Prognostic value of liver and kidney function parameters and their correlation with the ratio of urine-to-plasma paraquat in patients with paraquat poisoning.

Acute paraquat poisoning resulting from multiple organ failure usually has a high mortality rate. Liver and kidney, as the key oranges of paraquat detoxification and elimination, their injuries may suppress toxin excretion and enhance the toxicity of paraquat in other organs and worsen the prognosis. Therefore, we intended to explore the prognostic value of liver and kidney function parameters, and further evaluate their correlation with a more stable index urine-to-plasma paraquat (urine paraquat concentrations/plasma paraquat concentrations) instead of considering paraquat concentrations in plasma or urine alone. The study included 33 patients with acute paraquat poisoning admitted to four centres in China from January 2018 to December 2019. Seventeen patients (10 male/7 female) survived, whereas 16 patients (7 male/9 female, 48.48%) died from paraquat poisoning. Alanine aminotransferase (ALT) and the blood urea nitrogen (BUN) represent liver and kidney function parameters, respectively. The ratio of urine-to-plasma paraquat is negatively correlated with ALT (r = -0.94, P = 0 .02) and BUN (r = -0.82, P = 0.03). For receiver operating characteristic curve (ROC) analysis, ALT, BUN and urine-to-plasma paraquat have an AUC over 0.80. The study shows that the functional indexes of liver and kidney, as well as the ratio of urine-to-plasma paraquat, could be considered for evaluating the extent of organ injury and excretion rate of paraquat.

Biomarker evaluation of skeletal muscle toxicity following clofibrate administration in rats.

The use of sensitive biomarkers to monitor skeletal muscle toxicity in preclinical toxicity studies is important for the risk assessment in humans during the development of a novel compound. Skeletal muscle toxicity in Sprague Dawley Rats was induced with clofibrate at different dose levels for 7 days to compare standard clinical pathology assays with novel skeletal muscle and cardiac muscle biomarkers, gene expression and histopathological changes. The standard clinical pathology assays aspartate aminotransferase (AST), alanine aminotransferase (ALT), and creatine kinase (CK) enzyme activity were compared to novel biomarkers fatty acid binding protein 3 (Fabp3), myosin light chain 3 (Myl3), muscular isoform of CK immunoreactivity (three isoforms CKBB, CKMM, CKMB), parvalbumin (Prv), skeletal troponin I (sTnI), cardiac troponin T (cTnT), cardiac troponin I (cTnI), CKMM, and myoglobin (Myo). The biomarker elevations were correlated to histopathological findings detected in several muscles and gene expression changes. Clofibrate predominantly induced skeletal muscle toxicity of type I fibers of low magnitude. Useful biomarkers for skeletal muscle toxicity were AST, Fabp3, Myl3, (CKMB) and sTnI. Measurements of CK enzyme activity by a standard clinical assay were not useful for monitoring clofibrate-induced skeletal muscle toxicity in the rat at the doses used in this study.

Urinary (1)H-NMR-based metabolic profiling of children with NAFLD undergoing VSL#3 treatment.

BACKGROUND: Nowadays, non-alcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases in children. Our recent clinical trial demonstrated that dietary and VSL#3-based interventions may improve fatty liver by ultrasound and body mass index (BMI) after 4 months. OBJECTIVES: As in this short-term trial, as in others, it is impracticable to monitor response to therapy or treatment by liver biopsy, we aimed to identify a panel of potential non-invasive metabolic biomarkers by a urinary metabolic profiling. METHODS: Urine samples from a group of 31 pediatric NAFLD patients, enrolled in a VSL#3 clinical trial, were analyzed by high-resolution proton nuclear magnetic resonance spectroscopy in combination with analysis of variance-Simultaneous Component Analysis model and multivariate data analyses. Urinary metabolic profiles were interpreted in terms of clinical patient feature, treatment and chronology pattern correlations. RESULTS: VSL#3 treatment induced changes in NAFLD urinary metabolic phenotype mainly at level of host amino-acid metabolism (that is, valine, tyrosine, 3-amino-isobutyrate or ß-aminoisobutyric acid (BAIBA)), nucleic acid degradation (pseudouridine), creatinine metabolism (methylguanidine) and secondarily at the level of gut microbial amino-acid metabolism (that is, 2-hydroxyisobutyrate from valine degradation). Furthermore, some of these metabolites correlated with clinical primary and secondary trial end points after VSL#3 treatment: tyrosine and the organic acid U4 positively with alanine aminotransferase (R=0.399, P=0.026) and BMI (R=0.36, P=0.045); BAIBA and tyrosine negatively with active glucagon-like-peptide 1 (R=-0.51, P=0.003; R=-0.41, P=0.021, respectively). CONCLUSIONS: VSL#3 treatment-dependent urinary metabotypes of NAFLD children may be considered as non-invasive effective biomarkers to evaluate the response to treatment.

[URINE UNDER CHRONIC DYSFUNCTION OF RENAL ALLO-TRANSPLANT].

The study was organized to provide additional characteristic of chronic dysfunction of renal allo-transplant using such biomarkers of serum and urine as enzymes (alanine aminotransferase), aspartate aminotransferase, gamma- glutamiltransferase, alkaline phosphatase, N-acetyl-ß-D-glucosaminidase, interleukins (IL-2, IL-8, IL-10), beta-2- microglobulin. The chronic dysfunction of renal allo-transplant is characterized by increasing of concentration of IL-10 and beta-2-microglobulin in serum and increasing of concentration of beta-2-microglobulin, IL-2, IL-8 in urine and increasing of activity of N-acetyl-ß-D-glucosaminidase, alkaline phosphatase, aspartate aminotransferase, gamma-glutamiltransferase as compared with patients with satisfactory function of renal allo-transplant. The multivariant logistic regression analysis established that only activity of N-acetyl-ß-D-glucosaminidase in urine was reliably independently related to chronic dysfunction of renal allo-transplant. It is assumed that increasing of concentration of beta-2-microglobulin in serum testifies glomerular dysfunction and in urine--tubular dysfunction of renal allo-transplant. The enzymeuria indicates continuing damage of epithelium of proximal tubules of nephron. The classification of patients with satisfactory function and chronic dysfunction of renal allo-transplant established that the highest indicators of square under ROC-curves had concentration of beta-2-microglobulin in serum (0.858 ± 0.061) and urine (0.733 ± 0.079) and activity of N-acetyl-ß-D-glucosaminidase in urine (0.701 ± 0.061). To specify diagnosis of chronic dysfunction of renal allo-transplant the most useful (ratio of likelihood of positive result 10 and 11 correspondingly) are tests of beta-2- microglobulin in serum (more than 8.55 mkg/ml) and N-acetyl-ß-D-glucosaminidase/creatinine in urine (more than 34 nmol/(sl)/ mmol/l). These discoveries require further validation and confirmation by implementation of morphological analysis of bioptat of renal allo-transplant.

The Children's Hospital of Philadelphia's experience with donation after cardiac death.

OBJECTIVE: To describe our experience with pediatric donation after cardiac death. DESIGN: Retrospective chart review of all cases of donation after cardiac death from 1995 to 2005. SETTING: The Children's Hospital of Philadelphia pediatric intensive care unit. PATIENTS: Twelve patients who were pediatric organ donors after cardiac death. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Charts for 12 patients were located, and donation after cardiac death was confirmed. There were two females and ten males. Patient age ranged from 1 to 17 yrs (mean 8 yrs). Four patients had severe traumatic brain injury, and eight patients had hypoxic ischemic encephalopathy. The organs procured were 24 kidneys, eight livers, four lungs, and one pancreas. The organs transplanted were 23 kidneys, four livers, and one pancreas. Ten of 12 cases of withdrawal of life-sustaining support occurred in the operating room area; the other two occurred in the holding area and the postanesthesia care unit. Children received a wide range of medications at the time of extubation. No neuromuscular blockers were used. The time of extubation to time of death ranged from 4 mins to 30 mins, with a mean of 14.5 mins. Death was declared based on cardiac asystole confirmed by auscultation and transthoracic impedance, with organ procurement initiated 5 mins later. Regarding who initiated conversation about donation after cardiac death, nine cases were family initiated, one case was physician initiated, and in two there was a collaborative approach with the physician and representative from the organ procurement organization. Of the organs transplanted, all organs other than one kidney and one split liver graft were functioning at 1 yr post-transplant. CONCLUSIONS: Pediatric donation after cardiac death can be performed successfully; its impact on end-of-life care and bereavement needs further investigation.

The effects of bicarbonate and its combination with chelating agents used for the removal of depleted uranium in rats.

The effects of bicarbonate and its combination with the chelating agents, deferiprone (L1), 4,6-dimethyl-1-hydroxypyrimidin-2(1H)-one (AK-4), catechol-3,6-bis(methyleneimino-diacetic-acid) (CBMIDA), and ethane-1-hydroxy-1,1-bisphoshonate (EHBP) in removing depleted uranium (DU) for radiation emergency medicine were examined. After the intramuscular injection of DU in rats, various time schedules of bicarbonate and chelating agent administration were tested. The results indicate that the bicarbonate helps increase significantly the effects of LI and AK-4, while there were no effects of using bicarbonate alone. The effects of bicarbonate on CBMIDA were unclear, and the effects of EHBP were negative. Further studies are necessary to obtain distinctly synergic effects by the combination of chelating agents with bicarbonate.

Effect of vitamin B6 deficiency on glyoxylate metabolism in rats with or without glyoxylate overload.

We examined the effect of vitamin B6 deficiency on glyoxylate metabolism and hepatic alanine: glyoxylate aminotransferase (AGT) activity in rats with normal or high glyoxylate intake. Male rats were divided into four groups: a control group, a vitamin B6-free diet group, a glyoxylate water group, and a vitamin B6-free diet + glyoxylate water group. Each group was given special diet (control or vitamin B6-deficient diet) and drinking water (plain or 0.5% glyoxylate water) for 4 weeks, after which biochemical parameters and hepatic AGT mRNA level were measured. Compared with control rats, the urinary oxalate/creatinine ratio was higher in each of the other 3 groups. The urinary glycolate/creatinine ratio was also higher in the vitamin B6-free diet group and the vitamin B6-free diet + glyoxylate water group than the control group, while the urinary glycine/creatinine and citrate/creatinine ratio was lower in both groups. The hepatic AGT mRNA level was reduced in the vitamin B6-free diet group, but was increased in the glyoxylate water group than the control group. These results suggest that vitamin B6 is necessary for glyoxylate metabolism as a coenzyme of AGT. Especially in the presence of a high glyoxylate intake, vitamin B6 deficiency leads to severe hyperoxaluria and hypocituria.

Evaluation of renal enzymuria and cellular excretion as an marker of acute nephrotoxicity due to an overdose of paracetamol in Wistar rats.

INTRODUCTION: The present study was conducted to determine whether the urinary levels of excreted enzymes, gamma-glutamyltransferase (GGT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), aspartate (AST) and alanine aminotransferases (ALT), can efficiently indicate, within 24 h, an acute nephrotoxicity due to an overdose of paracetamol (PAR). METHODS: A baseline urine was collected from the experimental group. Thereafter, blood collected from the orbital sinus (1.0 ml) and paracetamol (650 mg/kg of body weight) was administered by gavage. After the drug administration, animals were returned to the metabolic cages and then urine was collected in the next 22 h. Blood and urine collection was performed at time 0+24 h (T(24)), as well as at times 48 and 72 h (T(48) and T(72)). After the last urine and blood collection, the rats were killed and the kidneys removed and prepared for histological examination. Plasma creatinine and urinary levels of creatinine (to determinate glomerular filtration rate-GFR), GGT, ALP, LDH, ALT and AST were measured. Kidney tissues were stained with hematoxylin and eosin stain for histological assessment. RESULTS: Urinary levels of GGT, ALP and LDH enzymes were significantly higher (P<0.05) at T(24) when compared to the levels at T(0) and returned to basal levels at T(48) and T(72). The number of urinary epithelial cells at T(24) was significantly higher when compared to the control time (T(0)) (P<0.001). The GFR was significantly reduced 24, 48 and 72 h after the drug administration. CONCLUSION: The number of urinary epithelial cells and urinary enzymes levels are a simple and low cost procedure that is available and can help in the detection of renal acute lesions.

A comparison of methods for measuring serum and urinary markers of bone metabolism in cats.

Biochemical markers of bone cell activity have recently been shown to be useful for monitoring skeletal health in domestic animals, including dogs and horses. The aim of this study was to evaluate a number of biochemical assays, originally developed for use in humans, for their ability to measure indicators of bone cell activity in serum and urine of normal cats over a range of ages. Bone alkaline phosphatase (BAP), a marker of bone formation, was measured in serum using wheatgerm lectin precipitation (WGL) and by ELISA. The curve derived from serial dilution of feline serum was parallel with the ELISA standard curve, indicating species cross-reactivity, and there was a significant relationship between assays (rs = 0.97, P < 0.001). Deoxypyridinoline (DPD), a marker of bone resorption, was measured in its total form in urine by HPLC and ELISA, and in its free form in serum and urine by ELISA. The dilution curve for free DPD in urine showed parallelism with the assay standard curve; however, the curves for total DPD in urine and serum did not. A significant relationship was established between total urinary DPD (HPLC) with total serum DPD (rs = 0.69, P < 0.001), and with free urinary DPD (rs = 0.95, P < 0.001) concentrations. Carboxy-terminal telopeptide of type I collagen (CTX) concentration, another marker of bone resorption, was measured in serum and urine by ELISA, and there was a significant relationship between assays (rs = 0.82, P < 0.001). CTX could not be measured reliably using an auto-analysis method. A significant relationship was established between total urinary DPD (HPLC) with serum CTX (rs = 0.59, P < 0.05), and urinary CTX (rs = 0.65, P < 0.001) concentrations. BAP (ELISA and WGL), total urinary DPD (HPLC), urinary CTX (ELISA), and serum CTX (ELISA) concentrations were significantly inversely correlated with age (rs = -0.66, -0.88, -0.61, -0.70, and -0.51, P < 0.05 respectively). Cats under two years of age had significantly higher BAP, total urinary DPD (HPLC), and urinary CTX concentrations compared to older cats. In conclusion, this study has shown that a number of commercially available assays provide reliable methods for non-invasively monitoring bone cell activity in cats and has shown that bone turnover decreases within the first two years of life, until complete skeletal maturity is attained. Future studies can now be directed at evaluating the potential clinical application of these methods.

Effects of coffee cherry, the residue left after removal of the beans from the coffee fruit, on mammary glands, automatic behavior and related parameters in mice.

To clarify the mechanisms of the anti-mammary tumor activity of coffee cherry (CC), the residue left after the removal of beans from the fruit, the effects in SHN mice of CC on plasma and urine component levels, mammary gland growth, spontaneous motor activity and several related parameters were examined. Hot water extract of CC was given to 2-month-old mice in drinking water (0.5%) for 60 days. The treatment prevented the elevation of plasma and urine levels of alanin amino-transferase and asparate aminotransferase, indicating that CC can protect against metabolic abnormality, which is a cause of the high mammary tumor susceptibility of SHN mice. It also resulted in an inhibition of the formation of precancerous mammary hyperplastic alveolar nodules. Neither food and water intake nor spontaneous motor activity was affected by CC. The findings provide novel information on the mechanism of the protective effect of CC on mammary tumorigenesis and confirm the usefulness of CC as a safe chemopreventive agent of mammary and other types of tumors.

Chloracne and morbidity after dioxin exposure (preliminary results).

In this paper, 159 cases of chloracne contamination, reported from 1969 to 1975, in TCDD-contaminated production of the herbicide 2,4,5-trichlorophenol (2,4,5-T) were followed for mortality and morbidity up to 1996, when blood and urine tests were performed on 50 of these chemical workers ('exposed') and matched controls. In exposed workers, the most frequent cause of sick leave was chloracne, which persisted in 32%. Neurological symptoms were reported frequently (44% sleep disturbance, 32% headache, 30% neuralgia). BSR, leucocytes, gamma-GT, S-G0T and S-GPT were significantly higher than in controls. The effects of exposure (P = 0.002) and alcohol (P = 0.002) on gamma-GT were found to be independent of each other.

Urinary enzyme changes in newborns with unconjugated hyperbilirubinemia.

Various changes in renal function caused by unconjugated hyperbilirubinemia in newborns have been suggested in previous reports. Disclosing an injury in renal tubulus epithelium is feasible by measurement of urinary enzymes. Thus, renal function tests and urinary enzymes in 25 terms newborns with unconjugated hyperbilirubinemia were evaluated before and after phototherapy. Ten healthy term newborns without hyperbilirubinemia formed the control group. Mean values of the variables obtained before and after phototherapy in the study group and in the controls were, respectively: urine osmolality (osm/kg H2O): 0.147 +/- 0.009, 0.174 +/- 0.011, and 0.153 +/- 0.018; endogenous creatinine clearance (mL/min per 1.73 m2): 45.7 +/- 2.15, 46.0 +/- 1.6 and 46.7 +/- 3.9; fractional excretion of sodium (%): 1.27 +/- 0.30, 0.79 +/- 0.19 and 1.24 +/- 0.07; tubular phosphorus reabsorption (%): 85.8 +/- 3.3, 87.8 +/- 2.8 and 86.6 +/- 1.7; urinary N-acetyl-beta-D glucosaminidase/creatinine (IU/mg): 0.617 +/- 0.226, 0.574 +/- 0.214 and 0.619 +/- 0.210; fractional excretion of alkaline phosphatase (%): 0.422 +/- 0.103, 1.001 +/- 0.374 and 0.596 +/- 0.201; fractional excretion of lactic dehydrogenase (LDH; %): 0.102 +/- 0.019, 0.121 +/- 0.023 and 0.119 +/- 0.041; fractional excretion of AST (%): 0.433 +/- 0.127, 0.530 +/- 0.113 and 0.502 +/- 0.074; fractional excretion of alanine aminotransferase (ALT; %) 0.856 +/- 0.413, 1.619 +/- 1.076 and 1.066 +/- 0.366. No significant difference was found between these values before and after phototherapy in the study group, or between the values before phototherapy in hyperbilirubinemic neonates and in the control group. In conclusion, unconjugated hyperbilirubinemia up to a serum level of 18.4 mg/dL in term neonates does not seem to result in injury of normal tubulus epithelium as shown by urinary enzyme levels.

Yeast, creatinine and false diagnosis of porphyria.

A distressingly common occurrence is the erroneous diagnosis of hepatic porphyria in patients with chronic abdominal pain in which either urinary porphyrins are elevated and/or Watson-Schwarz test is positive. This work investigates a characteristic case and points at possible pitfalls in establishing a diagnosis. In the patient described, spot urine analysis showed positive Watson-Schwarz test and increased porphyrins at three separate occasions, while normal values of precursors and porphyrins were recorded in 24-hrs. urinary collections during four hospitalization periods for acute abdominal pain. Various colorimetric and HPLC methods employed excluded the diagnosis of porphyria and led to resolving the discrepancy between home and hospital results. It was found that the false increase in porphyrins in the spot samples emerged from a substance present in yeast tablets which the patient was consuming. The positive Watson-Schwarz test obtained was probably the result of the fact that the urine samples were concentrated with creatinine values exceeding 400 mg%. The case reported above, as well as studies carried out in three healthy volunteers and in an AIP patient, led to the conclusion that in order to obtain reliable result, 24-hrs. urinary collections should be examined, rather than spot urine samples.

The assessment of nephrotoxic effect of organophosphorous pesticides based on the determination of the activity of some selected enzymes in urine.

Pesticides and their metabolites are excreted mainly by the kidneys. The effect of these compounds on the kidney parenchyma was evaluated on the basis of determinations of the activity of the following enzymes: alkaline phosphate, N-acetylglucosaminidase, lactate dehydrogenase, alanine aminotransferase, aspartate aminotransferase and arginase in urine of workers employed at the department producing organophosphorous pesticides (32 males and 53 females) as well as those employed at the production of chlorfenvinphos (35 males). The activity of most of the estimated enzymes was significantly higher as compared to control groups. The dynamic of changes of enzyme activity was traced in the workers employed at the department producing chlorfenvinphos over their first 18 months of employment.

Tubular toxicity is the main renal effect of contrast media.

The aim of this study is to evaluate the effects of contrast media on both tubular and glomerular function. Different parameters of tubular and glomerular function were determined before and at 1, 3, and 5 days after the intravascular administration of contrast media in 100 adult renal patients (plasma creatinine 0.6-10.8 mg/dL, mean: 1.3). Urinary activities of five tubular enzymes (alanine aminopeptidase, gamma-glutamyltransferase, alkaline phosphatase, lactate dehydrogenase, N-acetyl-beta-D-glucosaminidase) increased significantly on the first day after the administration of contrast media, indicating a tubular damage. Glomerular filtration rate and the conventional tests of glomerular function (plasma creatinine, creatinine clearance, and urinary proteins) presented only slight variations after the administration of contrast media. In conclusion, contrast media principally affected the renal tubule (as demonstrated by enzymuria), while their effects on glomerular function were very mild.

Effect of proximal tubular glucose transport blockade on urinary enzyme excretions in hyperglycemic rats.

To investigate proximal tubular dysfunction under hyperglycemic status, we infused 10% glucose solution into male Wistar rats with and without 0.16% phloridzin (a specific inhibitor of proximal tubular glucose transportation) and measured the urinary excretion rates of enzymes that are derived predominantly from proximal tubules. We used 10% mannitol solution and 0.9% saline as controls. Urinary excretion levels of N-acetyl-ss-D-glucosaminidase, alanine aminopeptidase, gamma-glutamyl transpeptidase and dipeptidyl aminopeptidase IV were significantly increased in the 10% glucose-loaded group. In contrast, these increased enzyme excretions were not observed in the 10% mannitol or 0.9% saline-loaded group. Moreover, addition of 0.16% phloridzin to 10% glucose solution completely prevented these increases in N-acetyl-beta-D-glucosaminidase, alanine aminopeptidase and gamma-glutamyl transpeptidase excretion, and slightly decreased dipeptidyl aminopeptidase IV excretion. At the end of the infusion study, a rise in renal cortical sorbitol concentration of the 10% glucose-loaded group was about 2 times higher than the 0.9% saline or 10% mannitol-loaded group. However, in the group that received both glucose and phloridzin, elevation of renal cortical sorbitol concentration was not observed. This study showed that glucose-load results in both abnormal enzymuria and renal cortical sorbitol accumulation; they were completely prevented by phloridzin.

Possible role of thioformamide as a proximate toxicant in the nephrotoxicity of thiabendazole and related thiazoles in glutathione-depleted mice: structure-toxicity and metabolic studies.

In mice depleted of GSH by treatment with buthionine sulfoximine (BSO), thiabendazole (TBZ) causes renal injury characterized by an increase in serum urea nitrogen (SUN) concentration and by tubular necrosis. Previous studies have shown that TBZ requires metabolic activation before it produces nephrotoxicity and that the structure contributing to the toxicity of TBZ is the thiazole moiety of the molecule. TBZ and its thiazole analogues were examined for the ability to increase SUN concentration and serum alanine aminotransferase activity in GSH-depleted mice. Unsubstituted thiazole and thiazoles with 4- and/or 5-, and no 2-, substituents caused marked increases in SUN concentration, suggesting nephrotoxicity. Furthermore, the nephrotoxic potency of these thiazoles decreased with the increasing number and bulk of the 4- and/or 5-substituents. On the other hand, the target organ (the kidney or liver) and the toxic potency of 4-methylthiazoles were markedly altered with the type of substituents at the 2-position. These observations and the known toxicity of thiono-sulfur compounds led us to the hypothesis that the nephrotoxic thiazoles, which lack 2-substituents, would undergo microsomal epoxidation of the C-4,5 double bond and, after being hydrolyzed, the resulting epoxide would then be decomposed to form thioformamide, a possibly toxic metabolite. Evidence for this hypothesis was provided by the results that thioformamide and tert-butylglyoxal as the accompanying fragment were identified as urinary metabolites in mice dosed with 4-tert-butylthiazole and that thioformamide caused a marked increase in SUN concentration when administered to mice in combination with BSO.

Observations on calcium oxalate stone formers.

Biochemical studies were performed on 22 adult patients with idiopathic recurrent calcium oxalate renal stone disease and 23 healthy controls. It was found that urinary glutamic-oxaloacetic acid transaminase (UGOT) and urinary glutamic-pyruvic acid transaminase (UGPT) activity was low and lactate dehydrogenase (LDH) and gamma-glutamyl transferase (gamma-GT) activity was high in the urine of calcium oxalate stone formers. No significant changes were observed in the activity of glutamic-oxaloacetic acid transaminase, glutamic-pyruvic acid transaminase and gamma-GT in their blood but a significant reduction was found in both LDH and alkaline phosphatase activity. It was concluded that the activity of UGOT and UGPT is reduced in patients with kidney stones.