Biomarkers Of Acute Kidney Injury Research Articles

Serum Dickkopf-3 as a biomarker for predicting acute kidney injury in postoperative intensive care patients.

Acute kidney injury (AKI) is a common and significant complication in the Intensive Care Unit (ICU), affecting more than half of all patients admitted. This condition is associated with increased morbidity and mortality, underscoring the urgent need for accurate and specific biomarkers to enable early diagnosis and intervention. Dickkopf-3 (DKK3) has emerged as a promising candidate biomarker for renal injury. We conducted a single-center, prospective cohort study from March 1 to July 1, 2023, enrolling 166 non-cardiac postoperative patients admitted to the ICU. Serum and urinary DKK3 levels were quantified using enzyme-linked immunosorbent assay (ELISA) kits. A multifactorial logistic regression model was constructed, incorporating changes in serum creatinine (ΔScr), cystatin C (CysC), serum DKK3 levels, and the serum DKK3 to urine DKK3 ratio. Elevated serum DKK3 levels were significantly associated with an increased incidence of AKI and a composite outcome of adverse events (AKI or death). The multifactorial logistic regression model exhibited excellent performance, with an area under the receiver operating characteristic curve (AUC) of 0.98. Decision curve analysis (DCA) demonstrated a net clinical benefit of utilizing serum DKK3 levels to guide treatment decisions, particularly at higher risk thresholds. Serum DKK3 is a robust diagnostic biomarker for AKI, effectively stratifying patients based on protein levels. The predictive model that incorporates DKK3 provides a valuable tool for clinical decision-making in the ICU setting. Further validation in larger and more diverse populations is warranted.

Peripheral Transcriptomics in Acute and Long-Term Kidney Dysfunction in SARS-CoV2 Infection.

Acute kidney injury (AKI) is common in SARS-CoV-2 infection and COVID-19, often leading to long-term kidney dysfunction. However, the transcriptomic features of AKI severity and its long-term effects are underexplored. We performed bulk RNA sequencing on peripheral blood mononuclear cells (PBMCs) from hospitalized SARS-CoV-2 patients and complemented these findings with proteomic data from the same cohort. We compared the functional enrichment findings with historical sepsis-AKI data and subsequently examined the association between molecular signatures and long-term kidney function changes. In 283 patients, 57 had mild AKI (stage 1) and 49 had severe AKI (stage 2 or 3). Following adjustments for age, sex, severity of infection, and pre-existing chronic kidney disease (CKD), we identified 6,432 differentially expressed genes (DEGs) in the severe AKI vs. control comparison, 840 in the mild AKI vs. control, and 1,213 in the severe vs. mild AKI comparison (FDR<0.05). Common pathways included unfolded protein response, cellular response to stress via eIF2, and IFN-g-mediated inflammatory response. Severe AKI was linked to pathways involved in mitochondrial dysfunction and endoplasmic reticulum stress. Proteomic analysis confirmed 40 established AKI and inflammation biomarkers, while gene-set enrichment of transcription regulators revealed additional biomarkers for severe AKI. Comparison with PBMC transcriptomics from sepsis-related AKI showed significant functional overlap (30%). Analysis of post-discharge eGFR data in 115 patients identified 177 DEGs for severe vs. control, 106 for mild vs. control, and 46 for severe vs. mild AKI. Key associations included kidney function decline related to carbohydrate and mitochondrial metabolism, inflammatory-response, and cardiovascular regulation. We demonstrate that severe AKI in SARS-CoV-2 infection is linked to mitochondrial dysfunction and ER stress. The functional overlap with sepsis-AKI suggests potential broader therapeutic applicability. Long-term kidney dysfunction is influenced by disruptions in cellular energy metabolism and immune response.

Magnetic structural color microspheres for the multiplex detection of acute kidney injury biomarkers

Magnetic structural color microspheres for the multiplex detection of acute kidney injury biomarkers

SuPAR, an emerging biomarker in acute kidney injury in ICU patients

SuPAR, an emerging biomarker in acute kidney injury in ICU patients

Acute kidney injury in paediatric kidney transplant recipients.

Acute kidney injury (AKI) in paediatric kidney transplant recipients is common. Infection including urinary tract infection (UTI) and rejection are the most common causes in children. Surgical complications often cause AKI early post-transplant, whereas BK polyomavirus nephropathy rarely occurs in the first month post-transplant. Understanding kidney physiology helps to appreciate the sensitivity of the allograft to AKI, more so than native kidneys. Although the cause of AKI is often multi-factorial, there may be an underlying process that is treatable. Eliciting the aetiology, in this regard, is of paramount importance. Pre-renal and post-renal causes of allograft dysfunction are important to distinguish from intrinsic kidney disease. Clinical information and examination of fluid balance, urine dipstick testing, blood tests, bladder and kidney transplant ultrasound, and kidney transplant biopsy remain vital assessment tools in narrowing the differential diagnosis. A careful prescribed and recreational drug history is always warranted as many drugs including supplements are nephrotoxic. Additional causes such as allograft rejection, recurrent disease, and calcineurin inhibitor toxicity need to be considered in cases of allograft dysfunction, which would not affect the native kidneys. Early detection and assessment of AKI is crucial in promoting recovery. Significant progress has been made in specific pathologies over the last 20years, which has improved kidney allograft survival rates considerably. Research into identifying AKI biomarkers to assist early diagnosis, before the serum creatinine rises, is ongoing.

Diagnostic potential of CDK1 and STAT1 in acute kidney injury associated with gastrointestinal cancers: a bioinformatics-based study.

Patients with gastrointestinal cancers are prone to acute kidney injury (AKI) due to treatment or disease progression, and current diagnostic methods exhibit insufficient sensitivity and specificity. This study aims to evaluate the potential value of CDK1 and STAT1 in the diagnosis of AKI in this patient population. A retrospective analysis was conducted on adjacent tissue, cancerous and the clinical data tissue from 150 gastrointestinal cancer patients treated at our hospital from May 2022 to May 2023. Differentially expressed genes (DEGs) associated with gastrointestinal cancer and kidney injury were identified through bioinformatics analysis. The expression of DEGs proteins in cancerous and adjacent tissues was assessed using immunohistochemical scoring (H scores). Patients were classified into AKI (n = 42) and non-AKI groups (n = 108) according to KDIGO AKI criteria. Univariate and multivariate logistic regression analyses were performed to investigate the influencing factors of AKI occurrence. Spearman correlation analysis was used to explore the relationship between DEGs and AKI biomarkers (Scr, BUN, MAU, and UA). The application value of DEGs in early diagnosis of AKI was evaluated using ROC curves. Bioinformatics analysis identified CDK1, STAT1, COL1A2, and COL1A1 as DEGs related to AKI in gastrointestinal cancer. Immunohistochemical analysis revealed elevated H scores for CDK1, STAT1, COL1A2, and COL1A1 in tumor tissues. Univariate analysis showed no significant differences in age, sex, marital status, education level, monthly income, disease type, cancer stage, or tumor markers (CEA, CA242, CA50) between AKI and non-AKI groups (P > 0.05). However, the AKI group exhibited significantly higher levels of MAU, UA, and H scores for CDK1, STAT1, COL1A2, and COL1A1 compared to the non-AKI group (P < 0.05). Multivariate logistic regression confirmed that MAU, UA, CDK1, and STAT1 are independent risk factors for AKI in gastrointestinal cancer patients. Correlation analysis indicated a significant positive association between CDK1, STAT1, and AKI biomarker levels (P < 0.05). ROC curve analysis demonstrated that CDK1 and STAT1 possess high diagnostic value for early detection of AKI in patients with gastrointestinal cancer, with enhanced efficacy when used in combination. CDK1 and STAT1 serve as early diagnostic indicators for the occurrence of AKI in gastrointestinal cancer patients.

Experimental study on early sensitive indexes of acute kidney injury in rats poisoned by diquat

Objective: To establish the model of acute kidney injury (AKI), search for more sensitive and reliable biomarkers. Methods: In April 2018, 100 male Wister rats aged 6 to 8 weeks were selected and randomly divided into experimental group (n=90) and control group (n=10). The experimental group was given Diachalefin (140 mg/kg body weight) by intragastric administration, while the control group was given saline intragastric administration. Ten rats in the experimental group were killed 0.5 h, 2 h, 6 h, 24 h, 3 d, 7 d, 14 d, 21 d and 28 d after intragastric administration, respectively. Serum creatinine (Cr), urea nitrogen (BUN) and uric acid (UA) were detected by automatic biochemical analyzer with 5 ml of blood from inferior vena cava puncture. Serum neutrophil gelatinase-associated lipid carrier protein (NGAL), kidney damage molecule-1 (KIM-1) and transforming growth factor-β1 (TGF-β1) levels were determined by enzyme-linked immunosorbent assay (ELISA). The data between groups were compared using two independent sample t tests. Results: The renal tissue structure of rats in the control group was not significantly abnormal, while the renal tissue cell damage of rats in the experimental group was obvious, which gradually increased with the extension of time in the early stage, and gradually recovered in the later stage. UA in experimental group reached its peak at 24 h after exposure and was still higher than that in control group at 14 d (P<0.05), Cr reached its peak at 7 d, and then gradually decreased, and there was no statistical significance between experimental group and control group at 28 d (P>0.05). BUN increased at 6 h after exposure and reached the highest value at 7~14 d (P<0.05). Blood NGAL increased at 0.5 h after exposure, reached its peak at 24 h, continued to increase at 3, 7 and 14 days (P<0.05), and began to decrease at 21 days. KIM-1 began to increase at 0.5 h, continued to peak at 24 h, 3 and 7 d after exposure, and began to decrease at 14 d, but it was still higher than that in control group (P<0.05). There was no significant difference in TGF-β1 at each time point (P>0.05). Western blot assay results: Compared with control group, there was no significant difference in the expression level of TGF-β1 in kidney tissue of experimental group (P>0.05). NGAL increased gradually from 2 h and was higher at 7 and 14 d, with statistical significance (P<0.05). KIM-1 increased at 2 h, decreased at 6 and 24 h, and increased again at 3 and 7 d. Conclusion: NGAL and KIM-1 can be used as early diagnostic biomarkers for diquat-induced acute kidney injury.

Determination of Urinary Neutrophil Gelatinase-Associated Lipocalin (uNGAL) Reference Intervals in Healthy Adult and Pediatric Individuals Using a Particle-Enhanced Turbidimetric Immunoassay.

Background: The current gold standards for diagnosing acute kidney injury (AKI) are an increase in serum creatinine and a decrease in urine output, which are inadequate for rapid diagnosis. Neutrophil gelatinase-associated lipocalin (NGAL) is a 25-kDa protein produced and secreted by injured kidney tubule epithelial cells, and can serve as an early urinary biomarker for AKI. ProNephro AKI (NGAL) is an immunoassay for the quantitative determination of NGAL in urine (uNGAL) that recently received FDA clearance. A multisite, cross-sectional study was conducted to establish reference intervals for uNGAL in apparently healthy individuals. Methods: Urine samples were collected from apparently healthy individuals aged ≥3 months who met all inclusion criteria and no exclusion criteria. Specimens were temporarily stored at room temperature or 2-8 °C, then transferred into urinalysis tubes before being frozen and shipped for testing. uNGAL testing was performed using the ProNephro AKI (NGAL) immunoassay on a Roche cobas c501 analyzer. Results: Of the 688 individuals screened, 677 were eligible, and 629 (91.4%) of those were deemed evaluable. The 95th and 97.5th percentile uNGAL values for all pediatric participants were below the clinical cutoff of 125 ng/mL. uNGAL values were statistically significantly higher for female vs. male participants in both adult (p = 0.003) and pediatric groups (p < 0.001), while differences were not statistically significant for age, site location, race, or ethnicity. Conclusions: This study provides normal reference intervals for uNGAL with the ProNephro AKI (NGAL) clinical chemistry immunoassay that may be useful for interpreting patient results.

Plasma neutrophil gelatinase-associated lipocalin as a single test rule out biomarker for acute kidney injury: A cross-sectional study in patients admitted to the emergency department.

Acute kidney injury (AKI) is a syndrome with high mortality and morbidity in part due to delayed recognition based on changes in creatinine. A marker for AKI based on a single measurement is needed and therefore the performance of a single measurement of plasma neutrophil gelatinase-associated lipocalin (pNGAL) to predict AKI in patients admitted to the emergency department was tested. Samples from the Triage study which included 6005 consecutive adult patients admitted to the emergency department were tested for pNGAL. The optimal cutoff for pNGAL was determined by the AUC and compared to AKI based on creatinine using different estimations of the premorbid kidney function. In 4833 patients, two or more plasma creatinine (pCr) measurements were available allowing the detection of AKI. The highest prevalence of AKI (10%) was found when defining AKI as an increase in pCr ≥26.5 μmol/L from the prior year's mean pCr. At these conditions the AUC for pNGAL to predict AKI was 85% giving an optimal cutoff of 142.5 ng/mL with a negative predictive value of 0.96, a positive predictive value of 0.35, a specificity of 0.87 and a sensitivity of 0.70. The study illustrates that the value of a single measurement of pNGAL is primarily in excluding AKI whereas it`s poorer in predicting the presence of AKI. When diagnosing AKI with pCr the optimal baseline pCr level is the mean of available pCr (mb-pCr) measurements from up to a year prior to the current event.

Preoperative leptin levels were associated with postoperative acute kidney injury in patients with acute type A aortic dissection

Objective Acute kidney injury (AKI) is a common surgical complication of acute type A aortic dissection (AAAD) and strongly associated with an unfavorable prognosis. Although elevated leptin levels have been identified as a potential risk factor for chronic kidney disease in middle-aged and elderly individuals, their association with AKI following AAAD surgery remains unknown. This study investigated the association between preoperative leptin levels and postoperative AKI in patients with AAAD. Methods This study included 159 patients with AAAD at Fujian Heart Medical Center. The Kidney Disease: Improving Global Outcomes standards were used to define and classify AKI. The receiver operating characteristic (ROC) curves were used to assess the ability of leptin levels to predict AKI. Binary logistic regression analysis was used to study the association between leptin level and AKI. Results The incidence of AKI was 33.96%. Leptin levels in the AKI group and stage 1, 2, and 3 AKI groups were higher than those in the non-AKI group (p < 0.05). Multivariate analysis revealed that elevated leptin levels were an independent risk factor for AKI (p < 0.001). ROC analysis of leptin detection for AKI showed an area under the curve of 0.71. The risk of AKI in the high-level group (leptin levels ≥3.62 ng/mL) was 3.87 times to the low-level group (leptin levels < 3.62 ng/mL). Conclusion Elevated leptin levels are associated with AKI, and plasma leptin may serve as a potential early blood biomarker for AKI in patients with AAAD.

Evaluation of urinary vanin-1 for the early prediction of cisplatin-induced acute kidney injury during neoadjuvant chemotherapy for esophageal cancer.

Cisplatin (CDDP) induces acute kidney injury (AKI) as a side effect during neoadjuvant chemotherapy (NAC). Urinary vanin-1 excretion may increase during CDDP treatment. We investigated whether urinary vanin-1 is an early biomarker for CDDP-induced AKI. Thirty patients were administered 80 mg/m2 CDDP on day 1 as NAC for esophageal cancer. Blood and urine samples were collected on days 1, 2, 3, 4, and 6 after CDDP administration. Serum creatinine (sCr) and urinary vanin-1 levels were measured. Creatinine clearance (cCr) and estimated glomerular filtration rate (eGFR) were calculated from sCr. Based on the change in sCr after CDDP administration, the AKI and non-AKI groups were defined using the Kidney Disease Improving Global Outcomes classification. Changes in sCr, cCr, eGFR, and urinary vanin-1 levels were compared between the two groups. A gradual increase in sCr and a decrease in eGFR were observed over time post-CDDP administration, with differences between the two groups becoming significant by day 4. However, urinary vanin-1 levels increased on day 3 after CDDP administration, and the difference between the two groups was significant on day 3. Receiver operating characteristic curves of urinary vanin-1 on day 3 revealed that a cut-off value of 3.17 ng urinary vanin-1/mg urinary creatinine yielded an area under the curve, sensitivity, and specificity of 0.83 (P < 0.05), 75.0%, and 22.7%, respectively. The non-AKI incidence below the cut-off value of urinary vanin-1 of 3.17 ng/mg uCr was 89.5%. Urinary vanin-1 is a superior minimally invasive biomarker for the early prediction of CDDP-induced AKI.

Combining cardiac and renal biomarkers to establish a clinical early prediction model for cardiac surgery-associated acute kidney injury: a prospective observational study.

Cardiac surgery-associated acute kidney injury (CSA-AKI) is a prevalent complication with poor outcomes, and its early prediction remains a challenging task. Currently available biomarkers for acute kidney injury (AKI) include serum cystatin C (sCysC) and urinary N-acetyl-β-D-glucosaminidase (uNAG). Widely used biomarkers for assessing cardiac function and injury are N-terminal pro B-type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI). In light of this, our study aimed to evaluate the effectiveness of these four biomarkers in predicting CSA-AKI. This prospective observational study enrolled adult patients who had undergone cardiac surgery. The clinical prediction model for CSA-AKI was developed using the least absolute shrinkage and selection operator (LASSO) regression method. The model's performance was assessed using the area under the curve of the receiver operating characteristic (ROC-AUC), decision curve analysis (DCA), and calibration curves. Furthermore, a separate validation cohort was constructed to externally validate the prediction model. Additionally, a risk nomogram was created to facilitate risk assessment and prediction. In the modeling cohort consisting of 689 patients and the validation cohort consisting of 313 patients, the total incidence of CSA-AKI was 33.4%. The LASSO regression identified several predictors, including age, history of hypertension, baseline serum creatinine (sCr), coronary artery bypass grafting combined with valve surgery, cardiopulmonary bypass duration, preoperative albumin, hemoglobin, postoperative NT-proBNP, cTnI, sCysC, and uNAG. The constructed clinical prediction model demonstrated robust performance, with a ROC-AUC of 0.830 (0.800-0.860) in the modeling cohort and 0.840 (0.790-0.880) in the validation cohort. Furthermore, both calibration and DCA indicated good model fit and clinical benefit. This study demonstrates that incorporating the immediately postoperative renal biomarkers, sCysC and uNAG, along with the cardiac biomarkers, NT-proBNP and cTnI, into a clinical early prediction model can significantly enhance the accuracy of predicting CSA-AKI. These findings suggest that a comprehensive approach combining both renal and cardiac biomarkers holds promise for improving the early detection and prediction of CSA-AKI.

Evaluation of Acute Kidney Injury (AKI) Biomarkers FABP1, NGAL, Cystatin C and IL-18 in an Indian Cohort of Hospitalized Acute-on-chronic Liver Failure (ACLF) Patients.

Acute-on-chronic liver failure (ACLF) is a complication of cirrhosis associated with systemic inflammation and organ dysfunction. In ACLF, the development of acute kidney injury (AKI) is associated with poor outcomes. FABP1, NGAL, Cys C and IL-18 have been shown to correlate with ACLF severity and mortality. Hence, our study aimed to evaluate the association of these biomarkers with organ dysfunctions, particularly AKI, in an Indian ACLF patient cohort. 151 study participants including ACLF (n= 91; with AKI n= 63, no-AKI n= 28), non-liver AKI (n= 30) and healthy controls (n= 30) were recruited. Serum ELISA was performed for biomarker estimation. Data interpolationand graphical representation were performed using GraphPad Prism and statistical analyses performed using STATA 14.0. FABP1 and Cys C levels were higher in ACLF-AKI patients compared to ACLF no-AKI (P-value ≤ 0.0005). Serum Cys C levels were significantly increased in non-liver AKI compared to ACLF-AKI (P-value ≤ 0.001). AUROC analysis showed better performance of Cys C (AUC 0.79; 95% CI (0.68-0.89)) compared to serum creatinine (AUC 0.71; 95% CI (0.61-0.82)) in discriminating AKI and no-AKI. Correlation analysis revealed positive correlations of FABP1 with creatinine and urea, Cys C with creatinine, urea and OF-Kidney, NGAL, and IL-18 with general markers of organ dysfunction. Plasma MTs) measured in a subset of ACLF patients were elevated in progression-to-AKI. Our study showed that in an Indian population of ACLF patients with a high short-term mortality, serum Cys C and FABP1 were elevated in ACLF-AKI, however did not have predictive potential for ACLF-AKI. Cys C levels were significantly higher in non-liver AKI patients vs. ACLF-AKI and correlated with markers of kidney dysfunction whereas NGAL and IL-18 represented higher inflammation and total organ dysfunction. Hence, we conclude that these biomarkers were elevated in ACLF-AKI but did not have predictive potential for AKI in ACLF.

Novel Biomarkers and Imaging Tests for AKI Diagnosis in Patients with Cancer.

The lack of non-invasive urine and blood-based biomarkers for the diagnosis of acute kidney injury (AKI) in patients with cancer is an area of significant unmet clinical need. Traditional non-invasive diagnostic tools that are currently utilized in the clinic, such as creatinine and cystatin C-based eGFR measurements, urinalysis, urine sediment exam, urine protein quantification, and urine electrolyte measurement, lack the sensitivity and specificity to distinguish between the various underlying etiologies of AKI in patients with cancer. Imaging-based diagnostics can be helpful to rule out urinary obstruction, but also lack sensitivity and specificity to diagnose the etiology of AKI. Kidney biopsy is often required for definitive diagnosis. As our scientific understanding of the biological pathways that are dysregulated in AKI has advanced, there has been considerable interest in developing new biomarkers for AKI. For example, the diagnosis of acute interstitial nephritis (AIN), which can occur in patients treated with immune checkpoint inhibitors (ICIs), promises to be revolutionized by the incorporation of urinary testing for inflammatory biomarkers such as C-X-C motif ligand 9 (CXCL9), tumor necrosis factor alpha (TNF-α), and interleukin 9 (IL-9). In the case of cisplatin administration, biomarkers such as neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule 1 (KIM-1) may improve prognostication, differentiating between persistent AKI resulting from acute tubular injury versus pre-renal azotemia. The development and validation of blood, urine and imaging biomarkers into widely utilized diagnostic tests will require a concerted effort, but could improve diagnosis, management and prognostication for a growing group of patients who are at high risk of developing AKI during the course of their illness.

Development and Validation of a Diagnostic Model for AKI Based on the Analysis of Ferroptosis-related Genes.

Acute kidney injury (AKI) is a common renal condition associated with various factors, including pre-renal, post-renal, and renal causes, with ischemia- reperfusion being a frequent contributor leading to tubular injury. Early identification of AKI is crucial but remains challenging. This study explored the molecular signature of AKI using gene microarray data from the GEO dataset, focusing on identifying ferroptosis-related features through three machine-learning algorithms. We also validated potential biomarkers through a hypoxia/ reoxygenation model. ROC curves, expression differences, and associations with immune cells were analyzed for the three markers to confirm their potential as AKI biomarkers, each demonstrating strong diagnostic ability. Combining these markers proved more effective. The combination of AEBP2, MDM2, and NR4A1 as diagnostic biomarkers for AKI not only enhances detection capability but also holds promise as a significant tool in clinical practice, providing patients with diagnostic and therapeutic guidance.

BIOMARKERS OF ACUTE KIDNEY INJURY OF BLOOD SERUM IN PATIENTS WITH THERMAL SKIN BURNS

The aim: to evaluate the dynamics of changes in the level of biomarkers of acute kidney injury – lipocalin and cystatin C in blood serum in patients with thermal skin burns.Materials and methods. The study included 74 patients with thermal skin burns of I-III degree with a skin lesion area of more than 25%, of which at least 15% are deep burns. Serum creatinine levels were determined using the kinetic Jaffe method. Lidocaine and cystatin C concentrations were studied by multiplex analysis on a flow cytofluorimeter.Results. It was found that the concentration of cystatin C in the blood serum during burn shock increases by 1,9 times, with burn toxemia and septicotoxemia - by 1,5 times in relation to the control group. The level of lipocalin in the blood serum of patients with thermal skin burns during the shock period increases by 5,5 times compared to the control group. During the period of burn toxemia and septicotoxemia, lidocaine concentration remained at a high level and exceeded the control values by 4,4 and 3,6 times, respectively.Conclusion. Lipocaine and cystatin C can be considered as early biomarkers of acute kidney injury in patients with thermal skin burns.

Can Novel Biomarkers Effectively Predict Acute Kidney Injury in Liver or Kidney Transplant Recipients?

Acute kidney injury (AKI) constitutes a common complication associated with liver or kidney transplantation, which may significantly impact the graft condition and perioperative mortality. Current AKI diagnostic criteria based on serum creatinine (sCr) and urine output alterations are widely utilized in routine clinical practice. However, the diagnostic value of sCr may be limited by various confounding factors, including age, sex, reduced or increased muscle mass, and pre-existing chronic kidney disease (CKD). Furthermore, sCr is rather a late indicator of AKI, as its concentration tends to increase only when the severity of the injury is enough to decrease the estimated glomerular filtration rate (eGFR). Recent expertise highlights the need for novel biomarkers in post-transplantation AKI diagnosis, prediction of event-associated mortality, or evaluation of indications for renal replacement treatment (RRT). Over the last decade, the diagnostic performance of various AKI biomarkers has been assessed, among which some showed the potential to outperform sCr in AKI diagnosis. Identifying susceptible individuals, early diagnosis, and prompt intervention are crucial for successful transplantation, undisturbed graft function in long-term follow-up, and decreased mortality. However, the research on AKI biomarkers in transplantation still needs to be explored. The field lacks consistent results, rigorous study designs, and external validation. Considering the rapidly growing prevalence of CKD and cirrhosis that are associated with the transplantation at their end-stage, as well as the existing knowledge gap, the aim of this article was to provide the most up-to-date review of the studies on novel biomarkers in the diagnosis of post-transplantation AKI.

Measurement of Apelin as a Biomarker and Its Relationship to Cystatin C, Copeptin, and Glomerular Filtration Rate in Serum of Patients with Acute Kidney Injury in Mosul City, Iraq

Abstract Background: There is a need for early and accurate diagnosis of acute kidney injury, as high levels of cystatin C, copeptin, and low apelin levels in serum can provide an early diagnosis of acute kidney injury in patients. Objectives: To measure the level of apelin as a biomarker in the blood serum of both control and acute kidney injury groups, and to find its relationship with each of cystatin C, copeptin, and estimated glomerular filtration rate of both groups. Materials and Methods: This study was conducted on 232 blood samples collected from males and females, 108 from control subjects and 124 from patients with acute kidney injury, aged between 35 and 56 years. Results: Serum apelin (pg/mL) levels decreased in the blood serum of the acute kidney injury patients group, increased both cystatin C and copeptin, and decreased estimated glomerular filtration rate compared to the control group. Conclusion: The results showed that serum apelin levels decreased in the blood serum of the acute kidney injury group, corresponding to an increase in the level of both cystatin C and copeptin levels and a decrease in the estimated glomerular filtration rate compared to the control group, which indicates the possibility that apelin is a strong predictive biomarker for acute kidney injury, and it can play a good preventive and therapeutic role in the future.

Research progress on biomarkers of sepsis-associated acute kidney injury

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. Sepsis-associated acute kidney injury (SA-AKI) is a common organ dysfunction of sepsis, and its incidence and mortality are increasing,which brings heavy economic burden to patients and society. Early diagnosis and effective intervention can block the occurrence and progression of SA-AKI effectively, improve prognosis, and reduce medical costs. Diagnosis on SA-AKI relies on urine volume and serum creatinine, which has the disadvantages of being easily disturbed and delaying. The identification of biomarkers in blood and urine can facilitate diagnosis and provide targeted therapy to enhance the management of SA-AKI. This article reviews the characteristics of a variety of SA-AKI biomarkers that have been found and validated, including pre-damage biomarkers, damage biomarkers and functional biomarkers, and explore the clinical value of newly discovered biomarkers related to the diagnosis and treatment of SA-AKI, such as blood uncoupling protein 2 (UCP2), Sestrin 2 protein and pannexin 1 (PANX1), to provide reference for the early diagnosis and effective treatment of SA-AKI.

Serum uromodulin associates with kidney function and outcome in a cohort of hospitalised COVID-19 patients

This study investigates the prevalence and evaluates the prognostic implications of acute kidney injury (AKI) in COVID-19 patients, with a novel emphasis on the evaluation of serum uromodulin (sUmod) as a potential kidney-specific biomarker. A cohort of hospitalised COVID-19 patients (n = 378) was examined for AKI using standard criteria. In addition to traditional urinary biomarkers, sUmod levels were analysed. Univariable and multivariable regression models were employed to evaluate the association of sUmod and AKI and in-hospital mortality. Levels of sUmod were significantly lower in patients with CKD (91.8 ± 60.7 ng/ml) compared to patients with normal kidney function (204.7 ± 91.7 ng/ml; p < 0.001). 151 patients (40.0%) presented with AKI at the time of hospital admission or developed an AKI during hospitalization. 116 patients (76.8%) had an AKI already at the time of hospital admission. COVID-19 patients with AKI had significantly lower levels of sUmod compared to patients without AKI during hospitalisation (124.8 ± 79.5 ng/ml) vs 214.6 ± 92.3 ng/ml; p < 0.001). The in-hospital mortality rate in this cohort of COVID-19 patients was 15.3%. Patients with AKI had a higher probability for in-hospital death (OR 5.6, CI 1.76 to 17.881, p = 0.004). Patients who died during hospital stay, had significantly lower sUmod levels (129.14 ± 89.56 ng/ml) compared to patients surviving hospitalisation (187.71 ± 96,64 ng/ml; p < 0.001). AKI is frequently associated with COVID-19 in hospitalized patients. Serum uromodulin may emerge as a promising biomarker for AKI in COVID-19 patients. Further research is warranted to explore its clinical application and refine risk stratification in this patient population.