Serum and urine acute kidney injury biomarkers in asphyxiated neonates

2012 ◽  
Vol 27 (9) ◽  
pp. 1575-1582 ◽  
Author(s):  
Kosmas Sarafidis ◽  
Eleni Tsepkentzi ◽  
Eleni Agakidou ◽  
Elisavet Diamanti ◽  
Anna Taparkou ◽  
...  
2019 ◽  
Vol 6 (5) ◽  
pp. 1981
Author(s):  
Hawwa M.S. Siddiqua ◽  
Mathew John ◽  
V. C. Manoj ◽  
Rati Santhakumar

Background: Acute kidney injury (AKI) is a sudden onset of kidney failure or kidney damage that happens within a few hours or a few days and can also affect other organs such as brain, heart and the lungs. Hence early diagnosis and intervention is needed to improve the outcome of the children. In these studies this objective was to determine if cystatin C is an early marker indicative of renal dysfunction in critically ill children and to determine if Cystatin C can detect Acute kidney injury earlier than serum creatinine.Methods: This prospective cohort study was undertaken in PICU at Jubilee Mission Medical College from December 2016- May 2018. Blood samples were collected from 34 critically ill children for serum creatinine estimation at 0,24 and 48 hours of admission and serum and urine were collected for cystatin C estimation at admission. Children were categorized into AKI and NON-AKI based on pRIFLE criteria. Comparison of cystatin C values with serum creatinine was performed and Statistical analysis was done using IBM SPSS version 20.Results: A total of 34 critically ill children were enrolled in this study, out of which 12 children progressed to AKI during the course of illness according to modified Pediatric Risk, Injury, Failure, Loss, End Stage Renal Disease (pRIFLE) criteria. We found a strong positive correlation between cystatin C at 0 hours and serum creatinine at 48 hours among AKI groups.Conclusions: Serum and Urine cystatin C are early markers to diagnose AKI in critically ill children. Serum cystatin C is more sensitive than urine cystatin C for the diagnosis of AKI.


2020 ◽  
Vol 245 (16) ◽  
pp. 1474-1489
Author(s):  
Chandrashekar Annamalai ◽  
Rajesh N Ganesh ◽  
Pragasam Viswanathan

Acute kidney injury causes significant morbidity and mortality. This experimental animal study investigated the simultaneous impact of iron and vitamin D on acute kidney injury induced by iohexol, an iodinated, non-ionic monomeric radiocontrast agent in Wistar rats. Out of 36 healthy male Wistar rats, saline was injected into six control rats (group 1) and iohexol into the remaining 30 experimental rats (groups 2 to 6 comprising six rats each). Biochemical, renal histological changes, and gene expression of iron-regulating proteins and 1 α-hydroxylase were analyzed. Urinary neutrophil gelatinase-associated lipocalin (NGAL), serum creatinine, urine protein, serum and urine catalytic iron, 25-hydroxyvitamin D3, 1,25-dihydroxyvitamin D3, and tissue lipid peroxidation were assayed. Rats injected with iohexol showed elevated urinary NGAL (11.94 ± 6.79 ng/mL), serum creatinine (2.92 ± 0.91 mg/dL), and urinary protein levels (11.03 ± 9.68 mg/mg creatinine) together with histological evidence of tubular injury and iron accumulation. Gene expression of iron-regulating proteins and 1 α-hydroxylase was altered. Serum and urine catalytic iron levels were elevated (0.57 ± 0.17; 48.95 ± 29.13 µmol/L) compared to controls (0.49 ± 0.04; 20.7 ± 2.62 µmol/L, P < 0.001). Urine catalytic iron positively correlated with tissue peroxidation (r = 0.469, CI 0.122 to 0.667, P = 0.004) and urinary NGAL (r = 0.788, CI 0.620 to 0.887, P < 0.001). 25-hydroxyvitamin D3 (61.58 ± 9.60 ng/mL) and 1,25-dihydroxyvitamin D3 (50.44 ± 19.76 pg/mL) levels increased simultaneously. In a multivariate linear regression analysis, serum iron, urine catalytic iron, and tissue lipid peroxidation independently and positively predicted urinary NGAL, an acute kidney injury biomarker. This study highlights the nephrotoxic potential of catalytic iron besides demonstrating a concurrent induction of vitamin D endogenously for possible renoprotection in acute kidney injury. Impact statement This work provides in-depth insights on catalytic iron-induced cytotoxicity and the resultant triggering of endogenous vitamin D synthesis in experimental acute kidney injury. Our results reveal significantly elevated levels of catalytic iron culminating in oxidant-mediated renal injury and a concomitant increase in 1,25-dihdyroxyvitamin D3 levels. Also, changes in other iron-related proteins including transferrin, ferritin, and hepcidin were observed both in the serum as well as in their mRNA expression. We consider all these findings vital since no connection between catalytic iron and vitamin D has been established so far. Furthermore, we believe that this work provides new and interesting results, with catalytic iron emerging as an important target in ameliorating renal cellular injury, possibly by timely administration of vitamin D. It also needs to be seen if these observations made in rats could be translated to humans by means of robust clinical trials.


Author(s):  
Stephen Wade Standage ◽  
Shenyuan Xu ◽  
Lauren Brown ◽  
Qing Ma ◽  
Adeleine Koterba ◽  
...  

Sepsis-associated acute kidney injury (SA-AKI) is a significant problem in the critically ill that causes increased death. Emerging understanding of this disease implicates metabolic dysfunction in its pathophysiology. This study sought to identify specific metabolic pathways amenable to potential therapeutic intervention. Using a murine model of sepsis, blood and tissue samples were collected for assessment of systemic inflammation, kidney function, and renal injury. Nuclear magnetic resonance (NMR)-based metabolomics quantified dozens of metabolites in serum and urine which were subsequently submitted to pathway analysis. Kidney tissue gene expression analysis confirmed implicated pathways. Septic mice had elevated circulating levels of inflammatory cytokines and increased levels of blood urea nitrogen and creatinine, indicating both systemic inflammation and poor kidney function. Renal tissue showed only mild histologic evidence of injury in sepsis. NMR metabolomic analysis identified the involvement of mitochondrial pathways associated with branched-chain amino acid (BCAA) metabolism, fatty acid oxidation, and de novo nicotinamide adenine dinucleotide (NAD+) biosynthesis in SA-AKI. Renal cortical gene expression of enzymes associated with those pathways was predominantly suppressed. Similar to humans, septic mice demonstrate renal dysfunction without significant tissue disruption, pointing to metabolic derangement as an important contributor to SA-AKI pathophysiology. Metabolism of BCAAs and fatty acids and NAD+ synthesis, which all center on mitochondrial function, appear to be suppressed. Developing interventions to activate these pathways may provide new therapeutic opportunities for SA-AKI.


2010 ◽  
Vol 37 (3) ◽  
pp. 493-501 ◽  
Author(s):  
Annick A. N. M. Royakkers ◽  
Johanna C. Korevaar ◽  
Jeroen D. E. van Suijlen ◽  
Lieuwe S. Hofstra ◽  
Michael A. Kuiper ◽  
...  

2016 ◽  
Vol 102 (1) ◽  
pp. 91-96 ◽  
Author(s):  
James McCaffrey ◽  
Ajaya Kumar Dhakal ◽  
David V Milford ◽  
Nicholas J A Webb ◽  
Rachel Lennon

Acute kidney injury (AKI) is a common condition in children admitted to hospital and existing serum and urine biomarkers are insensitive. There have been significant developments in stratifying the risk of AKI in children and also in the identification of new AKI biomarkers. Risk stratification coupled with a panel of AKI biomarkers will improve future detection of AKI, however, paediatric validation studies in mixed patient cohorts are required. The principles of effective management rely on treating the underlying cause and preventing secondary AKI by the appropriate use of fluids and medication. Further therapeutic innovation will depend on improving our understanding of the basic mechanisms underlying AKI in children.


2019 ◽  
Vol 25 (10) ◽  
pp. 1122-1133
Author(s):  
Mustafa M. Sinna ◽  
Faris M.N. Altaf ◽  
Osama F. Mosa

Background: High global incidence of acute kidney injury (AKI) is an observable complication in critically ill patients. Long-term disease and medication complexity contribute to devastating chronic kidney disease (CKD), diminishing quality of life. Objective: To establish new biomarkers to guide patient care and facilitate novel therapeutics development. Methods: Serum and urinary levels of creatinine, CysC, and NGAL were estimated in 86 renal patients and compared with healthy controls for AKI and CKD categorization. Creatinine and CysC measurements were used to estimate GFR. Kidney biopsies were prepared for light microscopy for further characterization. Patients’ demographic data were used in group association studies. Results: Thirty-six patients met the criteria for AKI and 50 for CKD. Both mean serum and urine creatinine levels were significantly elevated by 2.8 and 2.6, respectively, from baseline in 48 h in the AKI group but not CKD group. Mean serum Cystatin C (CysC) values were higher than controls but similar in both disease states, while urine levels were slightly higher in CKD patients, and remained steady by the end of the follow-up (EF-Up). Further, a significant 2.9-fold and 5.5-fold (p=0.001) increase in serum NGAL in AKI and CKD, respectively, and a dramatic 7.1-factor reduction in AKI group, but no appreciable change in the CKD group from admission to EF-Up were observed. Similarly, urine NGAL level for AKI and CKD increased 3.2-fold and 6-fold respectively, on admission, which decreased moderately with the AKI group (2.5-fold) but increased by a factor of 1-8 (10.7- fold; p=0.001) at EF-Up. ROC assessment curve revealed relatively higher NGAL performance at good predictive values than CysC (p < 0.009). Conclusion: Our data demonstrated creatinine elevation by a factor > 2 in 48 h in AKI group but not CKD group, which returned close to normal levels by the EF-Up, an indication of abrupt renal injury in AKI, compared with a persistent effect in the CKD group. Both serum and urine NGAL sensitivity and specificity provided powerful discriminative tool between AKI and CKD by reduction in the AKI group and an increase in the CKD group by the EF-UP, thus, contributing in establishing the basis for AKI and CKD classification. CysC, however, displayed less sensitivity than NGAL, indicating effects by enigmatic non-specific factors.


2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Pham Ngoc Huy Tuan ◽  
Dao Bui Quy Quyen ◽  
Huynh Van Khoa ◽  
Nguyen Duc Loc ◽  
Pham Van My ◽  
...  

Background. To evaluate the ratio of acute kidney injury (AKI) to chronic kidney disease (CKD) in sepsis-associated acute kidney injury (SA-AKI) patients of the intensive care unit (ICU) and predictive value of neutrophil gelatinase-associated lipocalin (NGAL) measured at the admission time in the progression of AKI to CKD. Methods. A study of 121 consecutive adult patients admitted to the intensive care unit (ICU) diagnosed as SA-AKI. AKI and CKD were defined based on Kidney Disease: Improving Global Outcomes (KDIGO) criteria. Glomerular filtration rate (GFR) was calculated by the CKD-EPI formula. Serum and urine NGAL was measured using the BioVendor Human Lipocalin-2/NGAL ELISA with a blood sample taken at hospital admission time. Results. The ratio of AKI to CKD in SA-AKI patients was 22.3%. Mean concentration of serum and urine NGAL in AKI to the CKD group was 790.99 ng/ml and 885.72 ng/ml, higher significantly than those of recovery patients (351.86 ng/ml and 264.68 ng/ml), p<0.001. eGFR, both serum and urine NGAL had a predictive value for AKI to CKD (eGFR: AUC=0.857, Se=74.1%, Spe=92.6%, p<0.001. Serum NGAL: AUC=0.868, Se=77.8%, Spe=91.5%. Urine NGAL: AUC=0.869, Se=77.8%, Spe=92.6%, p<0.001. Conclusion. Serum and urine NGAL, measuring at hospital admission time, were good prognostic biomarkers of AKI to CKD in SA-AKI patients.


2018 ◽  
Vol 18 (1) ◽  
Author(s):  
Zhenjiang Bai ◽  
Fang Fang ◽  
Zhong Xu ◽  
Chunjiu Lu ◽  
Xueqin Wang ◽  
...  

2021 ◽  
Vol 8 ◽  
pp. 205435812110196
Author(s):  
Erick D. McNair ◽  
Jennifer Bezaire ◽  
Michael Moser ◽  
Prosanta Mondal ◽  
Josie Conacher ◽  
...  

Background: Cardiac surgery–associated acute kidney injury (AKI) is an adverse outcome that increases morbidity and mortality in patients undergoing cardiac surgical procedures. To date, the use of serum creatinine levels as an early indicator of AKI has limitations because of its slow rise and poor predictive accuracy for renal injury. This delay in diagnosis may lead to prolonged initiation in treatment and increased risk for adverse outcomes. Objective: This pilot study explores serum and urine matrix metalloproteinases (MMPs)-2 and MMP-9 and their association, and potentially earlier detection of AKI in patients following cardiopulmonary bypass (CPB)–supported cardiac surgery. We hypothesize that increased activity of serum and urine levels MMP-2 and/ or MMP-9 are associated with AKI. Furthermore, MMP-2 and/ or MMP-9 may provide earlier identification of AKI as compared with serum levels of creatinine. Methods: During the study period, there were 150 CPB-supported surgeries, 21 of which developed AKI according to the Kidney Disease Improving Global Outcomes criteria. We then selected a sample of 21 matched cases from those patients who went through the surgery without developing AKI. Primary outcomes were the measurement via gel zymography of the serum and urine activity of MMP-2 and MMP-9 drawn at the following intervals: pre-CPB; 10-minute post-CPB; and 4-hour post-CPB time points. Secondary variables were the measurement of serum creatinine, intensive care unit (ICU) fluid balance, and length of ICU stay. Results: At the 10-minute and 4-hour post-CPB time points, the serum MMP-2 activity of AKI patients were significantly higher as compared with non-AKI patients ( P < .001 and P = .004), respectively. Similarly, at the 10-minute and 4-hour post-CPB time points, the serum MMP-9 activity of AKI patients was significantly higher as compared with non-AKI patients ( P = .001 and P = .014), respectively. The activity of urine MMP-2 and MMP-9 of AKI patients was significantly higher as compared with non-AKI patients at all 3 time points ( P = .004, P < .001, P < .001), respectively. Conclusion: Although the pilot study may have limitations, it has demonstrated that the serum and urine levels of activity of MMP-2 and MMP-9 are associated with the clinical endpoint of AKI and appear to have earlier rising levels as compared with those of serum creatinine. Furthermore, in depth, exploration is underway with a larger sample size to attempt validation of the analytical performance and reproducibility of the assay for MMP-2 and MMP-9 to aid in earlier diagnosis of AKI following CPB-supported cardiac surgery.


Sign in / Sign up

Export Citation Format

Share Document