N-acetyl-β-D-glucosaminidase Research Articles

Renal, gastrointestinal, and hemostatic effects of oral administration of meloxicam to Hispaniolan Amazon parrots (Amazona ventralis).

To investigate renal, gastrointestinal, and hemostatic effects associated with oral administration of multiple doses of meloxicam to healthy Hispaniolan Amazon parrots (Amazona ventralis). 12 Hispaniolan Amazon parrots. Birds were assigned to receive meloxicam oral suspension (1.6 mg/kg, PO, q 12 h) and 2.5 mL of tap water inserted into the crop by use of a gavage tube (n = 8) or the equivalent volume of tap water only (control group; 4) for 15 days. Urine and feces were collected 2 hours after treatment administration each day. Feces were evaluated for occult blood. Results of a CBC and serum biochemical analysis and measured N-acetyl-β-d-glucosaminidase (NAG) activity and whole blood clotting time were evaluated before, during, and after completion of treatments. Results of urinalysis and measured urine NAG activity were also evaluated. Birds treated with meloxicam had a significant increase in number of WBCs and decrease in PCV from before to after treatment. The PCV also decreased significantly, compared with results for the control group; however, WBC count and PCV for all birds remained within reference ranges throughout the study. One parrot treated with meloxicam had a single high value for urine NAG activity. Meloxicam administered orally at the dosage used in this study caused no apparent negative changes in several renal, gastrointestinal, or hemostatic variables in healthy Hispaniolan Amazon parrots. Additional studies to evaluate adverse effects of NSAIDs in birds will be needed.

Urinary N-acetyl-β-D-glucosaminidase (NAG) activity in the early detection of diabetic nephropathy

One of the serious outcomes of diabetes mellitus is nephropathy. Measurement of microalbuminuria is a routine clinical practice for screening the diabetic nephropathy, but the injury to the kidney may be happening even without microalbuminuria. The association between urinary enzyme activities of N-acetyl-β-D-glucosaminidase (NAG) and angiotensin converting enzyme (ACE) and urine microalbumin was assessed in this study to define the possible biofactor for detection of early diabetic nephropathy. Urinary enzyme activities of NAG and ACE and urine microalbumin of 24 h, serum ACE, and some other clinical features are investigated in 35 type 2 diabetic patients. Glycated hemoglobin (HbA1c), triglycerides, serum ACE, and urine NAG were significantly elevated in diabetic groups compared to the healthy controls. There was no relation between urine NAG and microalbuminuria except in the group of diabetic patients which had urine NAG activity upper than 25 IU/ml; there was a correlation between urine NAG and serum ACE. We may conclude that before the finding of microalbumin in urine, the elevated urine NAG, as an early indicator of renal damage, is associated with serum ACE which is related to kidney vascular microangiopathies.

Urinary biomarker N-acetyl-β-D-glucosaminidase can predict severity of renal damage in diabetic nephropathy.

BackgroundDiabetic nephropathy is a clinical diagnosis where proteinuria is present in a patient with diabetes. Early intervention can significantly improve the prognosis. However, imprecision of the currently available biomarkers have impaired effective therapies in a timely manner. Urinary N-acetyl-β-D-glucosaminidase (NAG) is excreted in abnormally high amounts in many renal diseases. The aim of this study was to evaluate urinary NAG as an early biomarker in detection of diabetic nephropathy and whether it parallels the severity of kidney damage in different stages of diabetic nephropathy.MethodsFifty patients with type 2 DM were classified into 3 groups (normoalbuminurea, microalbuminurea and macroalbuminurea) and 10 healthy subjects served as a control group. Urinary NAG, albumin and creatinine were measured. Blood urea, serum creatinine, serum albumin, total proteins, serum cholesterol, alanine aminotransferase (ALT), aspartate aminotransferase (AST), fasting and postprandial blood glucose, HbA1c and creatinine clearance were measured for all subjects.ResultsAll diabetic patients had a significantly higher level of urinary NAG compared to control. NAG value increased in parallel with the severity of renal involvement.ConclusionUrinary NAG expresses the degree of renal impairment in diabetic nephropathy.

Association between pulse wave velocity and a marker of renal tubular damage (N-acetyl-β-D-glucosaminidase) in patients without diabetes.

The authors assessed the association between the ratio of urinary activity of N-acetyl-β-D-glucosaminidase (NAG) to creatinine and the brachial-ankle pulse wave velocity (baPWV) in patients without overt diabetes mellitus (DM). This was a cross-sectional study of 233 patients who had an estimated glomerular filtration rate (eGFR) ≥30 mL/min/1.73 m(2) and no history of kidney disease. Patients were divided into two groups: high NAG group (>5.8 U/g creatinine) and low NAG group (≤5.8 U/g creatinine). Mean baPWVs of the high NAG group were significantly higher than those of the low NAG group in both the eGFR ≥30 and <60 tertiles and the eGFR ≥60 and <90 tertiles. The baPWV was positively correlated with NAG in all patients (r=0.341, P<.001). Stepwise multivariate regression analysis showed that the baPWV was significantly related with NAG, age, and systolic blood pressure. Elevated NAG is related to elevated arterial stiffness in patients without DM.

Urinary early kidney injury molecules in children with beta-thalassemia major

Background: The aim of this study was to investigate novel urinary biomarkers including N-acetyl-β-d-glucosaminidase (NAG), neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), and liver-type fatty acid binding protein (L-FABP) in children with β-thalassemia major (β-TM). Materials and methods: Totally, 52 patients (29 boys, 23 girls) with β-TM and 29 healthy controls (3–17 years) were included. Various demographic characteristics and blood transfusions/year, disease duration, and chelation therapy were recorded. Serum urea, creatinine, electrolytes, and ferritin and urinary creatinine, protein, calcium, phosphorus, sodium, potassium, and uric acid in first morning urine samples were measured and estimated glomerular filtration rate (eGFR) was calculated. Routine serum and urinary biochemical variables, urinary NAG to Creatinine (UNAG/Cr), UNGAL/Cr, UKIM-1/Cr, and UL-FABP/Cr ratios were determined. Results: Patients had similar mean serum urea, creatinine and eGFR levels compared with controls (p > 0.05 for all). The mean urinary protein to creatinine (UProtein/Cr) ratio was significantly higher in patients compared to the healthy subjects (0.13 ± 0.09 mg/mg and 0.07 ± 0.04 mg/mg, respectively; p < 0.001). Significantly increased UNAG/Cr (0.48 ± 0.58 vs. 0.23 ± 0.16, p = 0.026) and UNGAL/Cr (22.1 ± 18.5 vs. 11.5 ± 6.17, p = 0.01) ratios were found in β-TM patients compared with healthy controls. However, no differences were found in serum and urinary electrolytes or UKIM-1/Cr and UL-FABP/Cr ratios between patients and controls (p > 0.05). Significant correlations were found between urinary biomarkers and urinary electrolytes (p < 0.05). Conclusions: Our results suggest that urinary NAG and NGAL may be considered to be reliable markers to monitor renal injury in β-TM patients.

Variation of nephrotoxicity biomarkers by urinary storage condition in rats.

Recently, there has been an increase in the use of several nephrotoxicity biomarkers in preclinical experiments. In addition, it has been indicated that the result may have been influenced by secondary factors, such as sample storage condition or storage period. In this study, we have assessed the variation in urinary nephrotoxicity biomarkers as a result of urine storage conditions and storage period of the urine. Urine was sampled from specific pathogen-free Sprague-Dawley rats (19 weeks old), which were housed individually in hanged stainless steel wire mesh cages. Urine was stored at 20℃, at 4℃, or at −70℃ after sampling. The levels of the biomarkers such as beta-2 microglobulin (B2M), cystatin-C (Cys-C), N-acetyl-β- D-glucosaminidase (NAG), micro albumin (MA), micro protein (MP) were measured at 6, 24, 48 and 144 hr after sampling. The B2M level was significantly decreased at 6, 24, 48, and 144 hr compared to 0 hr at −70℃ (p < 0.05, p < 0.01, p < 0.05, and p < 0.05, respectively) and 24 and 144 hr at 20℃ (p < 0.01, p < 0.01, respectively). The Cys-C level was significantly decreased at 144 hr compared to 0 hr at 4℃ (p < 0.01), at 20℃ (p < 0.05) and at 70℃ (p < 0.01). MP and MA levels were not different for 144 hr in all storage conditions. Taken together, B2M and Cys-C levels were modulated by storage temperature and period. For the enhancement of test accuracy, it is suggested that strict protocols be established for samples to minimize the effects of the storage conditions on the detected levels of biomarkers.

Novel biomarkers of acute kidney injury: time for implementation?

Novel biomarkers of acute kidney injury: time for implementation?

Temporal changes in urinary levels of cadmium, N-acetyl-β-d-glucosaminidase and β2-microglobulin in individuals in a cadmium-contaminated area

Cadmium (Cd) is a metal that is toxic to renal tubules. If renal tubules are damaged by Cd, urinary excretion of N-acetyl-β-D-glucosaminidase (NAG) and beta 2-microglobulin (β2-MG) increases. The aim of this study was to describe the changing patterns of urinary Cd, NAG, and β2-MG levels over a 3-year period in individuals living in a Cd-contaminated area. This follow-up study included 191 residents (65.6±9.3 years) who were living in the vicinity of a copper refinery. Urinary levels of Cd, NAG activity, and β2-MG levels were measured, and their determinants and changing patterns were analyzed statistically. The natural logarithm of urinary Cd levels decreased significantly over time. Sex and intake of locally cultivated rice were significant determinants of urinary Cd concentration. Urinary NAG activity decreased over time. Age and urinary Cd concentration were significant determinants of urinary NAG activity in subjects with urinary Cd concentrations >5μg/g creatinine. In subjects whose urinary Cd concentrations were >2μg/g creatinine, diabetes was found to be a significant risk factor for high urinary NAG activity. The slope for temporal changes in urinary β2-MG levels was negative in subjects whose urinary Cd levels were <2μg/g creatinine but was positive in those whose urinary Cd levels were 2–5μg/g creatinine or >5μg/g creatinine. The urinary β2-MG levels found in individuals whose urinary Cd levels were >2μg/g creatinine suggest that previous Cd-induced renal tubular damage had occurred.

Trypanosoma cruzi antigens induce inflammatory angiogenesis in a mouse subcutaneous sponge model

Acute inflammation and angiogenesis are persistent features of several pathological conditions induced by biological agents leading to the resolution of local and systemic events. Glycoproteins derived from the protozoan Trypanosoma cruzi are suggested to mediate angiogenesis induced by inflammatory cells with still undescribed mechanisms. In this study, we investigated the effects of total antigen from trypomastigote forms of T. cruzi (Y strain), inoculated in sponges 24h after implantation in mice, on angiogenesis, inflammatory cell pattern and endogenous production of inflammatory and angiogenic mediators on days 1, 4, 7 and 14 post-implant. There was an increase in hemoglobin content and in the number of blood vessels associated with T. cruzi antigen stimuli on the 14th day, assessed by the hemoglobin of the implants and by morphometric analysis. However, these antigens were not able to increase type I collagen content on the 14th day. Parasite antigens also induced high production of vascular endothelial growth factor (VEGF) and inflammatory mediators TNF-alpha, CCL2 and CCL5 on the 7th day in sponges when compared to the unstimulated group. Neutrophils and macrophages were determined by measuring myeloperoxidase (MPO) and N-acetyl-β-d-glucosaminidase (NAG) enzyme activities, respectively. Only NAG was increased after stimulation with antigens, starting from day 4 and peaking at day 7. Together, these data showed that antigens from the Y strain of T. cruzi are able to promote inflammatory neovascularization probably induced by macrophage-induced angiogenic mediators in T. cruzi antigen-stimulated sponges in Swiss mice.

Association of urinary KIM-1, L-FABP, NAG and NGAL with incident end-stage renal disease and mortality in American Indians with type 2 diabetes mellitus.

Kidney injury molecule 1 (KIM-1), liver fatty acid-binding protein (L-FABP), N-acetyl-β-D-glucosaminidase (NAG) and neutrophil gelatinase-associated lipocalin (NGAL) are urinary biomarkers of renal tubular injury. We examined their association with incident end-stage renal disease (ESRD) and all-cause mortality in American Indians with type 2 diabetes. Biomarker concentrations were measured in baseline urine samples in 260 Pima Indians who were followed for a median of 14 years. HRs were reported per SD of creatinine (Cr)-normalised log-transformed KIM-1, NAG and NGAL, and for three categories of L-FABP. During follow-up, 74 participants developed ESRD and 101 died. Median concentrations of KIM-1/Cr, NAG/Cr and NGAL/Cr and the proportion of detectable L-FABP were highest in those with macroalbuminuria (p < 0.001 for KIM-1/Cr, NAG/Cr and L-FABP; p = 0.006 for NGAL/Cr). After multivariable adjustment, NGAL/Cr was positively associated with ESRD (HR 1.59, 95% CI 1.20, 2.11) and mortality (HR 1.39, 95% CI 1.06, 1.82); L-FABP/Cr was inversely associated with ESRD (HR [for highest vs lowest tertile] 0.40, 95% CI 0.19, 0.83). Addition of NGAL/Cr to models that included albuminuria and glomerular filtration rate increased the c-statistic for predicting ESRD from 0.828 to 0.833 (p = 0.001) and for death from 0.710 to 0.722 (p = 0.018). Addition of L-FABP/Cr increased the c-statistic for ESRD from 0.828 to 0.832 (p = 0.042). In Pima Indians with type 2 diabetes, urinary concentrations of NGAL and L-FABP are associated with important health outcomes, but they are unlikely to add to risk prediction with standard markers in a clinically meaningful way given the small increase in the c-statistic.

DisBa-01 inhibits angiogenesis, inflammation and fibrogenesis of sponge-induced-fibrovascular tissue in mice

Integrins are involved in a number of physio-pathological processes including wound healing, chronic inflammation and neoplasias. Blocking its activity is potentially of therapeutic value in these conditions. We investigated whether DisBa-01, a recombinant His-tag RGD-disintegrin from Bothrops alternatus snake venom, could modulate key events (inflammatory cell recruitment/activation, neovascularization and extracellular matrix deposition) of the proliferative fibrovascular tissue induced by polyether polyurethane sponge implants in mice. The hemoglobin content (μg/mg wet tissue), blood flow measurements (laser Doppler perfusion imaging) and number of vessels in the implants, used as indices of vascularization, showed that the disintegrin dose-dependently reduced angiogenesis in the implants relative to the Saline-treated group. DisBa-01 inhibited neutrophil and macrophage content as determined by the myeloperoxidase (MPO) and N-acetyl-β-D-glucosaminidase (NAG) activities, respectively. Similarly, down regulation of the fibrogenic component studied (collagen deposition) was observed in DisBa-01-treated implants. VEGF, bFGF, TNF-α, CXCL1 and CCL2 levels were also decreased by the disintegrin. The inhibitory effect of this αvβ3-blocking disintegrin on the angiogenic, inflammatory, and fibrogenic components of the fibrovascular tissue induced by the synthetic matrix extends the range of DisBa-01 actions and may indicate its therapeutic potential in controlling angiogenesis in fibroproliferative diseases.

PP-095 A RARE PRESENTATION OF HELLP SYNDROME AT 16TH WEEK OF GESTATION

Background: The prospects for children born with thalassemia currently include increased life expectancy and minimal or no organ damage. With the advances in the care of patients with β-thalassemia major (β-TM), there is a remarkable increasing prevalence of disrupted kidney functions due to various supposed factors. Therefore, early recognition of those likely to progress has become increasingly substantial. Serum creatinine and GFR, the current main diagnostic biomarkers, however, have several shortcomings for the evaluation of renal dysfunction. The aim of this study was to investigate novel urinary biomarkers including N-acetyl-b-Dglucosaminidase (NAG), neutrophil gelatinase-associated lipocalin (NGAL) urinary kidney injury molecule-1 (KIM-1), and liver-type fatty acid binding protein (L-FABP), to determine renal involvement in children with β-thalassemia major (β-TM). Methods: This prospective study involves measurements of the serum and urinary biochemical parameters, complete blood count, novel urinary biomarkers including urinary NAG to Creatinine (UNAG/Cr), UNGAL/Cr, UKIM-1/Cr and UL-FABP/Cr ratios and various demographic factors in 52 β-TM children and 29 healthy controls with comparable age and sex. Results: Patients had similar mean serum urea, creatinine and eGFR levels compared with controls (p>0.05 for all). The mean urinary protein to creatinine (UProtein/Cr) ratio was significantly higher in patients compared to the healthy subjects (0.13±0.09 mg/mg and 0.07±0.04 mg/mg, respectively; p=0.05). Significant correlations were found between urinary biomarkers and urinary electrolytes. Conclusion: Our results suggest that urinary NAG and NGAL may be

Mortality prediction by acute kidney injury biomarkers in comparison with serum creatinine

Objectives: To investigate the performance of acute kidney injury (AKI) biomarkers for mortality prediction.Materials and methods: Cutoff values of urinary L-type fatty acid-binding protein (L-FABP) and N-acetyl-β-d-glucosaminidase (NAG) for AKI diagnosis in ICU were determined in the derivation cohort. The performance of these AKI biomarkers for mortality prediction was evaluated in the validation cohort with stratification of serum-creatinine based AKI diagnosis.Results: Mortality in the AKI patients diagnosed by serum creatinine was increased remarkably when urinary L-FABP and NAG were positive.Conclusions: These AKI biomarkers can specifically detect high-risk patients among creatinine-base diagnosed AKI.

PP-096 URINARY EARLY KIDNEY INJURY MOLECULES IN CHILDREN WITH BETA-THALASSEMIA MAJOR

Background: The aim of this study was to investigate novel urinary biomarkers including N-acetyl-β-d-glucosaminidase (NAG), neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule...

Tubular reabsorption of high, middle and low molecular weight proteins according to the tubulo-interstitial damage marker N-acetyl-β-D-glucosaminidase in glomerulonephritis.

Proteinuria, the hallmark of glomerular diseases, is an independent predictor of end-stage renal disease (ESRD) progression. Proteinuria is a mixture of proteins of different molecular weight (MW) dependent on alterations of glomerular filtration barrier (GFB) and reabsorption impairment by proximal tubular epithelial cells (PTECs). We aimed to evaluate the excretion of different-MW proteins according to the tubulo-interstitial damage marker N-acetyl-β-D-glucosaminidase (NAG) in glomerulonephritides (GNs). In 189 patients [idiopathic membranous nephropathy (IMN) n = 84, primary focal segmental glomerulosclerosis (FSGS) n = 48, crescentic IgA nephropathy (CIgAN) n = 37, minimal change disease (MCD) n = 20] several urinary proteins were measured at biopsy: α2-macroglobulin/creatinine ratio; fractional excretion of IgG, transferrin, albumin and α1-microglobulin, and the NAG/creatinine ratio divided by estimated glomerular filtration rate (eGFR) (NAG/C/eGFR), as NAG excretion is dependent on functioning nephron mass. Protein excretion was compared between 4th vs. 1st quartile of NAG/C/eGFR. In IMN, FSGS and CIgAN high-MW proteins excretion (α2-macroglobulin, IgG) was greater than that of middle- (transferrin, albumin) and low-MW proteins (α1-microglobulin) in 4th vs. 1st quartile of NAG/C/eGFR; the mean fold excretion increase of high-MW proteins in 3 GNs was 74.9, higher than that of middle- (34.8) and low-MW proteins (12.0). Higher excretion of high-MW proteins may be dependent on lower reabsorption by PTECs. By contrast, in MCD the difference in excretion of different-MW proteins is probably due to high GFB selectivity. High-MW protein excretion is dependent on GFB alteration and reduced reabsorption; its prognostic significance is ominous because in several glomerular diseases progression is associated with high-MW protein excretion.

Curcumin prevents maleate-induced nephrotoxicity: Relation to hemodynamic alterations, oxidative stress, mitochondrial oxygen consumption and activity of respiratory complex I

The potential protective effect of the dietary antioxidant curcumin (120 mg/Kg/day for 6 days) against the renal injury induced by maleate was evaluated. Tubular proteinuria and oxidative stress were induced by a single injection of maleate (400 mg/kg) in rats. Maleate-induced renal injury included increase in renal vascular resistance and in the urinary excretion of total protein, glucose, sodium, neutrophil gelatinase-associated lipocalin (NGAL) and N-acetyl β-D-glucosaminidase (NAG), upregulation of kidney injury molecule (KIM)-1, decrease in renal blood flow and claudin-2 expression besides of necrosis and apoptosis of tubular cells on 24 h. Oxidative stress was determined by measuring the oxidation of lipids and proteins and diminution in renal Nrf2 levels. Studies were also conducted in renal epithelial LLC-PK1 cells and in mitochondria isolated from kidneys of all the experimental groups. Maleate induced cell damage and reactive oxygen species (ROS) production in LLC-PK1 cells in culture. In addition, maleate treatment reduced oxygen consumption in ADP-stimulated mitochondria and diminished respiratory control index when using malate/glutamate as substrate. The activities of both complex I and aconitase were also diminished. All the above-described alterations were prevented by curcumin. It is concluded that curcumin is able to attenuate in vivo maleate-induced nephropathy and in vitro cell damage. The in vivo protection was associated to the prevention of oxidative stress and preservation of mitochondrial oxygen consumption and activity of respiratory complex I, and the in vitro protection was associated to the prevention of ROS production.

Dahuang Fuzi Decoction ameliorates tubular epithelial apoptosis and renal damage via inhibiting TGF-β1-JNK signaling pathway activation in vivo

Ethnopharmacological relevanceDahuang Fuzi Decoction (DFD) is a traditional well-prescribed formula for the treatment of chronic kidney disease (CKD) in China. This study was carried out to examine the effects of DFD in adenine-induced tubular epithelial apoptosis and renal damage, in comparison with allopurinol (AP), then to clarify the therapeutic mechanisms in vivo. Materials and methodsA rat model of renal damage was created by adenine. Rats in Normal and Vehicle groups received distilled water, while rats in DFD and AP groups received DFD and AP, respectively. Proteinuria; urinary N-acetyl-β-d-glucosaminidase (NAG) levels; the blood biochemical parameters; renal histopathology damage; transferase-mediated dUTP nick-end labeling (TUNEL)-staining; the key molecular protein expressions in mitochondrial and transforming growth factor (TGF)-β1-c-JunNH2-terminal kinase (JNK) pathways were examined, respectively. ResultsAdenine administration induced severe renal damages, as indicated by the mass proteinuria, the heavy urinary NAG, and the marked histopathological injury in tubules and interstitium. This was associated with the activation of TGF-β1-JNK signaling pathway and tubular epithelial apoptosis. DFD treatment, however, significantly prevented proteinuria and urinary NAG elevation, and attenuated tubular epithelial apoptosis. It suppressed the protein expressions of Bax and cleaved caspase-3, whereas it enhanced the protein expression of Bcl-2. Furthermore, it also suppressed the protein levels of TGF-β1 as well as phosphorylated-JNK (p-JNK). ConclusionDFD alleviated adenine-induced tubular epithelial apoptosis and renal damage in vivo, presumably through the suppression of TGF-β1-JNK pathway activation.

Identification of local angiogenic and inflammatory markers in the menstrual blood of women with endometriosis

The aim of this study was to evaluate the presence of myeloperoxidase (MPO), N-acetyl-β-D-glucosaminidase (NAG), tumor necrosis factor alpha (TNF-α) and vascular endothelial growth factor (VEGF) in peripheral and menstrual blood in women with (n=10) and without (n=7) endometriosis. NAG and MPO activities were evaluated by enzymatic methods, whereas TNF-α and VEGF by immunoassay. No significant differences were found for these markers, neither in menstrual nor in peripheral blood between groups. Menstrual blood NAG (P=0.039) and MPO (P=0.0117) activities in the endometriosis group were significantly higher than in peripheral blood. NAG and MPO presented positive linear correlation in peripheral (P=0.07; r=0.641) and menstrual blood (P=0.01; r=0.603). These findings point to the existence of an increased local inflammatory activity in women with endometriosis.

Malondialdehyde, antioxidant enzymes, and renal tubular functions in children with iron deficiency or iron-deficiency anemia.

We aimed to investigate the effects of iron deficiency (ID) or iron-deficiency anemia (IDA) on oxidative stress and renal tubular functions before and after treatment of children. A total of 30 children with a diagnosis of IDA constituted the IDA group and 32 children with a diagnosis of ID constituted the ID group. Control group consisted 38 age-matched children. Serum ferritin, soluble transferrin receptor (sTfR), serum, and urinary sodium (Na), potassium (K), calcium (Ca), phosphorus (P), creatinine (Cr), uric acid (UA), urinary N-acetyl-β-D-glucosaminidase (NAG) levels, and intra-erythrocyte malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) levels were measured before and after iron therapy in the IDA and ID groups, whereas it was studied once in the control group. We have divided the study group in groups according to age (infants <2 years, children 3-9 years, and adolescents 10-15 years). Patients with IDA (infant, adolescent) and ID (infant, children, and adolescent) had a significantly high level of MDA in post-treatment period in comparison to those of healthy control. Patients with IDA (children, adolescent) and ID (infant, children) had a significantly high level of pre-treatment GSH-Px than controls. Post-treatment SOD was lower in IDA (children and adolescent) groups than control and post-treatment CAT was lower in IDA and ID (adolescent) groups than control. These findings show that ferrous sulfate used in the treatment of ID or IDA could lead to oxidative stress; however, a marked deterioration of in proximal renal tubular functions was not seen.

Early prediction of acute kidney injury biomarkers after endovascular stent graft repair of aortic aneurysm: a prospective observational study

BackgroundAcute kidney injury (AKI) is a common and serious condition usually detected some time after onset by changes in serum creatinine (sCr). Although stent grafting to repair aortic aneurysms is associated with AKI caused by surgical procedures or the use of contrast agents, early biomarkers for AKI have not been adequately examined in stent graft recipients. We studied biomarkers including urinary neutrophil gelatinase-associated lipocalin (NGAL), blood NGAL, N-acetyl-β-d-glucosaminidase (NAG), microalbumin (Alb), and liver fatty acid-binding protein (L-FABP) as prospective early biomarkers for AKI in patients who had received stent graft repairs of aortic aneurysms.MethodsIn addition to pre-surgical sampling, at 2 to 6 h and at 1, 3 to 4, and 5 days or later (until stable) after surgery, urine and serum biomarkers were sampled from 47 patients who underwent stent graft repair of aortic aneurysms.ResultsUsing Acute Kidney Injury Network criteria, 6 (14%) of 42 retained patients developed AKI. NGAL corrected with urine Cr (NGAL/Cr) values demonstrated the best predictive value for AKI (97% specificity, 83% sensitivity at a 65.1 μg/gCr cutoff). The area under the receiver-operator characteristic curve of NGAL/Cr value 2 h after surgery was 0.9. Although NGAL/Cr, L-FABP corrected with urine Cr (L-FABP/Cr), L-FABP, NAG, and Alb corrected by urine Cr (Alb/Cr) all reached peak values before AKI detection by sCr in AKI patients, all biomarkers reached the cutoff value before AKI detection after adaption of cutoff value.ConclusionsAfter stent graft repair of aortic aneurysm, NGAL/Cr is a potentially useful early biomarker for AKI.