OBJECTIVETo estimate the biological exposure limit (BEL) using benchmark dose (BMD) based on two sets of data from occupational epidemiology.

METHODSCadmium-exposed workers were selected from a cadmium smelting factory and a zinc product factory. Doctors, nurses or shop assistants living in the same area served as a control group. Urinary cadmium (UCd) was used as an exposure biomarker and urinary beta2-microgloburin (B2M), N-acetyl-13-D-glucosaminidase (NAG) and albumin (ALB) as effect biomarkers. All urine parameters were adjusted by urinary creatinine. Software of BMDS (Version 1.3.2, EPA.U.S.A) was used to calculate BMD.

RESULTSThe cut-off point (abnormal values) was determined based on the upper limit of 95% of effect biomarkers in control group. There was a significant dose response relationship between the effect biomarkers (urinary B2M, NAG; and ALB) and exposure biomarker (UCd). BEL value was 5 microg/g creatinine for UB2M as an effect biomarker, consistent with the recommendation of WHO. BEL could be estimated by using the method of BMD. BEL value was 3 microg/g creatinine for UNAG as an effect biomarker. The more sensitive the used biomarker is, the more occupational population will be protected.

CONCLUSIONBMD can be used in estimating the biological exposure limit (BEL). UNAG is a sensitive biomarker for estimating BEL after cadmium exposure.

Acetylglucosaminidase ; urine ; Albuminuria ; urine ; Biomarkers ; urine ; Cadmium ; toxicity ; urine ; Dose-Response Relationship, Drug ; Female ; Humans ; Male ; Occupational Exposure ; Spectrophotometry, Atomic ; beta 2-Microglobulin ; urine

OBJECTIVEBased on two sets of data from occupational epidemiology, Benchmark dose (BMD) was applied to estimate biological exposure limit (BEL).

METHODSCadmium exposed workers were selected from a cadmium smelting and a zinc products factory and control group was selected from doctors or nurses and staff from shops living in the same area; Urinary cadmium (UCd) was used as exposure biomarker and urinary beta(2) microglobulin (UBM), NAG (UNAG) and albumin (UALB) were as effect biomarkers. All urine parameters were adjusted by urinary creatinine. Software of BMDS (Version 1.3.2, EPA.U.S) was used to calculate BMD.

RESULTSCalculated abnormal prevalence was based on the upper limit of 95% of effect biomarkers in control group; There are significant dose response relationship between the prevalence of effect biomarkers (UBM, UNAG and UALB) and exposure biomarker (UCd); BEL was 5 microg/g creatinine for UBM as effect biomarker, It consists with the recommendation of WHO; BEL was 3 microg/g creatinine for UNAG as effect biomarker; BEL can be estimated by using the method of BMD; the more sensitive biomarker would used, the more occupational people would protected.

CONCLUSIONThe application of BMD in estimating biological exposure limit (BEL) is proper. UNAG is suggested as most sensitive biomarker to be used to estimate BEL for cadmium exposure.

Acetylglucosaminidase ; urine ; Albuminuria ; urine ; Biomarkers ; urine ; Cadmium ; adverse effects ; urine ; Dose-Response Relationship, Drug ; Female ; Humans ; Male ; Occupational Exposure ; Reference Values ; beta 2-Microglobulin ; urine

Acetylglucosaminidase ; urine ; Adult ; Biomarkers ; urine ; Clinical Enzyme Tests ; Female ; Humans ; Insecticides ; poisoning ; Kidney Diseases ; chemically induced ; urine ; Male ; Middle Aged ; Organophosphate Poisoning ; Poisoning ; urine

OBJECTIVETo use the data of occupational epidemiology to estimate the benchmark dose (BMD) of renal dysfunction induced by lead.

METHODSBlood lead was considered as an exposure biomarker, while urinary total protein (TP), urinary beta(2)-microglobulin (beta(2)-MG) and urinary N-Acetyl-beta-D-glucosaminidase (NAG) were considered as effect biomarkers reflecting the damage of renal function. The dichotomized (binary) data was used as effect endpoints. The BMD and BMD lower limit (BMDL) of blood lead were estimated at the 10% benchmark response using BMDS version 1.3.1.

RESULTSThere was an increased prevalence of hyper-TP-uria, hyper-beta(2)-MG-uria and hyper-NAG-uria with an increasing blood lead concentration. There was obviously dose-response relationship between blood lead and TP, beta(2)-MG and NAG, respectively. The BMD and BMDL of blood lead affecting renal function were estimated to be 323.6 - 754.3 microg/L and 274.2 - 541.5 microg/L. The BMDL of blood lead was ranged from low to high as NAG, TP and beta(2)-MG. The urinary NAG activity might be served as a sensitive biomarker in detecting early renal dysfunction.

CONCLUSIONIt should be feasible to use the BMD approach to set up the reference dose (RfD) and reference concentration (RfC). BMD approach might provide a new and better way for setting up the RfD/RfC.

Acetylglucosaminidase ; urine ; China ; epidemiology ; Clinical Chemistry Tests ; methods ; standards ; Humans ; Lead ; blood ; Lead Poisoning ; blood ; epidemiology ; urine ; Occupational Exposure ; analysis ; Prevalence ; Proteinuria ; urine ; beta 2-Microglobulin ; urine

Acetylglucosaminidase ; urine ; Albuminuria ; physiopathology ; Child, Preschool ; Female ; Humans ; Infant ; Kidney ; physiopathology ; Male ; Seizures, Febrile ; physiopathology

OBJECTIVETo study the diagnostic method for early renal injury in the workers exposed to mercury (Hg).

METHODSThe contents of urinary Hg were determined by chemical method. Urinary microalbumin (mALB), beta(2)-microglodulin (beta(2)-MG) and retinol binding protein (RBP) levels were measured with total quantitative enzyme immunoassay. The activities of urinary N-acetyl-beta-D-glucosaminidase (NAG) and gamma-glutamyl transferase (gamma-GT) were determined by rate methods. Urinary creatinine (Cr) was measured by using picric acid method.

RESULTSThe levels of urinary BRP, beta(2)-MG, NAG and gamma-GT in exposed workers [(439.7 +/- 201.4), (141.4 +/- 56.3) micro g/g Cr and (12.3 +/- 5.7), (60.3 +/- 18.5) U/g Cr respectively] were significantly higher than those in controls (P < 0.05, P < 0.01). The levels were increased gradually with the increasing contents of urinary Hg. The positive detection rate for single or two combined indexes was rather lower whereas that for 4 combined indexes was as high as 85.5%. A positive correlation was noted between the contents of urinary Hg and urinary BRP, beta(2)-MG, NAG and gamma-GT (r: 0.466, 0.379, 0.323, 0.311, P < 0.05). Urinary RBP was correlated to urinary beta(2)-MG, NAG and gamma-GT (r: 0.362, 0.354, 0.332, P < 0.05).

CONCLUSIONCombined detection of urinary RBP, beta(2)-MG, NAG and gamma-GT is a sensitive method for the diagnosis of early renal injury in the workers exposed to Hg.

Acetylglucosaminidase ; urine ; Adult ; Albuminuria ; urine ; Creatinine ; urine ; Female ; Humans ; Kidney ; injuries ; physiopathology ; Kidney Diseases ; etiology ; urine ; Male ; Mercury Poisoning ; complications ; Middle Aged ; Occupational Exposure ; adverse effects ; Retinol-Binding Proteins ; urine ; gamma-Glutamyltransferase ; urine

This study was aimed to evaluate renal dysfunction during three weeks after the burn injuries in 12 patients admitted to the Hallym University Hankang Medical Center with flame burn injuries (total body surface area, 20-40%). Parameters assessed included 24-hr urine volume, blood urea nitrogen, serum creatinine, creatinine clearance, total urinary protein, urinary microalbumin, 24-hr urinary N-acetyl--D-glucosaminidase (NAG) activity, and urinary malondialdehyde (MDA). Statistical analysis was performed using repeated measures ANOVA test. The 24-hr urine volume, creatinine clearance, and urinary protein significantly increased on day 3 post-burn and fell thereafter. The urine microalbumin excretion showed two peak levels on day 0 post-burn and day 3. The 24-hr urinary NAG activity significantly increased to its maximal level on day 7 post-burn and gradually fell thereafter. The urinary MDA progressively increased during 3 weeks after the burn injury. Despite recovery of general renal function through an intensive care of burn injury, renal tubular damage and lipid peroxidation of the renal tissue suggested to persist during three weeks after the burn. Therefore, a close monitoring and intensive management of renal dysfunction is necessary to prevent burn-induced acute renal failure as well as to lower mortality in patients with major burns.
Acetylglucosaminidase/*urine ; Adult ; Aged ; Albuminuria/etiology ; Biological Markers ; Burns/*complications ; Female ; Human ; Kidney Diseases/*diagnosis/urine ; Kidney Failure, Acute/diagnosis ; Lipid Peroxidation ; Male ; Malondialdehyde/*urine ; Middle Age

OBJECTIVETo research the impairment of renal function and the combined effects of arsenic and cadmium exposure in population residing in polluted area, and to calculate the benchmark doses of urinary arsenic (UAs) and cadmium (UCd) in renal dysfunction.

METHODSThe concentrations of Uas and UCd were used as as exposure biomarker. Urinary beta(2)-microglobulin (Ubeta(2)-MG), N-acetyl-beta-glucosaminidase (UNAG), and albumin were calculated as biomarkers of renal dysfunction. The benchmark dose (BMD) and the lower confidence limit of the benchmark dose (BMDL) were calculated. Totally 245 patients were enrolled in the study, them, of 122 were from the exposed area, and 123 from the control area.

RESULTSUAs and UCd concentrations in the exposed group were shown significantly higher than those in the control group (P < 0.01). The levels of Ubeta(2)-MG, UNAG and urinary albumin in the exposed group were significantly higher than those of the controls (P < 0.01). There existed positive correlation among the concentrations of UAs, UCd, Ubeta(2)-MG, urinary albumin and UNAG, showing a significant dose-effect relationship. The combination of cadmium and arsenic caused even more renal injury than by chemicals alone in a same dose. The BMD/BMDL of UAs were estimated as 121.91-171.88 microg/g Cr and 102.11-144.44 microg/g Cr. Of UCd, the BMD/BMDL were 1.05-1.48 microg/g Cr and 0.88-1.24 microg/g Cr.

CONCLUSIONSThis study indicates the combination of cadmium and arsenic might cause even more renal injury than by chemicals given alone, and cadmium might cause potential arsenic nephrotoxicity during long-term coexposure to arsenic and cadmium in human beings. It also suggests that UAs and UCd should be kept below 102.11 and 0.88 microg/g creatinine as to preventing renal damage from coexposure to arsenic and cadmium. The BMD method should be used in calculating the BMD of UAs and UCd on renal dysfunction.

Acetylglucosaminidase ; urine ; Arsenic ; adverse effects ; urine ; Biomarkers ; urine ; Cadmium ; adverse effects ; urine ; China ; epidemiology ; Dose-Response Relationship, Drug ; Environmental Exposure ; Female ; Humans ; Kidney Diseases ; chemically induced ; epidemiology ; Kidney Function Tests ; Male ; Risk Factors ; beta 2-Microglobulin ; urine

OBJECTIVE: To study correlation between urinary retinol binding protein (RBP) content and renal tubular damage. METHODS: A total of 1 353 healthy people and 186 patients with renal tubular damage diagnosed by renal biopsy were enrolled. The indicators such as endogenous creatinine clearance rate (Ccr), creatinine(Cr), urinary retinol binding protein(RBP), urinary β(2)-microglobulin(β(2)-MG), urinary N-acety1-beta-D-glucosaminidase (NAG), urine specific gravity(SG), urine osmolality of the 2 groups were examined and compared. Score of tubulointerstitial impairing and all indicators were analyzed by Spearman rank correlation analysis, and the sensitivity and specificity of indicators were calculated. RESULTS: Renal tubular damage was positively correlated with urinary RBP, β2-MG, NAG (r=0.863, P<0.001; r=0.777, P<0.001; r=0.374, P=0.002, respectively), while negatively correlated with urine osmolaling, SG (r=-0.519, P<0.001; r=-0.624, P<0.001, respectively). The specificity and sensitivity for renal tubular damage of RBP were 91.03% and 72.06%. CONCLUSION RBP is an idea marker for renal tubular damage, and is useful to diagnose renal tubular damage and assess the extent of the damage.
Acetylglucosaminidase ; urine ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; Biomarkers ; urine ; Case-Control Studies ; Creatinine ; urine ; Female ; Humans ; Kidney Diseases ; pathology ; Kidney Tubules ; pathology ; Male ; Middle Aged ; Retinol-Binding Proteins, Cellular ; urine ; Young Adult ; beta 2-Microglobulin ; urine

OBJECTIVESTo test the hypothesis that urine N-acetyl-beta-D-glucosaminidase (NAG) is a nearly biomarker for acute kidney injury in patients with acute paraquat poisoning.

METHODSForty-four patients with paraquat intoxication and 40 age and gender-matched healthy control participants were recruited. The urine N-acetyl-beta-D-glucosaminidase was determined by spectrophotometric methods.

RESULTSThe urine N-acetyl-beta-D-glucosaminidase activities in the patients with paraquat poisoning were higher than the corresponding values in the control participants (P<0.01); The prevalence rate of mortality was significantly higher in subjects with N-acetyl-beta-D-glucosaminidase activities ≥25 U/g Cr than in those N-acetyl-beta-D-glucosaminidase activities <25 Ulg Cr (34.4% vs 16.7%, P<0.01).

CONCLUSIONSThe urine N-acetyl-beta-D-glucosaminidase could be used as an early biomarker for acute kidney injury and predictor of mortality inpatients with acute paraquat intoxication.

Acetylglucosaminidase ; urine ; Acute Kidney Injury ; chemically induced ; diagnosis ; Adolescent ; Adult ; Aged ; Female ; Humans ; Male ; Middle Aged ; Paraquat ; poisoning ; Young Adult