Biomarkers Of Kidney Injury Research Articles

Effects of the Vitamin D3 on Alleviating the Oxidative Stress Induced by Diquat in Wenchang Chickens

Vitamin D3 (VD3) is an indispensable micronutrient in livestock and poultry feed. Its function in antioxidant stress has been reported. We investigate whether the addition of different concentrations of VD3 to the diet affects the production performance, slaughter performance, meat quality, organ index, and gut injury on the diquat (DQ)-induced model of oxidative stress in Wenchang chickens. Four hundred and eighty one-day-old chickens were randomly divided into six groups: control (basal diet), 4000 VD (basal diet + VD3 4000 IU per kg feed intake), 1000 VD+DI (DQ, basal diet + VD3 1000 IU per kg feed intake), 2000 VD+DI (DQ, basal diet + VD3 2000 IU per kg feed intake), and 4000 VD+DI (DQ, basal diet + VD3 4000 IU per kg feed intake). The results showed that the addition of VD3 to the diet promoted DQ-induced weight loss and reduced ADFI, slaughter rate, splenic index, and pH after 1 h and 24 h in the leg muscles. VD3 decreased the increase in content of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) among proinflammatory cytokines (p < 0.05) and increased the reduction in anti-inflammatory cytokines content of interleukin-10 (IL-10) (p < 0.05) induced by DQ. In addition, liver and kidney injury biomarkers and the intestinal permeability index in serum were disordered after treatment with DQ (p < 0.05). VD3 perfected the increase of D-lactic acid (D-LA), diamine oxidase (DAO), total cholesterol (T-CHO), creatinine (CR), blood urea nitrogen (BUN), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C) content, aspartate transaminase (AST), alanine transaminase (ALT), and lactate dehydrogenase (LDH) activity (p < 0.05); it increased the decrease of albumin (ALB) content (p < 0.05). Meanwhile, VD3 regulated the intestinal morphology and intestinal barrier. Moreover, DQ induced a decrease in total antioxidant capacity and antioxidant enzyme activity in the serum, liver, and jejunum (p < 0.05), and an increase in malonaldehyde (MDA) content (p < 0.05). However, the addition of different levels of VD3 could alleviate the above phenomenon of oxidative stress in Wenchang chickens to different degrees. Thus, this research suggested that the addition of VD3 can relieve the DQ-induced oxidative stress of Wenchang chickens, and the level of VD3 acquisition is positively correlated with the remission effect.

Urinary levels of kidney injury molecule-1 (KIM-1) and interleukin-18 (IL-18) in children and adolescents with hyperuricemia

PurposeHyperuricemia may lead to silent tissue damage and increase the risk of some diseases, including kidney diseases. Increased serum uric acid concentration induces inflammatory pathways and promotes kidney damage. This study aimed to determine whether hyperuricemia influences the levels of urinary kidney injury markers in children and adolescents with hyperuricemia, assessed by the urinary concentrations of interleukin-18, a biomarker of inflammation, and kidney injury molecule-1 (KIM-1), a biomarker of kidney injury. Material and methodsThe study included 73 children and adolescents (32 males and 41 females) aged 2–18 years. They were divided into two groups: hyperuricemia (HU) group (n ​= ​48) and normouricemia – reference group (R) (n ​= ​25). The concentrations of urinary interleukin-18 and KIM-1 were measured using an ELISA kit and were normalized for urinary creatinine (cr.) concentration. ResultsThe median interleukin-18/cr. Levels in the HU group were significantly higher than in the R group (median, Q1-Q3) 21.83 (11.32–35.96) and 12.68 (7.11–24.04), respectively, (p ​< ​0.05). The KIM-1/cr. in the HU group and the R group were (median, Q1-Q3) 0.79 (0.45–1.03) and 0.81 (0.59–1.01), respectively, and the difference was not significant. KIM-1/cr. did not differ between the groups. Interleukin-18/cr. ratio correlated positively with serum uric acid concentration (r ​= ​0.24, p ​< ​0.05). ConclusionsInterleukin-18/cr., but not KIM-1/cr. was higher in children with hyperuricemia. Hyperuricemia results in increased IL-18 in urine, in absence of other markers of kidney injury, suggesting inflammation in the kidney. Additional studies on the adults should be done, to confirm this hypothesis.

Metabolomic identification of predictive and early biomarkers of cisplatin-induced acute kidney injury in adult head and neck cancer patients.

Cisplatin causes acute kidney injury (AKI) in approximately one third of patients. Serum creatinine and urinary output are poor markers of cisplatin-induced AKI. Metabolomics was utilized to identify predictive or early diagnostic biomarkers of cisplatin-induced AKI. Thirty-one adult head and neck cancer patients receiving cisplatin (dose ≥70 mg/m2) were recruited for metabolomics analysis. Urine and serum samples were collected prior to cisplatin (pre), 24-48 h after cisplatin (24-48 h) and 5-14 days (post) after cisplatin. Based on serum creatinine concentrations measured at the post timepoint, 11/31 patients were classified with clinical AKI. Untargeted metabolomics was performed using liquid chromatography-mass spectrometry (LC-MS). Metabolic discrimination was observed between "AKI" patients and "no AKI" patients at all timepoints. Urinary glycine, hippuric acid sulfate, 3-hydroxydecanedioc acid and suberate were significantly different between AKI patients and no AKI patients prior to cisplatin infusion. Urinary glycine and hippuric acid sulfate were lower (-2.22-fold and -8.85-fold), whereas 3-hydroxydecanedioc acid and suberate were higher (3.62-fold and 1.91-fold) in AKI patients relative to no AKI patients. Several urine and serum metabolites were found to be altered 24-48 h following cisplatin infusion, particularly metabolites involved with mitochondrial energetics. We propose glycine, hippuric acid sulfate, 3-hydroxydecanedioc acid and suberate as predictive biomarkers of predisposition to cisplatin-induced AKI. Metabolites indicative of mitochondrial dysfunction may serve as early markers of subclinical AKI.

Identification of AGXT2, SHMT1, and ACO2 as important biomarkers of acute kidney injury by WGCNA.

Acute kidney injury (AKI) is a serious and frequently observed disease associated with high morbidity and mortality. Weighted gene co-expression network analysis (WGCNA) is a research method that converts the relationship between tens of thousands of genes and phenotypes into the association between several gene sets and phenotypes. We screened potential target genes related to AKI through WGCNA to provide a reference for the diagnosis and treatment of AKI. Key biomolecules of AKI were investigated based on transcriptome analysis. RNA sequencing data from 39 kidney biopsy specimens of AKI patients and 9 normal subjects were downloaded from the GEO database. By WGCNA, the top 20% of mRNAs with the largest variance in the data matrix were used to construct a gene co-expression network with a p-value < 0.01 as a screening condition, showing that the blue module was most closely associated with AKI. Thirty-two candidate biomarker genes were screened according to the threshold values of |MM|≥0.86 and |GS|≥0.4, and PPI and enrichment analyses were performed. The top three genes with the most connected nodes, alanine-glyoxylate aminotransferase 2(AGXT2), serine hydroxymethyltransferase 1(SHMT1) and aconitase 2(ACO2), were selected as the central genes based on the PPI network. A rat AKI model was constructed, and the mRNA and protein expression levels of the central genes in the model and control groups were verified by PCR and immunohistochemistry experiments. The results showed that the relative mRNA expression and protein levels of AGXT2, SHMT1 and ACO2 showed a decrease in the model group. In conclusion, we inferred that there is a close association between AGXT2, SHMT1 and ACO2 genes and the development of AKI, and the down-regulation of their expression levels may induce AKI.

Mineral bone disorders and kidney disease in hospitalized children with sickle cell anemia.

Mineral bone disorders (MBD) are common in sickle cell anemia (SCA). Frequent vaso-occlusive crises (VOC) further impact MBD in children with SCA. We evaluated the prevalence of markers of SCA-related MBD (sMBD) in hospitalized children and assessed the relationship between sMBD and individual mineral abnormalities with kidney disease. We prospectively recruited 185 children with SCA hospitalized with a VOC. Serum measures of mineral bone metabolism (calcium, phosphate, parathyroid hormone, 25-hydroxy vitamin D, FGF23, osteopontin) were measured at enrollment. The primary outcome was markers of sMBD defined as a composite of hypocalcemia, hyperphosphatemia, hyperparathyroidism, or deficiency in 25-OH vitamin D. Secondary outcomes included individual abnormalities in mineral metabolism. The Kidney Disease: Improving Global Outcomes (KDIGO) guidelines were used to define SCA-associated acute kidney injury (AKI). AKI was further assessed using urine NGAL as a marker of tubular injury. Acute kidney disease (AKD) was defined as a composite of AKI, an eGFR < 90 ml/min per 1.73 m2 using the Cystatin C GFR equation, or evidence of structural injury (positive biomarker test or albuminuria). The mean age of children was 8.9 years and 41.6% were female. The prevalence of sMBD was 47.6%, with hypocalcemia the most frequent abnormality (29.9%, 55/184) followed by hyperphosphatemia (20.7%, 38/184), hyperparathyroidism (8.7%, 16/185), and vitamin D deficiency (5.4%, 10/185). There was no association between sMBD and sKDIGO-defined AKI using serial changes in creatinine or when incorporating biomarkers to define AKI. However, the presence of AKD was associated with a 2.01-fold increased odds of sMBD (95% CI 1.05 to 3.83) and was driven by a decrease in eGFR (OR, 2.90 95% CI: 1.59 to 5.29). When evaluating individual mineral abnormalities, hypocalcemia was associated with AKD and low eGFR while hyperparathyroidism was associated with low eGFR, AKI and structural injury. Vitamin D deficiency was associated with structural kidney injury. Vitamin D deficiency, hyperparathryoidism, and increases in FGF23 and osteopontin predicted mortality (p < 0.05 for all). MBD is common among children with SCA hospitalized with VOC. Biomarkers of kidney injury and bone health may help risk stratify children at risk of sMBD. Routine evaluation of sMBD in children with SCA may improve long-term bone health.

Urine neutrophil gelatinase-associated lipocalin as a biomarker of acute kidney injury and prognosis in decompensated chronic liver disease: A prospective study.

Acute kidney injury (AKI) heralds deterioration in patients with decompensated chronic liver disease (DCLD). Serum creatinine (sCr), a component of the model for end-stage liver disease-sodium (MELD-Na) prognostic score, has limitations in patients with DCLD. We evaluated the prognostic role of urine neutrophil gelatinase-associated lipocalin (NGAL) in DCLD and its ability to sub-type AKI. Total 147consecutive patients hospitalized between June 2018 andJune 2020 for complications of DCLD were evaluated. Urine NGAL was estimated and demographic, clinical and biochemical parameters recorded at baseline. Participants were followed up till theend of study period or mortality, whichever came earlier. Primary outcomes included all-cause mortality and time to death after index hospitalization. Secondary outcomes included thepresence and type of AKI, need for intensive care unit (ICU) stay, length of ICU/hospital stay, in-hospital mortality, development of new-onset/recurrent AKI and recurrent hospitalization after index admission. Urine NGAL was highest in acute tubular necrosis (ATN), lowest in pre-renal azotemia (PRA) and intermediate in hepatorenal syndrome (HRS-AKI). Urine NGAL (p = 0.0208) was superior to sCr (p = 0.0388) and inferior to fractionated excretion of sodium (FENa) (p = 0.0013) in stratifying AKI. A cut-off of 203.9ng/mL discriminated between HRS and PRA with sensitivity 77.8% and specificity 68.7%. Urine NGAL correlated with MELD-Na score, need for ICU stay, in-hospital mortality and mortality at three and sixmonths. Two-year survival was significantly lower in patients with urine NGAL > 205ng/mL. Addition of log-urine-NGAL score did not improve predictive performance of MELD-Na. Urine NGAL could identify AKI sub-types and correlated with short-term clinical outcomes, including mortality.

Evaluation The role of Trefoil Factor1 as early stage biomarker in patients with Nephrolithiasis

Nephrolithiasis is a public health problem that affect large scale ofpeoples around the world. naturally, there are many substances ,proteins,lipids, glycosaminoglycans and inorganic compounds, work as kidneystone inhibitors in the normal renal tubular fluid that inhibit crystalgrowth, aggregation, and/or adhesion to renal surfaces, among thisinhibitors we investigate the concentration of trefoil factor 1 (TFF1) as astone formation inhibitor and kidney injury biomarker in serum of 75kidney stone patients and 15 healthy subjects using ELISA technique.The results shows no significant changes within patients groups whileshows that TFF1 levels were significantly increased in stone patientswhen compared with the healthy controls (P≤0.05), which support thefact that it could use as early marker of kidney injury (KI) .The resultsalso revealed no significant changes within patients groups while therewas a significant changes between patients and controls for both bloodurea and serum creatinine levels in renal stone patients in comparison tothe apparently healthy control subjects (P ≤0.05). Further investigationare needed to show the inhibitory effect of TFF1 in urine of kidney stonepatients.

Impact of Vancomycin Loading Doses and Dose Escalation on Glomerular Function and Kidney Injury Biomarkers in a Translational Rat Model.

Vancomycin-induced kidney injury is common, and outcomes in humans are well predicted by animal models. This study employed our translational rat model to investigate temporal changes in the glomerular filtration rate (GFR) and correlations with kidney injury biomarkers related to various vancomycin dosing strategies. First, Sprague-Dawley rats received allometrically scaled loading doses or standard doses. Rats that received a loading dose had low GFRs and increased urinary injury biomarkers (kidney injury molecule 1 [KIM-1] and clusterin) that persisted through day 2 compared to those that did not receive a loading dose. Second, we compared low and high allometrically scaled vancomycin doses to a positive acute kidney injury control of high-dose folic acid. Rats in both the low- and high-dose vancomycin groups had higher GFRs on all dosing days than the positive-control group. When the two vancomycin groups were compared, rats that received the low dose had significantly higher GFRs on days 1, 2, and 4. Compared to low-dose vancomycin, the KIM-1 was elevated among rats in the high-dose group on dosing day 3. The GFR correlated most closely with the urinary injury biomarker KIM-1 on all experimental days. Vancomycin loading doses were associated with significant losses of kidney function and elevations of urinary injury biomarkers. In our translational rat model, both the degree of kidney function decline and urinary biomarker increases corresponded to the magnitude of the vancomycin dose (i.e., a higher dose resulted in worse outcomes).

Determination of HMGB1 in hepatitis B virus-related acute-on-chronic liver failure patients with acute kidney injury: Early prediction and prognostic implications.

Background: Acute kidney injury (AKI) is a frequent complication in patients with hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF) and is associated with high rates of mortality. We aimed to estimate serum high mobility group protein 1 (HMGB1) levels in hepatitis B virus-related acute-on-chronic liver failure patients and analyze their clinical value in the development and outcomes of Acute kidney injury. Methods: A total of 251 consecutive patients with hepatitis B virus-related acute-on-chronic liver failure were enrolled in this retrospective study. Using the International Club of Ascites staging criteria of Acute kidney injury, 153 patients developed Acute kidney injury. The clinical data of patients were collected and serum levels of high mobility group protein 1 were measured by ELISA. All patients were followed up until death or for a minimum of 3months. Early prediction and prognostic implications of high mobility group protein 1 in Hepatitis B Virus-Related Acute-on-Chronic Liver Failure Patients with Acute Kidney Injury were investigated in different cohorts, including a propensity score-matched ACLF cohort. Results: Among all individuals with hepatitis B virus-related acute-on-chronic liver failure, the incidence of Acute kidney injury was 61.0% (153/251). The patients who developed stage 2/3 Acute kidney injury showed the highest high mobility group protein 1 levels, followed by those who developed stage 1 Acute kidney injury, and those without Acute kidney injury showed the lowest high mobility group protein 1 levels. Moreover, high mobility group protein 1 levels were significantly higher in non-survivors than in survivors among hepatitis B virus-related acute-on-chronic liver failure patients with Acute kidney injury. Furthermore, analysis of the area under the receiver operating characteristic curve (AUROC) indicated that serum high mobility group protein 1 levels (pre-matching: AUC = 0.740; post-matching: AUC = 0.661) may be a potential predictive factor for Acute kidney injury development and that high mobility group protein 1 (AUC = 0.727) might be a reliable biomarker for prognosis in patients with Acute kidney injury. Conclusion: In patients with hepatitis B virus-related acute-on-chronic liver failure, Acute kidney injury is universal. Acute kidney injury and its stages negatively influence the 90-day transplant-free mortality rate. Serum high mobility group protein 1 levels can serve as a positive predictor of Acute kidney injury development, and high mobility group protein 1 might also be a prognostic biomarker for Acute kidney injury among hepatitis B virus-related acute-on-chronic liver failure patients.

Association between Serum Soluble α-Klotho and Urinary Albumin Excretion in Middle-Aged and Older US Adults: NHANES 2007-2016.

(1) Background: Preclinical and clinical studies on the anti-aging effect of α-Klotho are emerging. Urinary albumin excretion (UAE) is a well-known biomarker of kidney injury and generalized damage in the cardiovascular system. However, the potential relationship between α-Klotho and UAE is limited and controversial. This study aimed to quantify this relationship in the general middle-aged and elderly population from the National Health and Nutrition Survey (NHANES) 2007-2016. (2) Methods: Serum α-Klotho was measured by enzyme-linked immunosorbent assay. UAE was assessed by the albumin-to-creatinine ratio (ACR). After adjusting for several confounding variables, the relationship between α-Klotho and ACR was analyzed by weighted multivariable logistic regression, subgroup analysis, and interaction tests. A generalized additive model (GAM) with smooth functions using the two-piecewise linear regression model was used to examine the potential nonlinear relationship between α-Klotho and ACR. (3) Results: Among 13,584 participants aged 40-79 years, we observed an independent and significant negative correlation between α-Klotho and ACR (β = -12.22; 95% CI, -23.91, -0.53, p = 0.0448) by multivariable logistic regression analysis, especially in those with age ≥ 60 years, pulse pressure (PP) ≥ 60 mmHg, hypertension or diabetes. We further discovered the nonlinear relationship between α-Klotho and ACR by GAM, revealing the first negative and then positive correlations with an inflection point of 9.91 pg/mL between α-Klotho and ACR. (4) Conclusions: A dose-response relationship between α-Klotho and ACR was demonstrated, and the negative correlation therein indicated that α-Klotho has potential as a serum marker and prophylactic or therapeutic agent despite its metabolic and effective mechanisms needing to be further explored.

Renal medicine in the intensive care unit: a narrative review.

Kidney disease, both acute and chronic, is commonly encountered on the intensive care unit. Due to the role the kidneys play in whole body homeostasis, it follows that their dysfunction has wide-ranging implications and can affect prescribing and therapeutic management. This narrative review discusses the pathophysiology of acute kidney injury and chronic kidney disease, and how this relates to critically unwell patients. We cover several aspects of the management of renal dysfunction on the critical care unit, exploring some of the recurrent themes within the literature, including type and timing of kidney replacement therapy, management of acute kidney injury, as well as discussing how novel biomarkers for acute kidney injury may help to identify patients suffering from acute kidney injury as well as risk stratifying these patients. We discuss how early involvement of specialist nephrology services can improve outcomes in patients with kidney disease as well as offer valuable diagnostic and specialist management advice, particularly for patients with established end stage kidney disease and patients who are already known to nephrology services. We also explore some of the ongoing research questions that need to be answered within this arena.

Acute kidney injury in patients with myocardial infarction and percutaneous coronary interventions: laboratory markers and the influence on the frequency of recurrent cardiovascular events

Highlights. Biomarkers of acute kidney injury and their effect on the frequency of recurrent coronary events in patients with myocardial infarction after percutaneous coronary interventions.Aim. To study biomarkers of acute kidney injury (AKI) and prognosis, as well as the frequency of recurrent cardiovascular events in patients with myocardial infarction and percutaneous coronary interventions.Methods. 166 patients with myocardial infarction and performed percutaneous coronary interventions were studied, divided into 2 groups: with acute kidney injury (n = 91) and without it (n = 50), the control group consisted of 25 people. All patients underwent standard general clinical and biochemical blood tests to assess the level of C-reactive protein, markers of myocardial necrosis, natriuretic peptide (NTproBNP), microalbuminuria (MAU). In both groups, the glomerular filtration rate (GFR) was calculated using the CKD-EPI formula. An increase in serum creatinine by 26.5 mmol/L or more during the first 3 days from the value at admission was the reason for the study of the level of Kidney Injury Molecule-1 (KIM-1) and interleukin 18 (IL-18) in urine on the 3rd and 14th days from hospitalization. All patients underwent coronary angiography and stenting of the infarct-dependent artery. 6 months and 1 year after discharge for this acute coronary event, repeated examinations of patients were performed to assess the frequency of repeated cardiovascular events and kidney function.Results. It was revealed that the creatinine level in the examined patients did not differ statistically significantly at admission, but there was a decrease in the filtration function of the kidneys in patients with AKI. On the third day of hospitalization, there was an increase in creatinine levels in the first group of patients with a decrease in GFR. The level of the KIM-1 and IL-18 molecules on the 3rd day of hospitalization in the first group was higher than the corresponding indicator of the comparison group. Also, patients with AKI showed a significant increase in the level of NTproBNP and MAU in the early period of kidney damage. When studying correlations, it was revealed that the level of MAU in the group with AKI is interrelated with the indicator of C-reactive protein and creatinine on the 3rd day of hospitalization. Also, a positive statistically significant correlation was found between the level of the KIM-1 molecule, IL-18, creatinine level on the 3rd day of hospitalization, NTproBNP and the level of MAU. During the follow-up of patients 6 months and a year after discharge, unstable angina pectoris, myocardial infarction, as well as progression of chronic heart failure were more often detected in the group with AKI. A persistent decrease in kidney function after a year was observed in most patients of the first group.Conclusion. The data obtained indicate the influence of acute kidney injury on the progression of renal dysfunction and the frequency of recurrent cardiovascular events, which is confirmed by the obtained associative relationships of the level of the KIM-1 molecule, creatinine and GFR with the prognosis of cardiovascular disease.

The preoperative plasma histamine level as a possible protective biomarker for postoperative acute kidney injury

Acute kidney injury (AKI) is a life-threatening complication of acute type A aortic dissection (ATAAD) patients. Increasing evidence suggests that histamine ameliorates the pathology of renal injury. However, data on the association between histamine levels and postoperative AKI in ATAAD patients are limited. The purpose of our study was to explore the incidence and independent risk factors of postoperative AKI, with special emphasis on the relationship between preoperative plasma histamine levels and the severity of postoperative ATAAD-AKI. This retrospective single-center study evaluated 160 patients with ATAAD admitted to the Beijing Anzhen Hospital aortic surgery database between April 2020 and December 2021. Univariate and multivariate logistic regression analyses were performed to determine the potential risk factors for postoperative ATAAD-AKI. A subgroup analysis was performed to investigate the association between preoperative plasma histamine levels and the severity of postoperative ATAAD-AKI or continuous renal replacement therapy (CRRT). ATAAD-AKI occurred in 84 of 160 patients (52.5%), including 32 with stage 1 (38.1%), 14 with stage 2 (16.7%), 38 with stage 3 (45.2%), and 34 (21.3%) received postoperative CRRT. The in-hospital mortality rate was 19.0% (16/84) in the AKI group and 2.6% (2/76) in the non-AKI group (P = .02). Preoperative lower plasma histamine levels (odds ratio [OR], 1.31; 95% confidence interval [CI], 1.10-1.52; P = .004) were an important factor related to postoperative ATAAD-AKI in multivariate logistic regression analysis. Subgroup analysis revealed that low preoperative plasma histamine level was independently associated with postoperative ATAAD-AKI (stage 3) (OR, 1.38; 95% CI, 1.10-1.73; P = .005) and CRRT (OR, 1.44; 95% CI, 1.13-1.79; P = .008). Low preoperative plasma histamine level was an independent prognostic indicator of postoperative AKI in patients with ATAAD, especially for postoperative AKI (stage 3) and CRRT. Preoperative plasma histamine levels may serve as potential protective biomarkers of postoperative ATAAD-AKI.

Elevated levels of biomarkers of oxidative stress and renal injury linked to nitrogenous flame retardants exposure in e-waste dismantling site: A case study in China

Nitrogenous flame retardants (NFRs) have aroused worldwide public concern as their nephrotoxic effect. However, knowledge regarding the pathogenesis mechanism of their exposure to induce kidney injury remains largely unknown. In this study, eight NFRs, four oxidative stress biomarkers (OSBs), and one kidney injury biomarker, namely neutrophil gelatinase-associated lipocalin (NGAL), were measured in urine specimens collected from residents living around e-waste disassembly and reference areas, representing two exposure scenarios. Significant higher concentrations of Σ8NFR (median: 70.6 vs. 33.8 μg/g Cre) and five biomarkers (124 vs. 97.4 μg/g Cre) were found in urines of populations living in e-waste site compared to those in the reference site (p < 0.05). Primary NFRs exhibited significant positive associations with OSBs and NGAL regardless of the population examined, implying that chronic NFRs exposure could induce oxidative stress and kidney damage. By using structure equation model, we found that oxidative stress, particularly DNA and RNA oxidation mediated 16.1% of the total effect of NFRs on NGAL in e-waste related people, but not on the general population. Overall, this study suggests long-term chronic exposure to NFRs can induce oxidative stress and renal injury in humans but the pathogenesis mode may be scenario-specific.

Urinary Neutrophil Gelatinase-Associated Lipocalin, Cystatin C and Clusterin as Biomarkers for Acute Kidney Injury in Cattle with Tropical Theileriosis

Urinary Neutrophil Gelatinase-Associated Lipocalin, Cystatin C and Clusterin as Biomarkers for Acute Kidney Injury in Cattle with Tropical Theileriosis

Urinary Proteomics Unveil Prognostic Biomarkers in Acute Kidney Injury with Decompensated Cirrhosis

Urinary Proteomics Unveil Prognostic Biomarkers in Acute Kidney Injury with Decompensated Cirrhosis

Marathon running and cell-cycle arrest biomarkers of acute kidney injury.

Endurance exercise is known to cause a rise in serum creatinine. It is not known to what extent this rise reflects renal stress and a potential acute kidney injury (AKI). Increases in Insulin Like Growth Factor Binding Protein 7 (IGFBP7) and Tissue Inhibitor of Metalloprotinases-2 (TIMP-2), urinary biomarkers of cell cycle arrest and renal stress, are associated with the development of AKI in clinical populations. Repeated measures study. Runners were recruited at the 2019 Brighton Marathon (UK) and provided urine and blood samples at baseline, immediately post-race and 24 h post-race. Serum creatinine, urinary creatinine and urinary IGFBP7 and TIMP-2 were analysed from the samples. Seventy nine participants (23 females, 56 males), aged 43 ± 10 yrs. (mean ± SD), finish time 243 ± 40mins were included for analysis. Serum creatinine increased over the race by 40 ± 26% (p < 0.001), TIMP-2 increased by 555 ± 697% (p < 0.001) and IGFBP7 increased by 1094 ± 1491% (p < 0.001) over the race. A subset of twenty-two participants supplied samples 24 h post-race, reporting values similar to baseline for all variables. This study is the first to report large rises in IGFBP7 and TIMP-2 following marathon running. This suggests that rises in creatinine are not fully explained by changes in production and clearance and marathon running induces a state of kidney stress and potential injury.

Early diagnostic biomarkers for acute kidney injury using cisplatin-induced nephrotoxicity in rat model

Chronic kidney diseases (CKD) caused by acute kidney injury (AKI) results rapid and reversible loss in renal function. A real-time, highly accurate, and sensitive acute kidney injury biomarker is urgently required in order to keep these patients alive and prevent end stage renal disease and related complications that include hypertension, fluid and electrolyte retention, metabolic acidosis, anemia, stroke etc. This study was designed to develop a specific and sensitive model for the early identification of renal damage in male albino rats. Using a single intraperitoneal dose of cisplatin (10 mg/kg body weight) to the rats, the various duration-dependent nephrotoxic activities were compared using multiple physiological, biochemical, genomic, and histopathological markers. We looked into when renal dysfunction would start occurring after receiving a single high dose of cisplatin while blood urea nitrogen (BUN) and serum creatinine (sCr) remained normal. Following a single cisplatin injection, various measurements were taken in plasma, urine, and/or kidney tissues of rats euthanized on days 1, 2, 3, 5, and 7. When the urine kidney injury molecule (KIM-1), interleukine 18 (IL-18), nephrin, neutrophil gelatinase-associated lipocalin (NGAL) and serum cystatin C (Cys C) levels are greatly raised on day 3 after cisplatin treatment, BUN and sCr levels remain normal. Nephrotoxicity of cisplatin is also indicated by the upregulated mRNA expression of KIM-1, IL-18, Cys C, and NGAL and downregulated expression of nephrin in kidney tissue at very initial stage. Protein expression of KIM-1, IL-18 and NGAL level of kidney tissues was upregulated indicated confirmatory results done by western blot. Utilising an array of kidney impairment indicators has emerged as an earlier, more effective, and more reliable technique to diagnose AKI when compared to the most sophisticated signs now available.

Urinary Mitochondrial Deoxyribonucleic Acid: A Novel Biomarker of Coronavirus Disease 2019-associated Acute Kidney Injury in Renal Transplant Recipients

Abstract Background: Acute kidney injury (AKI) is one of the common manifestations of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection. An early identification of AKI is of paramount importance to modulate the management of AKI, limiting the severity, avoiding nephrotoxic medicines, and modifying the drug dose depending on renal function. Aim: To determine the utility of urinary mitochondrial deoxyribonucleic acid (umt-DNA) and neutrophil gelatinase-associated lipocalin (NGAL) in predicting coronavirus disease 2019 (COVID-19)-associated AKI and mitochondrial stress. Materials and Methods: Live-related renal transplant recipients (RTRs) (n = 66), who acquired SARS-CoV-2 infection and were admitted to a COVID hospital were included and subclassified into AKI (n = 19) with &gt; 1.5-fold rise in serum creatinine level from the pre-COVID-19 serum creatinine level, and non-AKI (n = 47) whose serum creatinine value remained stable, or a rise of &lt;1.5-fold of the baseline values of pre-COVID-19. A 50 mL urine sample was collected and urinary mt-DNA and NGAL was determined by the reverse transcriptase-polymerase chain reaction and enzyme-linked immunosorbent assays methods. Results: Both the urinary mitochondrial gene NADH dehydrogenase (ND-1) and NGAL level were significantly higher in the AKI group compared to non-AKI. The mean ND-1 gene Ct in the AKI group was (19.44 ± 2.58 a.u) compared to non-AKI (21.77 ± 3.60; P = 0.013). The normalized ND-1 gene cycle of threshold (Ct) in AKI was 0.79 ± 0.11 a.u compared to non-AKI (0.89 ± 0.14; P = 0.007). The median urinary NGAL level in AKI group was (453.53; range, 320.22–725.02, 95% confidence interval [CI]) ng/mL compared to non-AKI (212.78; range, 219.80–383.06, 95% CI; P = 0.015). The median urine creatinine normalized uNGAL was 4.78 (0.58–70.39) ng/mg in the AKI group compared to 11.26 ng/mg (0.41–329.71) in the non-AKI group. The area under curve of ND-1 gene Ct was 0.725, normalized ND-1 Ct was 0.713, uNGAL was 0.663, and normalized uNGAL was 0.667 for detecting the AKI and mitochondrial stress. Conclusions: Urinary mt-DNA quantification can detect the post-COVID mitochondrial distress with higher sensitivity than uNGAL in RTRs.

Comparison of Fixed and Ramping Voltage Extracorporeal Shockwave Lithotripsy with Acute Kidney Injury Biomarkers: Prospective Randomized Clinical Study

Comparison of Fixed and Ramping Voltage Extracorporeal Shockwave Lithotripsy with Acute Kidney Injury Biomarkers: Prospective Randomized Clinical Study