent CIAKI. If this result is confirmed, we will be able to set up CIAKI prevention protocols, thus expanding the number of patients who will undergo contrast-enhanced exams.

Critically ill patients are susceptible to serious infections due to their compromised conditions and extensive use of medical devices, often requiring empiric broad-spectrum antimicrobial therapy. Failure of antimicrobial therapy in this vulnerable population has a direct impact on the patient's survival; hence, selecting the optimal dosage is critical. This population, however, exhibits complex and diverse disease-related physiological changes that can markedly alter antimicrobial disposition. Inflammatory cytokines overexpressed in the systemic inflammatory response syndrome increase vascular permeability, leading to higher volume of distribution for hydrophilic antimicrobials. These cytokines also downregulate metabolic enzyme activities, reducing the clearance of their substrates. Hypoalbuminemia can increase the volume of distribution and clearance of highly protein-bound antimicrobials. Acute kidney injury decreases, while augmented renal clearance increases the clearance of antimicrobials primarily excreted by the kidneys. Furthermore, continuous renal replacement therapy and extracorporeal membrane oxygenation used in critical illness substantially affect antimicrobial pharmacokinetics. The complex interplay of multiple factors observed in critically ill patients poses a significant challenge in predicting the pharmacokinetics of antimicrobials. Therapeutic drug monitoring is the most effective tool to address this issue, and is proactively recommended for vancomycin, teicoplanin, aminoglycosides, voriconazole, β-lactams, and linezolid in critically ill patients. To streamline this process, model-informed precision dosing is expected to promote personalized medicine for this population.

Diabetic nephropathy (DN) is a prevalent complication and serious microvascular of diabetes mellitus. After previous studies, we found that phenylethanol glycosides (CPhGs) derived from Cistanche tubulosa (Schenk) Wight exerts antidiabetic and renoprotective effects. However, the effects of CPhGs on DN remain incompletely understood. The study aimed to examine the effects of CPhGs on DN in rats and explore the underlying mechanism involved. A DN rat model was established by streptozotocin (STZ) combined with a high-fat diet. Reagent kits were used to assess the extent to which CPhGs ameliorate hyperglycemia, insulin resistance (IR), renal dysfunction, kidney oxidative stress, and peripheral inflammation. Histology and immunohistochemical staining were used to detect the changes in renal tissue structure and the expression levels of α-smooth muscle actin (α-SMA) and collagen I. Furthermore, we analyzed the cecal contents of DN rats to investigate the effect of CPhGs on gut microbiota by using 16S rRNA sequencing and broad-spectrum metabolite profiling. The results showed that CPhGs demonstrated a range of advantageous outcomes in DN, encompassing the enhancement of kidney function and alleviation of hyperglycemia, IR, renal injury, oxidative stress, and peripheral inflammatory reactions. In addition, CPhGs regulated the abundance of the [Eubacterium]_coprostanoligenes_group, Oscillospiraceae_UCG-005, etc. to modulate the gut microbiota. CPhGs significantly upregulated the content of vitamin B6 and tyrosyl-tryptophan and downregulated histamine, L-methionine, etc. In summary, the therapeutic efficacy of CPhGs on DN rats may be achieved by modulating the gut microbiota and cecal metabolites to restore the metabolic disorders of vitamin B6, histidine, etc.

Heavy metals (e.g., cadmium, lead, mercury, etc.) can infiltrate the human body via diverse routes, with a propensity to accumulate in the kidney cortex, thereby precipitating kidney dysfunction. Vitamin D has been implicated in mitigating the oxidative stress and inflammatory reactions triggered by heavy metal exposure. However, the interplay between heavy metal toxicity and vitamin D deficiency in the context of incipient kidney injury remains an underexplored area of research.

Utilizing data from the National Health and Nutrition Examination Survey spanning from 2001 to 2004, Our methodology leveraged spline smoothing within the framework of generalized additive models to more vividly elucidate the impact of heavy metal exposure and serum vitamin D levels on the trajectory of early kidney injury biomarkers (including albumin-to-creatinine ratio, β-2 microglobulin (B2M), cystatin C (CYST), and estimated glomerular filtration rate (eGFR) (serum creatinine(SCr)-based(eGFR), CYST-based eGFR, and SCr-CYST-based eGFR). Furthermore, we conducted an interaction analysis to assess the combined effects of heavy metal exposure and vitamin D deficiency on early kidney injury.

The cohort comprised 2,422 adults. Our results indicated that cadmium levels were positively correlated with B2M, CYST, and negatively correlated with eGFRc, eGFRs. Similarly, lead levels showed a positive correlation with ACR, B2M, and CYST, and negative correlation with eGFRc, eGFRc&s. In contrast, mercury levels were negatively correlated with B2M, CYST and positively correlated with eGFRc. In addition, there was an interaction between lead exposure and vitamin D deficiency in early kidney injury indicators (P for interaction: B2M: 0.028, CYST: 0.038, eGFRc&s: 0.011).

This study suggests a correlation between exposure to cadmium and lead and an increased risk of early kidney injury. It highlights the potential importance of targeted vitamin D supplementation and reduction in lead exposure in mitigating early kidney injury. However, these findings warrant validation through further prospective research.

Given the previously reported harmful effects of abdominal fat burden on kidney function, we aim to investigate the relationship between major adverse kidney events within 30 days (MAKE30) and abdominal obesity in acute necrotizing pancreatitis (ANP) patients and explore the underlying risk factors.

A retrospective cohort study of all patients admitted within 72 h after the first episode of ANP to a tertiary center between June 2015 and June 2019 was conducted. Automatic image analysis software was used to calculate the area of subcutaneous adipose tissue (SAT), visceral adipose tissue (VAT) and skeletal muscle from computed tomography scans at the umbilical level. The potential risk factors of MAKE30 were analyzed by logistic regression.

A total of 208 eligible ANP patients were enrolled, with an incidence of 23% for MAKE30. VAT area was more closely associated with the development of MAKE30, with an area under the ROC curve of 0.69 (cutoff value 200 cm2, 63.8% sensitivity and 66.7% specificity). Multivariate logistic regression analysis demonstrated that VAT area [OR 1.01 (1.01-1.02); p < 0.001] was an independent risk factor in predicting MAKE30. Patients with a VAT area > 200 cm2 had more requirements of renal replacement therapy (32% vs. 12%, P < 0.001), and a significantly higher incidence of other poor clinical outcomes (all p < 0.05).

Early assessment of the VAT area may help identify ANP patients at high risk of MAKE30, suggesting that it could be a potential indicator for adverse kidney events.

Acute kidney injury (AKI), a global public health concern that increases the risk of death, end-stage renal disease, and prolonged hospital admissions. As of this point, supportive measures like fluid resuscitation and replacement therapy for renal failure are the only treatments available for treating AKI. Asparagus racemosus (AR) also known as Shatavari, belongs to family Liliaceae and is considered exceptional in Ayurvedic medicine due to its versatility in treating and preventing a variety of illnesses.

The purpose of this study is to determine the effectiveness of chloroform fraction of Asparagus racemosus (CFAR) against cisplatin (CP) induced AKI.

HPLC was used to analyze the presence of bioactive phytocompounds in CFAR using standard quercetin. Further LC-MS study indicated the existence of different bioactive compounds. Normal Rat Kidney (NRK-52E) cells were used to study the nephroprotective effect of CFAR. Cells were untreated, treated or cotreated with CP (20 μM) and CFAR (5, 25, 50, 100, 200 and 400μg/mL) for 24 h. After 24 h of treatment, cell viability assay and assay of apoptosis parameters were performed. The CFAR at the dose of 50 mg, 100 mg and 200 mg/kg/day was administered orally for 15 days and acute kidney injury was induced in rats by intraperitoneal injection of CP (10 mg/kg body weight) at the 10th day of experimentation. Biochemical studies were performed to evaluate kidney function; protein expression by Western blot and mRNA expression of related gene were studied from the kidney tissues to evaluate the effects of CFAR. Histopathological analysis was done to investigate the structural abnormalities and fibrosis of renal tissues.

Our result reported that CFAR contain many bioactive phytomolecules having many pharmacological properties. Cell viability assay and assay of apoptosis reported that different doses of CFAR could reduced CP-induced cell death and cell apoptosis. The levels of kidney injury markers (BUN, sCr and eGFR), inflammatory markers (Interleukin-18, KIM-1, Cys-C, NF-kB and NGAL), and antioxidant markers (SOD, GSH, CAT, Nrf2 and Bcl2) and lipid peroxidation (MDA) were settled to a normal level by the oral administration of high doses (100 and 200 mg/kg body weight) of CFAR after intraperitoneal injection of CP as suggested by biochemical, histopathological, protein and gene expression studies.

In conclusion, CFAR at the high doses (100 and 200 mg/kg body weight) could able to protect the kidneys from CP induced oxidative stress and inflammation due to presence of bioactive phytomolecules that prevent the activation of oxidative stress induced signalling cascades leading to kidney damage.

Acute kidney injury (AKI) is a severe and prevalent syndrome, primarily observed in intensive care units (ICUs) and perioperative settings. The discovery of a new biomarker for kidney function and injury, capable of overcoming the limitations of traditional markers, has the potential to improve the diagnosis and management of AKI. Proenkephalin A 119-159 (PENK) has emerged as a novel biomarker for AKI and has been validated in various clinical settings. It has demonstrated a faster response to AKI compared to creatinine and has been shown to predict successful weaning from renal replacement therapy in the ICU. PENK has also shown promise as an AKI biomarker in perioperative patients. Additionally, PENK has been proven to be effective in estimating mortality and morbidity in patients undergoing cardiac surgery, and those with traumatic brain injury or ischemic stroke. Incorporating PENK into a novel estimation of the glomerular filtration rate, referred to as the PENK-Crea equation, has yielded promising results.

Objectives  Neurosurgical patients often receive 0.9% normal saline (NS) during the perioperative period. Theoretically, a balanced salt solution (BSS) is better than 0.9% saline. We compared the effects of two different fluids on acid-base balance, renal function, and neurological outcome in patients who underwent clipping following subarachnoid hemorrhage from a ruptured intracranial aneurysm. Materials and Methods  Patients in group NS ( n  = 30) received 0.9% saline and group BSS ( N  = 30) received BSS (Plasmalyte-A) in the perioperative period for 48 hours. Comparison of arterial pH, bicarbonate, and base deficit measured preoperatively, intraoperatively (first and second hour), and postoperatively (at 24 and 48 hours) was the primary outcome of the study. The secondary outcome compared serum electrolytes, renal function tests, urine neutrophil gelatinase-associated lipocalin (NGAL), serum cystatin C, and the neurological outcome using modified Rankin score (MRS) at discharge, 1, and 3 months. Results  In group NS, significantly low pH at 1-hour intraoperative period was seen compared with group BSS (7.37 ± 0.06 vs. 7.40 ± 0.05, p  = 0.024). The bicarbonate level in group NS was significantly lower and the base deficit was higher at second intraoperative hour (bicarbonate: 17.49 vs. 21.99 mEq/L, p  = 0.001; base deficit: 6.41 mmol/L vs. 1.89 mmol/L, p  = 0.003) and at 24 hours post-surgery (bicarbonate: 20.38 vs. 21.96 mEq/L, p  = 0.012; base deficit: 3.56 mmol/L vs. 2.12 mmol/L, p  = 0.034)). Serum creatinine was higher in group NS at 24 hours (0.66 vs. 0.52 mg/dL, p  = 0.013) and 48 hours (0.62 vs. 0.53 mg/dL, p  = 0.047). Serum urea, electrolytes, cystatin, urine NGAL, and MRS were comparable. Conclusion  In neurosurgical patients undergoing clipping for ruptured intracranial aneurysm, using a BSS during the perioperative period is associated with a better acid-base and renal profile. However, the biomarkers of kidney injury and long-term outcomes were comparable.

Contrast-induced nephropathy (CIN) can lead to serious complications following percutaneous coronary intervention (PCI). Urine N-Acetyl-β-D-glucosaminidase (uNAG) and serum homocysteine (sHCY) are both potential predictors for CIN detection, but their combination has not been explored. We aimed to combine uNAG and sHCY as predictors for the early detection of CIN and for prognosis prediction in patients after PCI.

A total of 232 consecutive patients who underwent PCI at a university hospital were recruited for this study. According to the European Society of Urology and Reproduction (ESUR) criterion, CIN is defined as an elevation of serum creatinine (sCr) by ≥25% or ≥0.5 mg/dl from baseline within 48 h. We assessed the use of individual biomarkers (uNAG and sHCY) measured around PCI and their combinations for CIN detection and prognosis prediction. Receiver operating characteristic curves (ROC) and area under the curve (AUC) were used to evaluate the predictive efficiency of potential predictors.

In total, 54 (23.28%) patients developed CIN. Concentrations of uNAG and sHCY increased significantly in CIN subjects (p < 0.05) than non-CIN. CIN could be predicted by uNAG and sHCY but not by creatinine at an early stage. At pre-PCI, 0, 12, 24, and 48 h after PCI, the AUC-ROC value of uNAG in calculating total CIN was 0.594, 0.603, 0.685, 0.657, and 0.648, respectively. The AUC-ROC value of sHCY in calculating total CIN was 0.685, 0.726, 0.771, 0.755, and 0.821, respectively. The panel of uNAG plus sHCY detected CIN with significantly higher accuracy than either individual biomarker alone and earlier than sCr. For detecting total CIN, this panel yielded AUC-ROCs of 0.693, 0.754, 0.826, 0.796, and 0.844 at pre-PCI, 0, 12, 24, and 48 h after PCI, respectively, which were superior to those of the individual biomarkers. For predicting the incidence of major adverse cardiovascular events (MACE) within 30 days to 12 months, the AUC-ROC values for uNAG and sHCY measured before discharge were 0.637 and 0.826, respectively. The combined panel yielded an AUC-ROC of 0.832. The combined detection did not significantly enhance the predictive capability for MACE in patients with CIN. The CIN group and the non-CIN group showed no significant difference in the Coronary Heart Disease Intensive Care Unit (CCU) stay time, hospital stay time, demand for renal replacement therapy, CCU mortality rate, and in-hospital mortality rate.

The uNAG and sHCY panel demonstrated better sensitivity and specificity for predicting the diagnosis and prognosis of CIN in patients after PCI, earlier than sCr. The combination of these biomarkers revealed a significantly superior discriminative performance for CIN detection and prognosis compared to using uNAG or sHCY alone.

Early recognition and timely intervention for AKI in critically ill patients were crucial to reduce morbidity and mortality. This study aimed to use biomarkers to construct a optimal machine learning model for early prediction of AKI in critically ill patients within seven days.

The prospective cohort study enrolled 929 patients altogether who were admitted in ICU including 680 patients in training set (Jiefang Campus) and 249 patients in external testing set (Binjiang Campus). After performing strict inclusion and exclusion criteria, 421 patients were selected in training set for constructing predictive model and 167 patients were selected in external testing for evaluating the predictive performance of resulting model. Urine and blood samples were collected for kidney injury associated biomarkers detection. Baseline clinical information and laboratory data of the study participants were collected. We determined the average prediction efficiency of six machine learning models through 10-fold cross validation.

In total, 78 variables were collected when admission in ICU and 43 variables were statistically significant between AKI and non-AKI cohort. Then, 35 variables were selected as independent features for AKI by univariate logistic regression. Spearman correlation analysis was used to remove two highly correlated variables. Three ranking methods were used to explore the influence of 33 variables for further determining the best combination of variables. The gini importance ranking method was found to be applicable for variables filtering. The predictive performance of AKIMLpred which constructed by the XGBoost algorithm was the best among six machine learning models. When the AKIMLpred included the nine features (NGAL, IGFBP7, sCysC, CAF22, KIM-1, NT-proBNP, IL-6, IL-18 and L-FABP) with the highest influence ranking, its model had the best prediction performance, with an AUC of 0.881 and an accuracy of 0.815 in training set, similarly, with an AUC of 0.889 and an accuracy of 0.846 in validation set. Moreover, the performace was slightly outperformed in testing set with an AUC of 0.902 and an accuracy of 0.846. The SHAP algorithm was used to interpret the prediction results of AKIMLpred. The web-calculator of AKIMLpred was shown for predicting AKI with more convenient(https://www.xsmartanalysis.com/model/list/predict/model/html?mid=8065&symbol=11gk693982SU6AE1ms21). AKIMLpred was better than the optimal model built with only routine tests for predicting AKI in critically ill patients within 7 days.

The model AKIMLpred constructed by the XGBoost algorithm with selecting the nine most influential biomarkers in the gini importance ranking method had the best performance in predicting AKI in critically ill patients within 7 days. This data-driven predictive model will help clinicians to make quick and accurate diagnosis.

The effects of exercise therapy (ET) on renal function in chronic kidney disease (CKD) remain unclear.

In a randomized controlled trial (UMIN-CTR number: UMIN000038415), we investigated whether ET affects renal function in CKD; eligible patients had undergone renal biopsy in the past 3 months. We stratified patients by disease (immunoglobulin A [IgA] nephropathy, n = 16; diabetic nephropathy, n = 4; benign nephrosclerosis, n = 13; and other CKD types, n = 13) and randomized them to 12 weeks' observation and 24 weeks' ET comprising home-based aerobic exercise 3×/week and resistance training 2×/week (intervention group) or usual care (non-intervention group). Primary endpoint was creatinine-based estimated glomerular filtration rate (eGFR) or serum cystatin C-based eGFR (eGFRcys). Secondary endpoints included urinary protein and exercise tolerance.

Seventy patients were enrolled, 50 fulfilled the inclusion criteria, but 4 discontinued before randomization. No items significantly differed between week 0 to 24 in either group (intervention group, n = 23; non-intervention group, n = 23) or between groups at week 24 (intention-to-treat population) in the total study population. The eGFRcys slope showed no significant intergroup difference in the observation period, but eGFRcys improved significantly in IgA nephropathy patients (n = 16) in the intervention group (stratified comparison; week 0, 48.3 ± 18.2; week 24, 51.6 ± 17.6; p = 0.043). In these patients, urinary protein was significantly worse at week 24 in the non-intervention group (p = 0.046) and worsened significantly less in the intervention group (p = 0.039).

ET did not improve renal function overall in CKD patients but might help maintain renal function in patients with IgA nephropathy.

Fibroblast growth factor 21 (FGF21) shows great therapeutic potential in metabolic, neurodegenerative and inflammatory diseases. However, current FGF21 administration predominantly relies on injection rather than oral ingestion due to its limited stability and activity post-gastrointestinal transit, thereby hindering its clinical utility. Milk-derived exosomes (mEx) have emerged as a promising vehicle for oral drug delivery due to their ability to maintain structural integrity in the gastrointestinal milieu. To address the challenge associated with oral delivery of FGF21, we encapsulated FGF21 within mEx (mEx@FGF21) to protect its activity post-oral administration. Additionally, we modified the surface of mEx@FGF21 by introducing transferrin (TF) to enhance intestinal absorption and transport, designated TF-mEx@FGF21. In vitro results demonstrated that the surface modification of TF promoted FGF21 internalization by intestinal epithelial cells. Orally administered TF-mEx@FGF21 showed promising therapeutic effects in septic mice. This study represents a practicable strategy for advancing the clinical application of oral FGF21 delivery.

Contrast-induced nephropathy (CIN) is a form of acute kidney injury (AKI) occurring in patients undergoing cardiac catheterization, such as coronary angiography (CAG) or percutaneous coronary intervention (PCI). Although the conventional criterion for CIN detection involves a rise in creatinine levels within 72 h after contrast media injection, several limitations exist in this definition. Up to now, various meta-analyses have been undertaken to assess the accuracy of different biomarkers of CIN prediction. However, the existing body of research lacks a cohesive overview. To address this gap, a comprehensive umbrella review was necessary to consolidate and summarize the outcomes of prior meta-analyses. This umbrella study aimed to offer a current, evidence-based understanding of the prognostic value of biomarkers in predicting CIN.

A systematic search of international databases, including PubMed, Scopus, and Web of Science, from inception to December 12, 2023, was conducted to identify meta-analyses assessing biomarkers for CIN prediction. Our own meta-analysis was performed by extracting data from the included studies. Sensitivity, specificity, positive likelihood ratio, and negative likelihood ratio were assessed using Meta-Disc and CMA softwares.

Twelve studies were ultimately included in the umbrella review. The results revealed that neutrophil gelatinase-associated lipocalin (NGAL) exhibited the highest area under the curve (AUC), followed by cystatin-C, urinary kidney injury molecule-1 (uKIM-1), and brain natriuretic peptide (BNP) with AUCs of 0.91, 0.89, 0.85, and 0.80, respectively. NGAL also demonstrated the highest positive likelihood ratio [effect size (ES): 6.02, 95% CI 3.86-9.40], followed by cystatin-C, uKIM-1, and BNP [ES: 4.35 (95% CI 2.85-6.65), 3.58 (95% CI 2.75-4.66), and 2.85 (95% CI 2.13-3.82), respectively]. uKIM-1 and cystatin-C had the lowest negative likelihood ratio, followed by NGAL and BNP [ES: 0.25 (95% CI 0.17-0.37), ES: 0.25 (95% CI 0.13-0.50), ES: 0.26 (95% CI 0.17-0.41), and ES: 0.39 (0.28-0.53) respectively]. NGAL emerged as the biomarker with the highest diagnostic odds ratio for CIN, followed by cystatin-C, uKIM-1, BNP, gamma-glutamyl transferase, hypoalbuminemia, contrast media volume to creatinine clearance ratio, preprocedural hyperglycemia, red cell distribution width (RDW), hyperuricemia, neutrophil-to-lymphocyte ratio, C-reactive protein (CRP), high-sensitivity CRP, and low hematocrit (P < 0.05).

NGAL demonstrated superior diagnostic performance, exhibiting the highest AUC, positive likelihood ratio, and diagnostic odds ratio among biomarkers for CIN, followed by cystatin-C, and uKIM-1. These findings underscore the potential clinical utility of NGAL, cystatin-C and uKIM-1 in predicting and assessing CIN.

Acute kidney injury (AKI) is a complex syndrome that might be induced by different causes and is associated with an increased morbidity and mortality. Therefore, it is a very heterogeneous syndrome and establishing a "one size fits all" treatment approach might not work. This review aims to examine the potential of personalized treatment strategies for AKI.

The traditional diagnosis of AKI is based on changes of serum creatinine and urine output, but these two functional biomarkers have several limitations. Recent research identified different AKI phenotypes based on clinical features, biomarkers, and pathophysiological pathways. Biomarkers, such as Cystatin C, NGAL, TIMP2∗IGFBP7, CCL14, and DKK-3, have shown promise in predicting AKI development, renal recovery, and prognosis. Biomarker-guided interventions, such as the implementation of the KDIGO bundle, have demonstrated an improvement in renal outcomes in specific patient groups.

A personalized approach to AKI treatment as well as research is becoming increasingly important as it allows the identification of distinct AKI phenotypes and the potential for targeted interventions. By utilizing biomarkers and clinical features, physicians might be able to stratify patients into subphenotypes, enabling more individualized treatment strategies. This review highlights the potential of personalized AKI treatment, emphasizing the need for further research and large-scale clinical trials to validate the efficacy of these approaches.

Broadly neutralizing monoclonal antibodies (mAbs) are being developed for HIV-1 prevention. Hence, these mAbs and licensed oral pre-exposure prophylaxis (PrEP) (tenofovir-emtricitabine) can be concomitantly administered in clinical trials. In 48 US participants (men and transgender persons who have sex with men) who received the HIV-1 mAb VRC01 and remained HIV-free in an antibody-mediated-prevention trial (ClinicalTrials.gov #NCT02716675), we conduct a post-hoc analysis and find that VRC01 clearance is 0.08 L/day faster (p = 0.005), and dose-normalized area-under-the-curve of VRC01 serum concentration over-time is 0.29 day/mL lower (p < 0.001) in PrEP users (n = 24) vs. non-PrEP users (n = 24). Consequently, PrEP users are predicted to have 14% lower VRC01 neutralization-mediated prevention efficacy against circulating HIV-1 strains. VRC01 clearance is positively associated (r = 0.33, p = 0.03) with levels of serum intestinal Fatty Acid Binding protein (I-FABP), a marker of epithelial intestinal permeability, which is elevated upon starting PrEP (p = 0.04) and after months of self-reported use (p = 0.001). These findings have implications for the evaluation of future HIV-1 mAbs and postulate a potential mechanism for mAb clearance in the context of PrEP.

The study of trimethylamine oxide (TMAO), a metabolite of gut microbiota, and heart failure and chronic kidney disease has made preliminary achievements and been summarized by many researchers, but its research in the field of cardiorenal syndrome is just beginning. TMAO is derived from the trimethylamine (TMA) that is produced by the gut microbiota after consumption of carnitine and choline and is then transformed by flavin-containing monooxygenase (FMO) in the liver. Numerous research results have shown that TMAO not only participates in the pathophysiological progression of heart and renal diseases but also significantly affects outcomes in chronic heart failure (CHF) and chronic kidney disease (CKD), besides influencing the general health of populations. Elevated circulating TMAO levels are associated with adverse cardiovascular events such as HF, myocardial infarction, and stroke, patients with CKD have a poor prognosis as well. However, no study has confirmed an association between TMAO and cardiorenal syndrome (CRS). As a syndrome in which heart and kidney diseases intersect, CRS is often overlooked by clinicians. Here, we summarize the research on TMAO in HF and kidney disease and review the existing biomarkers of CRS. At the same time, we introduced the relationship between exercise and gut microbiota, and appropriately explored the possible mechanisms by which exercise affects gut microbiota. Finally, we discuss whether TMAO can serve as a biomarker of CRS, with the aim of providing new strategies for the detection, prognostic, and treatment evaluation of CRS.

Drug-induced nephrotoxicity accounts for up to 60% of cases of acute kidney injury (AKI) in hospitalized patients and is associated with increased morbidity and mortality in both adults and children. Antibiotics are one of the most common causes of drug-induced nephrotoxicity. Mechanisms of antibiotic-induced nephrotoxicity include glomerular injury, tubular injury or dysfunction, distal tubular obstruction from casts, and acute interstitial nephritis (AIN) mediated by a type IV (delayed-type) hypersensitivity response. Clinical manifestations of antibiotic-induced nephrotoxicity include acute tubular necrosis (ATN), AIN, and Fanconi syndrome. Given the potential nephrotoxic effects of antibiotics on critically ill patients, the use of novel biomarkers can provide information to optimize dosing and duration of treatment and can help prevent nephrotoxicity when traditional markers, such as creatinine, are unreliable. Use of novel kidney specific biomarkers, such as cystatin C and urinary kidney injury molecule-1 (KIM-1), may result in earlier detection of AKI, dose adjustment, or discontinuation of antibiotic and development of nonnephrotoxic antibiotics.

Severity of acute kidney injury (AKI) confers higher odds of mortality. Timely recognition and early initiation of preventive measures may help mitigate the injury further. Novel biomarkers may aid in the early detection of AKI. The utility of these biomarkers across various clinical settings in children has not been evaluated systematically.

To synthesize the currently available evidence on different novel biomarkers for the early diagnosis of AKI in pediatric patients.

We searched four electronic databases (PubMed, Web of Science, Embase, and Cochrane Library) for studies published between 2004 and May 2022.

Cohort and cross-sectional studies evaluating the diagnostic performance of biomarkers in predicting AKI in children were included.

Participants in the study included children (aged less than 18 years) at risk of AKI.

We used the QUADAS-2 tool for the quality assessment of the included studies. The area under the receiver operating characteristics (AUROC) was meta-analyzed using the random-effect inverse-variance method. Pooled sensitivity and specificity were generated using the hierarchical summary receiver operating characteristic (HSROC) model.

We included 92 studies evaluating 13,097 participants. Urinary NGAL and serum cystatin C were the two most studied biomarkers, with summary AUROC of 0.82 (0.77-0.86) and 0.80 (0.76-0.85), respectively. Among others, urine TIMP-2*IGFBP7, L-FABP, and IL-18 showed fair to good predicting ability for AKI. We observed good diagnostic performance for predicting severe AKI by urine L-FABP, NGAL, and serum cystatin C.

Limitations were significant heterogeneity and lack of well-defined cutoff value for various biomarkers.

Urine NGAL, L-FABP, TIMP-2*IGFBP7, and cystatin C showed satisfactory diagnostic accuracy in the early prediction of AKI. To further improve the performance of biomarkers, they need to be integrated with other risk stratification models.

PROSPERO (CRD42021222698). A higher resolution version of the Graphical abstract is available as "Supplementary information".

Acute kidney injury (AKI) is a frequent and severe condition in intensive care units (ICUs). In 2020, the Acute Dialysis Quality Initiative (ADQI) group proposed a new stage of AKI, referred to as stage 1S, which represents subclinical disease (sAKI) defined as a positive biomarker but no increase in serum creatinine (sCr). This study aimed to determine and compare the urinary peptide signature of sAKI as defined by biomarkers.

This is an ancillary analysis of the prospective, observational, multinational FROG-ICU cohort study. AKI was defined according to the Kidney Disease Improving Global Outcome definition (AKIKDIGO). sAKI was defined based on the levels of the following biomarkers, which exceeded the median value: neutrophil gelatinase-associated lipocalin (pNGAL, uNGAL), cystatin C (pCysC, uCysC), proenkephalin A 119-159 (pPENKID) and liver fatty acid binding protein (uLFABP). Urinary peptidomics analysis was performed using capillary electrophoresis-mass spectrometry. Samples were collected at the time of study inclusion.

One thousand eight hundred eighty-five patients had all biomarkers measured at inclusion, which included 1154 patients without AKI (non-AKIKDIGO subgroup). The non-AKIKDIGO subgroup consisted of individuals at a median age of 60 years [48, 71], among whom 321 (27.8%) died. The urinary peptide signatures of sAKI, regardless of the biomarkers used for its definition, were similar to the urinary peptide signatures of AKIKDIGO (inflammation, haemolysis, and endothelial dysfunction). These signatures were also associated with 1-year mortality.

Biomarker-defined sAKI is a common and severe condition observed in patients within intensive care units with a urinary peptide signature that is similar to that of AKI, along with a comparable prognosis.

Acute kidney injury is a common comorbidity in patients with intracerebral hemorrhage. Although there are predictive models to determine risk of AKI in patients in critical care or post-surgical scenarios or in general medical floors, there are no models that specifically determine the risk of AKI in patients with ICH.

Clinical features and laboratory tests were selected by previous studies and LASSO (least absolute shrinkage and selection operator) regression. We used multivariable logistic regression with a bidirectional stepwise method to construct ICH-AKIM (intracerebral hemorrhage-associated acute kidney injury model). The accuracy of ICH-AKIM was measured by the area under the receiver operating characteristic curve. The outcome was AKI development during hospitalization, defined as KDIGO (Kidney Disease: Improving Global Outcomes) Guidelines.

From four independent medical centers, a total of 9649 patients with ICH were available. Overall, five clinical features (sex, systolic blood pressure, diabetes, Glasgow coma scale, mannitol infusion) and four laboratory tests at admission (serum creatinine, albumin, uric acid, neutrophils-to-lymphocyte ratio) were predictive factors and were included in the ICH-AKIM construction. The AUC of ICH-AKIM in the derivation, internal validation, and three external validation cohorts were 0.815, 0.816, 0.776, 0.780, and 0.821, respectively. Compared to the univariate forecast and pre-existing AKI models, ICH-AKIM led to significant improvements in discrimination and reclassification for predicting the incidence of AKI in all cohorts. An online interface of ICH-AKIM is freely available for use.

ICH-AKIM exhibited good discriminative capabilities for the prediction of AKI after ICH and outperforms existing predictive models.

To evaluate the performance of kidney-specific biomarkers (neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), and cystatin-C) in early detection of acute kidney injury (AKI) following cardiac arrest (CA) when compared to serum creatinine.

Adult CA patients who had kidney-specific biomarkers of AKI collected within 12 h of return of spontaneous circulation (ROSC) were included. The association between renal biomarker levels post-ROSC and the development of KDIGO stage III AKI within 7 days of enrollment were assessed as well as their predictive value of future AKI development, neurological outcomes, and survival to discharge.

Of 153 patients, 54 (35%) developed stage III AKI within 7 days, and 98 (64%) died prior to hospital discharge. Patients who developed stage III AKI, compared to those who did not, had higher median levels of creatinine, NGAL, and cystatin-C (p < 0.001 for all). There was no statistically significant difference in KIM-1 between groups. No biomarker outperformed creatinine in the ability to predict stage III AKI, neurological outcomes, or survival outcomes (p > 0.05 for all). However, NGAL, cystatin-C, and creatinine all performed better than KIM-1 in their ability to predict AKI development (p < 0.01 for all).

In post-CA patients, creatinine, NGAL, and cystatin-C (but not KIM-1) measured shortly after ROSC were higher in patients who subsequently developed AKI. No biomarker was statistically superior to creatinine on its own for predicting the development of post-arrest AKI.

Sepsis is a syndrome caused by an imbalance in the inflammatory response of the body caused by an infection that leads to organ dysfunction, with the kidney being one of the most commonly affected organs. Sepsis-related acute kidney injury (SAKI) is strongly linked to increased mortality and poor clinical outcomes. Early diagnosis and treatment can significantly reduce patient mortality. On the other hand, the pathogenesis of SAKI is not fully understood, and early diagnosis of SAKI is a clinical challenge. Therefore, the current review describes biomarkers of acute kidney injury in sepsis and discusses the various pathogenic mechanisms involved in the progression of acute kidney injury in sepsis to develop new clinical treatment avenues.

While acute kidney injury (AKI) after hematopoietic cell transplant (HCT) has been well-described in pediatric patients, literature regarding the long term renal consequences of HCT-related AKI, the development of chronic kidney disease (CKD), and CKD care in pediatric patients post-HCT is limited. CKD affects almost 50% of patients after HCT with multifactorial etiology including infection, nephrotoxic medications, transplant-associated thrombotic microangiopathy, graft-versus-host disease, and sinusoidal obstruction syndrome. As renal function declines in CKD, eventually progressing to end stage kidney disease (ESKD), mortality increases and is more than 80% among patients requiring dialysis. Using society guidelines and current literature, this review summarizes definitions and etiologies of and management strategies among patients with AKI and CKD post-HCT with an emphasis on albuminuria, hypertension, nutrition, metabolic acidosis, anemia, and mineral bone disease. The goal of this review is to aid early identification and intervention in patients with renal dysfunction prior to development of ESKD, and to discuss ESKD and renal transplant in these patients post-HCT.

Besides impaired respiratory function and immune system, COVID-19 can affect renal function from elevated blood urea nitrogen (BUN) or serum creatinine (sCr) levels to acute kidney injury (AKI) and renal failure. This study aims to investigate the relationship between Cystatin C and other inflammatory factors with the consequences of COVID-19.

A total of 125 patients with confirmed Covid-19 pneumonia were recruited in this cross-sectional study from March 2021 to May 2022 at Firoozgar educational hospital in Tehran, Iran. Lymphopenia was an absolute lymphocyte count of less than 1.5 × 109/L. AKI was identified as elevated serum Cr concentration or reduced urine output. Pulmonary consequences were evaluated. Mortality was recorded in the hospital one and three months after discharge. The effect of baseline biochemical and inflammatory factors on odds of death was examined. SPSS, version 26, was used for all analyses. P-vale less than 0.05 was considered significant.

The highest amount of co-morbidities was attributed to COPD (31%; n = 39), dyslipidemia and hypertension (27%; n = 34 for each) and diabetes (25%; n = 31). The mean baseline cystatin C level was 1.42 ± 0.93 mg/L, baseline creatinine was 1.38 ± 0.86 mg/L, and baseline NLR was 6.17 ± 4.50. Baseline cystatin C level had a direct and highly significant linear relationship with baseline creatinine level of patients (P < 0.001; r: 0.926). ). The average score of the severity of lung involvement was 31.42 ± 10.80. There is a direct and highly significant linear relationship between baseline cystatin C level and lung involvement severity score (r = 0.890, P < 0.001). Cystatin C has a higher diagnostic power in predicting the severity of lung involvement (B = 3.88 ± 1.74, p = 0.026). The mean baseline cystatin C level in patients with AKI was 2.41 ± 1.43 mg/L and significantly higher than patients without AKI (P > 0.001). 34.4% (n = 43) of patients expired in the hospital, and the mean baseline cystatin C level of this group of patients was 1.58 ± 0.90 mg/L which was significantly higher than other patients (1.35 ± 0.94 mg/L, P = 0.002).

cystatin C and other inflammatory factors such as ferritin, LDH and CRP can help the physician predict the consequences of COVID-19. Timely diagnosis of these factors can help reduce the complications of COVID-19 and better treat this disease. More studies on the consequences of COVID-19 and knowing the related factors will help treat the disease as well as possible.

Acute kidney injury (AKI) following cardiopulmonary bypass (CPB) is associated with increased morbidity and mortality. Serum Cystatin C (CysC) is a novel biomarker synthesized by all nucleated cells that may act as an early indicator of AKI following infant CPB. Prospective observational study of infants (< 1 year) requiring CPB during cardiac surgery. CysC was measured at baseline and 12, 24, 48, and 72 h following CPB initiation. Each post-op percent difference in CysC (e.g. %CysC12h) from baseline was calculated. Clinical variables along with urine output (UOP) and serum creatinine (SCr) were followed. Subjects were divided into two groups: AKI and non-AKI based upon the Kidney Disease Improving Global Outcomes (KDIGO) classification. AKI occurred in 41.9% (18) of the 43 infants enrolled. Patient demographics and baseline CysC levels were similar between groups. CysC levels were 0.97 ± 0.28 mg/L over the study period, and directly correlated with SCr (R = 0.71, p < 0.0001). Although absolute CysC levels were not significant between groups, the %CysC12h was significantly greater in the AKI group (AKI: - 16% ± 22% vs. Non-AKI - 28% ± 9% mg/L; p = 0.003). However, multivariate analysis demonstrated that a lower UOP (Odds Ratio:0.298; 95% CI 0.073, 0.850; p = 0.02) but not %CysC12h was independently associated with AKI. Despite a significant difference in the %CysC12h, only UOP was independently associated with AKI. Larger studies of a more homogenous population are needed to understand these results and to explore the variability in this biomarker seen across institutions.

Acute kidney injury (AKI), acute kidney disease (AKD) and CKD (chronic kidney disease) were a continuous process. There has been little discussion of risk factors for AKD in the population undergoing surgery for acute type A aortic dissection (AAAD).

The main objective of this study was to investigate the risk factors for AKD after surgery for acute type A aortic dissection and the impact of AKD on early and late mortality.

AKI was to be defined as an increase in serum creatinine to >0.3 mg/dL or 1.5 times above baseline within 7 days. AKD was defined as the kidney damage within 90 days after AKI. Logistic regression models were performed to identify the risk factors of AKD and the association between AKD and early mortality after AAAD surgery.

Patients with AKI after AAAD surgery admitted in ICU from March 2009 to September 2021 were included.

Among the 328 patients who developed AKI after AAAD surgery, 98 patients (29.9%) progressed to AKD. Multivariable analysis revealed that AKI stage 2 (OR, 3.032) and AKI stage 3 (OR, 4.001) have been shown to be independent risk factors for the development of AKD. AKD (OR, 3.175) proved to be an independent risk factor for early mortality, while no significant difference in late mortality was observed between patients in the AKD and non-AKD groups.

The severity of AKI after surgery of AAAD was independently associated with AKD. The occurrence of AKD had a negative impact on early mortality.

ChiCTR, ChiCTR1900021290. Registered 12 February 2019, http://www.chictr.org.cn/showproj.aspx?proj=35795.

Acute kidney injury (AKI) after total aortic arch replacement (TAAR) is frequent and associated with adverse outcomes, whereas its early detection remains a challenge. Serum cystatin C (sCysC) and urinary N-acetyl-β-d-glucosaminidase (uNAG) are clinically available renal biomarkers, but their combination for AKI detection requires more evidence. This study aimed to assess the discriminative abilities of these biomarkers in AKI after TAAR.

Patients undergoing TAAR were included in this prospective observational study. The AKI prediction model was developed and internal verificated, and the significance of each variable was analyzed by random forest (RF). Finally, the best predictive critical values of sCysC and uNAG were explored by the AUC-ROC curve.

The AUC-ROC of the prediction model was substantially enhanced by adding sCysC and uNAG (0.909 vs 0.844, p < 0.001), and the clinical utility and risk reclassification were significantly improved. Additionally, the RF showed that sCysC and uNAG ranked first and second. The AUC-ROC for each were 0.864 and 0.802 respectively, and the cut-off values were 1.395 mg/L and 31.90 U/g Cre respectively.

The prediction model incorporating functional marker sCysC and tubular injury marker uNAG can improve the discriminative abilities of AKI after TAAR.

To evaluate renal function damage in children with duplex kidneys.

A total of 355 duplex kidneys, 110 urinary tract infection (UTI) kidneys without abnormalities, and 104 kidneys with primary unilateral vesicoureteral reflux (VUR) were reviewed. Clinical data including age at diagnosis, body weight, history of UTI, ureteroceles, ectopic ureteral opening, VUR grade, serum creatinine level, cystatin C level, renal scarring, split renal function in dimercaptosuccinic acid scans, and effective renal plasma flow (ERPF) were analyzed.

Duplex kidneys had a higher grade of VUR and renal scarring. Split renal function in unilateral duplex kidneys (45.58 ± 12.85%) was much lower than that in contralateral duplex kidneys (56.33 ± 11.90%) and controls (50.00 ± 11.38%) (P < 0.001 and P = 0.014, respectively). Both left and right split renal functions in bilateral duplex kidneys were similar to those ipsilateral to the controls (P = 0.906 and P = 0.932, respectively). However, the total ERPFs in the left, right, and bilateral duplex kidneys were significantly lower than that in the control group (P = 0.003, P = 0.001, and P = 0.003, respectively). The total ERPFs in the left and right unilateral duplex kidneys were similar. ERPF in unilateral duplex kidneys (106.70 ± 48.05 mL/min/m²) was significantly lower than that in contralateral duplex kidneys (150.18 ± 49.01 mL/min/m²) or those ipsilateral to controls (145.98 ± 41.16 mL/min/m²) (P < 0.001 and P < 0.001, respectively).

Duplex kidneys are usually accompanied by a higher grade of VUR, more severe renal scarring, and renal function impairment. Split renal function in duplex kidneys often declines significantly. Notably, the evaluation of split renal function in bilateral duplex kidneys should be performed cautiously.

The definition of acute kidney injury (AKI), despite improvements in criteria, continues to be based on the level of serum creatinine and urinary output that do not specifically indicate tubular function or injury, or glomerular function or injury that is not significant enough to warrant acute hospitalization of the patient. Finding novel biomarkers of AKI has become a major focus nowadays in nephrology to overcome the further complications of end stage renal disease (ESRD). Many compounds, such as KIM 1, IL 18, NGAL, uromodulin, calprotectin, vanin 1, galactin 3, platelet-derived growth factor (PDGF), urinary Na⁺/H⁺ exchanger isoform 3 (NHE3), retinol binding protein (RBP) and Cystatin C, are released from the renal tubules and thus any alterations in tubular function can be detected by measuring these parameters in urine. Additionally, glomerular injury can be detected by measuring immunoglobulin G, nephrin, podocalyxin, podocin, transferrin, netrin-1, pyruvate kinase M2, etc. in urine. These novel biomarkers will be useful for timing the initial insult and assessing the duration of AKI. According to available research, these biomarkers could be applied to assess the onset of AKI, distinguishing between kidney injury and dysfunction, directing the management of AKI, and enhancing disease diagnosis. Therefore, we intend to present recent developments in our understanding of significant biomarkers implicated in various aspects of renal damage. Numerous biomarkers are implicated in various pathophysiological processes that follow renal injury, and can improve prognosis and risk classification.

Some studies have reported to use some predictors before extracorporeal membrane oxygenation (ECMO) initiation to predict the acute kidney injury (AKI) risk. However, injury during the ECMO operation and the response of patients to ECMO may significantly influence the prognosis, and they are unpredictable before ECMO initiation. This study aims to develop a potential model based clinical characteristics at the 2-hour time point during ECMO for the early prediction of AKI in patients receiving ECMO.

139 patients who underwent ECMO were enrolled in this study. The clinical characteristics and the laboratory examinations at 2-hour time point during ECMO were recorded. The least absolute shrinkage and selection operator (LASSO) regression method was performed to select predictors, and logistic regression and a nomogram were used to establish the prediction model. The area under curve (AUC) of the receiver operating characteristic and calibration curve were used to analyze the discrimination and calibration of the model. K-fold cross-validation method was performed to validate the accuracy of this model.

Among the 139 patients receiving ECMO, 106 participants (76.26%) developed AKI. Four predictive variables including ECMO model, serum creatinine (Scr-2h), uric acid(UA-2h), and serum lactate (Lac-2h) at the 2-hour time point during ECMO were filtered from 39 clinical parameters by LASSO regression. These four predictors were incorporated to develop a model for predicting AKI risk using logistic regression. The AUC of the model was 0.905 (0.845-0.965), corresponding to 81.1% sensitivity, 90.9% specificity and 83.5% accuracy. Moreover, this model showed good consistency between observed and predicted probability based on the calibration curve (P > 0.05). The validation performed by K-fold cross-validation method showed that the accuracy was 0.874 ± 0.006 in training sets, 0.827 ± 0.053 in test sets, indicating a good capability for AKI risk prediction. Finally, a nomogram based on this model was constructed to facilitate its use in clinical practice.

The nomogram incorporating Scr-2h,Lac-2h, UA-2h, and ECMO model may facilitate the individualized prediction of the AKI risk among patients undergoing ECMO.

To diagnose renal function using a biochip capable of detecting SERS and to assess Raman measurements taken from a bilateral renal ischemia model and the feasibility of early diagnosis was done. After generating a bilateral renal ischemia rat model, blood and urine were collected. After confirming the presence of renal injury and function, liquid drops were placed onto a Raman chip whose surface had been enhanced with Au-ZnO nanorods. SERS biomarkers that diffused into the nanogaps were selectively amplified. Raman signals varied based on the severity of the renal function, and these differences were confirmed statistically. These results confirm that renal ischemia leads to renal dysfunction and that surface-enhanced Raman spectroscopy and a machine learning algorithm can be used to track signals in the urine from the release of SERS biomarkers.

While an association between postoperative acute kidney injury (AKI) and adverse events exists, the incidence and impact of postoperative AKI after pancreaticoduodenectomy for pancreatic ductal adenocarcinoma remain unclear. This study aimed to diagnose AKI and investigate the risk factors for and prognostic value of postoperative AKI.

Clinical characteristics of patients who underwent pancreaticoduodenectomy between 2013 and 2020 at a high-volume centre were collected retrospectively. The Kidney Disease Improving Global Outcomes criteria were used to diagnose AKI. A 1:2 propensity score matching (PSM) was used to minimise bias between the AKI and non-AKI groups. Short-term surgical and long-term survival outcomes were compared between groups. Multivariate logistic regression analysis assessed the independent risk factors for AKI development, major complications, and 30-day mortality.

Postoperative AKI occurred in 10.7% of 1312 patients. Total bilirubin level > 250 μmol/L (odds ratio [OR]: 3.24; p < 0.001), estimated glomerular filtration rate < 60 ml/min/1.73 m² (OR: 2.30; p = 0.048), and intraoperative estimated blood loss >1000 ml (OR: 2.96; p = 0.001) were independent risk factors for postoperative AKI. After PSM, higher incidences of major complications (p < 0.001) and 30-day mortality (p < 0.001) were observed in the AKI group than in the non-AKI group. There was no difference in long-term overall survival outcomes between both groups (p = 0.535). AKI was an independent predictor of major complications (OR: 3.06; p < 0.001) and 30-day mortality (OR: 2.87; p = 0.034).

Postoperative AKI is common after pancreaticoduodenectomy for pancreatic ductal adenocarcinoma and has a predictive effect on major complications and 30-day mortality. Therefore, prevention and proper management of postoperative AKI are required in clinical practice.

Acute kidney injury (AKI) is a complex syndrome with a high incidence and considerable morbidity in critically ill patients. Renal replacement therapy (RRT) remains the mainstay of treatment for AKI. There are at present multiple disparities in uniform definition, diagnosis, and prevention of AKI and timing of initiation, mode, optimal dose, and discontinuation of RRT that need to be addressed. The Indian Society of Critical Care Medicine (ISCCM) AKI and RRT guidelines aim to address the clinical issues pertaining to AKI and practices to be followed for RRT, which will aid the clinicians in their day-to-day management of ICU patients with AKI.

Mishra RC, Sodhi K, Prakash KC, Tyagi N, Chanchalani G, Annigeri RA, et al. ISCCM Guidelines on Acute Kidney Injury and Renal Replacement Therapy. Indian J Crit Care Med 2022;26(S2):S13-S42.

We have recently shown that minor subclinical creatinine dynamic changes enable the excellent detection of acute kidney injury (AKI) within 6-12 h after cardiac surgery. The aim of the present study was to examine a combination of neutrophil gelatinase-associated lipocalin (NGAL), cystatin C (CysC) and creatinine for enhanced AKI detection early after cardiac surgery. Elective patients with normal renal function undergoing cardiac surgery using cardiopulmonary bypass were enrolled. Concentrations of plasma NGAL, serum CysC and serum creatinine were determined after the induction of general anesthesia, at the termination of the cardiopulmonary bypass and 2 h thereafter. Out of 119 enrolled patients, 51 (43%) developed AKI. A model utilizing an NGAL, CysC and creatinine triple biomarker panel including sequential relative changes provides a better prediction of cardiac surgery-associated acute kidney injury than any biomarker alone already 2 h after the termination of the cardiopulmonary bypass. The area under the receiver-operator curve was 0.77, sensitivity 77% and specificity 68%.