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PubMed1993

Urinary albumin excretion rate and puberty in non-diabetic children and adolescents.

Slightly elevated urinary albumin excretion rate (microalbuminuria) is a marker of early diabetic nephropathy, but it is unclear if the established definition of microalbuminuria (20-200 micrograms/min) is correct for children and adolescents. We investigated the albumin excretion rate, albumin/creatinine ratio and urinary albumin concentration in 150 healthy schoolchildren and adolescents to (a) obtain a reference value for albumin excretion rate, (b) relate albumin excretion to pubertal stages and (c) evaluate albumin/creatinine ratio and morning albumin concentration as screening methods for elevated albumin excretion rate. Albumin concentration was measured by immunoturbidimetry in timed overnight urine samples. The albumin excretion showed a skewed distribution (geometric mean 3.2 micrograms/min, 95 percentile 15.1 micrograms/min). In girls, a peak in the albumin excretion rate was found at the pubertal stage 4 (Tanner) and in boys at stage 5. Albumin/creatinine ratio of 2.5 mg/mmol as a screening level for elevated albumin excretion (15 micrograms/min) showed a high positive (0.88) and negative (0.99) predictive value.

Adolescent↗
PubMed2000

Temporal patterns and quantification of excretion of Mycobacterium avium subsp paratuberculosis in sheep with Johne's disease.

OBJECTIVES: To determine the frequency of excretion of Mycobacterium avium subsp paratuberculosis in Merino sheep with Johne's disease and to quantify excretion in a group of Merino sheep. DESIGN: A pen and laboratory experiment. PROCEDURE: Seven sheep selected from an affected flock on the basis of acid-fast bacilli in the sheep's faeces were housed and total daily faecal output was collected, weighed and subjected to culture for M avium subsp paratuberculosis. An end-point titration method was used to enumerate viable M avium subsp paratuberculosis in a 15 day pooled sample from five sheep that had acid-fast bacilli in their faeces while housed. RESULTS: Four sheep with subclinical multibacillary Johne's disease excreted M avium subsp paratuberculosis each day for 11 days of cultural observation. A further three sheep were intermittent excreters but lacked other evidence of infection with M avium subsp paratuberculosis. The average number of viable bacteria excreted was 1.09 x 10(8) per gram of faeces while total daily excretion was 8.36 x 10(10) viable M avium subsp paratuberculosis per sheep. Examination of faecal smears stained with Ziehl Neelsen was an unreliable means of assessing daily excretion in individual animals except in those with severe lesions. CONCLUSION: Excretion of M avium subsp paratuberculosis in Merino sheep with multibacillary Johne's disease occurred daily, proving that environmental contamination can be continuous on farms with endemic ovine Johne's disease. Faecal culture is a useful method for detecting infection as it does not appear to be affected by the timing of collection of a sample from sheep with multibacillary disease however, to maximise the sensitivity of disease surveillance using faecal culture, sampling rates should be adjusted to take account of the proportions of multibacillary and paucibacillary cases.

Animals↗
PubMed1988

Effect of butylated hydroxyanisole on hepatic glucuronidation and biliary excretion of drugs in mice.

Inhibition of glucuronidation by depletion of UDP-glucuronic acid from liver impairs the hepatobiliary transport of glucuronidated xenobiotics. However, it is not known if enhancement of hepatic glucuronidation increases the biliary excretion of these compounds. Therefore, the effect of treatment with butylated hydroxyanisole (BHA), which increases hepatic glucuronidation capacity, on the biliary excretion of compounds undergoing glucuronidation was studied in mice. BHA-feeding (1% for 10 days) increased hepatic UDP-glucuronic acid content by 240% and enhanced hepatic UDP-glucuronosyltransferase activities (expressed per kg body weight) toward valproic acid, phenolphthalein, iopanoic acid and bilirubin 220, 180, 120 and 60%, respectively. BHA treatment did not influence the biliary excretion of unmetabolized cholephils, phenol-3,6-dibromphthalein disulphonate and phenolphthalein glucuronide, but enhanced that of phenolphthalein (+108%), iopanoic acid (+63%) and bilirubin (+33%) as glucuronides. However, these increases were apparent only in the initial phase of excretion. In contrast, BHA markedly decreased (-43%) the biliary excretion of valproic acid glucuronides. Simultaneously, BHA increased the urinary excretion of the glucuronides of phenolphthalein (+48%), iopanoic acid (+450%) and valproic acid (+150%). A shift in the distribution of iopanoic acid and valproic acid and metabolites from liver to kidney was also apparent in BHA-fed mice. Thus, enhanced glucuronidation does not facilitate the biliary excretion of all glucuronidated compounds and only transiently increases others. It is likely that this phenomenon is the result of the glucuronides readily entering the plasma and being excreted by the kidney.

Animals↗
PubMed1993

Urinary excretion of hexafluoroisopropanol glucuronide and fluoride in patients after sevoflurane anaesthesia.

The excretion of sevoflurane metabolites in the urine collected every 12 h after sevoflurane anaesthesia was measured by ion exchange chromatography. A metabolite, which was converted on incubation with glucuronidase to hexafluoroisopropanol was detected in the urine. The maximum excretion was found in the first 12 h after anaesthesia, none was found in the last collection 3 days after anaesthesia. The excretion half-life for the metabolite was calculated to be 55 h. A significant increase in the urinary excretion of organic and inorganic fluoride was also observed during the first 12 h after anaesthesia. The cumulative organic and inorganic fluoride excretion in the 3 days after sevoflurane anaesthesia was 1588 and 856 mumol, respectively (ratio = 1.85). The excreted half-lives for organic and inorganic fluoride were calculated to be 4028 and 2069 min, respectively. Our study showed that a hexafluoroisopropanol glucuronide is excreted in the urine, and the major part of urinary metabolites of sevoflurane, organic and inorganic fluoride, are excreted within 2 days of sevoflurane inhalation in man.

1-Propanol↗
PubMed1970

Studies on the excretion of [14C]histamine and its metabolites by the rabbit kidney.

1. After intravenous administration of [(14)C]histamine in rabbits, the urinary excretion of [(14)C]histamine and [(14)C]histamine metabolites was examined over a period of 4 hr.2. It was found that [(14)C]histamine was excreted in the unchanged form only in small amounts (6-7%), while 54-71% was eliminated in the form of its metabolites.3. Under normal conditions, the percentage excretion of metabolites, but not of histamine, showed a dose dependence. With the higher [(14)C]histamine dose, a significantly smaller proportion of the dose given was excreted as metabolites than with the lower dose. The proportion of unchanged [(14)C]histamine excreted remained constant.4. Pre-treatment with histamine infusions, or with mepyramine maleate, caused an increase in the excretion of [(14)C]histamine metabolites while the excretion of [(14)C]histamine remained unchanged.5. Pre-treatment with a diuretic, a combination of mersalyl and theophylline, did not influence the excretion of [(14)C]histamine nor of its metabolites.

Animals↗
PubMed1983

Effect of vasopressin on prostaglandin excretion in conscious dogs.

A controversy persists around the effect of vasopressin on urinary prostaglandin excretion. In an attempt to explain part of this controversy, in the present study we re-investigated the effect of vasopressin on urinary prostaglandin excretion in conscious dogs after water loading and during hydropenia. In water diuresis, during the administration of arginine vasopressin or 1-deamino-8-D-arginine vasopressin, prostaglandin excretion and urine flow decreased in parallel. Prostaglandin E2 excretion fell from 1086 +/- 454 to 353 +/- 122 and from 754 +/- 216 to 226 +/- 74 pg min-1 as urine flow decreased by 74 and 66% with arginine vasopressin and 1-deamino-8-D-arginine vasopressin, respectively. In hydropenia both arginine vasopressin and 1-deamino-8-D-arginine vasopressin increased prostaglandin E2 excretion (from 85 +/- 15 to 261 +/- 82 pg min-1; and from 115 +/- 33 to 272 +/- 66 pg min-1, respectively), while urine flow remained practically unchanged. The changes in prostaglandin F2 alpha excretion were similar to those observed with prostaglandin E2. Plasma renin activity was reduced during arginine vasopressin infusion but was unaltered during 1-deamino-8-D-arginine vasopressin infusion. These results indicate that, in the conscious dog, urine flow is a major determinant of prostaglandin excretion but they also show that when large changes in urine flow are avoided vasopressin may increase urinary prostaglandin excretion.

Animals↗
PubMed1984

Effect of aldosterone on urinary kallikrein and prostaglandin excretion in the rat.

In an attempt to study the interrelationship between aldosterone, Na balance, prostaglandin (PG) and kallikrein excretion, we investigated the influence of adrenalectomy and aldosterone administration on kallikrein and PG excretion during dietary manipulation of extracellular volume in Sprague-Dawley rats. Adrenalectomy decreased while aldosterone administration increased urinary kallikrein and PG excretion during both low and high Na intake. Aldosterone induced a prompt change in Na/K ratio; however, kallikrein and PG excretion increased gradually during the 7 days of treatment. When the animals were forced into a negative Na balance during the administration of aldosterone by reducing their Na intake, kallikrein and PG excretion still increased but to a lesser extent than on a constant diet. In adrenalectomized rats given only vehicle, shifting the diet to a low Na intake caused a decrease in kallikrein and PG excretion. Corticosterone failed to correct the changes evoked by adrenalectomy, and it did not reproduce the effects of aldosterone. It is concluded that the effect of aldosterone on kallikrein and PG excretion is not mediated by changes in extracellular volume; however, in the absence of aldosterone a change in Na balance itself may influence kallikrein and PG excretion.

Adrenalectomy↗
PubMed2005

P-glycoprotein plays a major role in the efflux of fexofenadine in the small intestine and blood-brain barrier, but only a limited role in its biliary excretion.

Fexofenadine is a selective, nonsedating H(1)-receptor antagonist approved for symptoms of allergic conditions, which is mainly excreted into feces via biliary excretion. The purpose of this study is to investigate its pharmacokinetics in mice and rats to determine the role of P-glycoprotein (P-gp) in its biliary excretion. In mice, biliary excretion clearance (17 ml/min/kg) accounted for almost 60% of the total body clearance (30 ml/min/kg). Comparing the pharmacokinetics after intravenous and oral administration indicated that the bioavailability of fexofenadine was at most 2% in mice. Knockout of Mdr1a/1b P-gp did not affect the biliary excretion clearance with regard to both plasma and liver concentrations, whereas the absence of P-gp caused a 6-fold increase in the plasma concentration after oral administration. In addition, the steady-state brain-to-plasma concentration ratio of fexofenadine was approximately 3-fold higher in Mdr1a/1b P-gp knockout mice than in wild-type mice. Together, these results show that P-glycoprotein plays an important role in efflux transport in the brain and small intestine but only a limited role in biliary excretion in mice. In addition, there was no difference in the biliary excretion between normal and hereditarily multidrug resistance-associated protein 2 (Mrp2)-deficient mutant rats (Eisai hyperbilirubinemic rats) and between wild-type and breast cancer resistance protein (Bcrp) knockout mice. These results suggest that the biliary excretion of fexofenadine is mediated by unknown transporters distinct from P-gp, Mrp2, and Bcrp.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2006

Differential involvement of Mrp2 (Abcc2) and Bcrp (Abcg2) in biliary excretion of 4-methylumbelliferyl glucuronide and sulfate in the rat.

The hepatic excretion of hydrophilic conjugates, end products of phase II metabolism, is not completely understood. In the present studies, transport mechanism(s) responsible for the biliary excretion of 4-methylumbelliferyl glucuronide (4MUG) and 4-methylumbelliferyl sulfate (4MUS) were studied. Isolated perfused livers (IPLs) from Mrp2-deficient (TR(-)) Wistar rats were used to examine the role of Mrp2 in the biliary excretion of 4MUG and 4MUS. After a 30-micromol dose of 4-methylumbelliferone, cumulative biliary excretion of 4MUG was extensive in wild-type rat IPLs (25 +/- 3 micromol) but was negligible in TR(-) livers (0.4 +/- 0.1 micromol); coadministration of the Bcrp and P-glycoprotein inhibitor GF120918 [N-(4-[2-(1,2,3,4-tetrahydro-6,7-dimethoxy-2-isoquinolinyl)ethyl]-phenyl)-9,10-dihydro-5-methoxy-9-oxo-4-acridine carboxamide] had no effect on 4MUG biliary excretion in wild-type rat IPLs. In contrast, biliary excretion of 4MUS was partially maintained in Mrp2-deficient rat IPLs. Recovery of 4MUS in bile was approximately 50 to 60% lower in both control TR(-) (149 +/- 8 nmol) and wild-type IPLs with GF120918 coadministration (176 +/- 30 nmol) relative to wild-type control livers (378 +/- 37 nmol) and was nearly abolished in TR(-) IPLs in the presence of GF120918 (13 +/- 8 nmol). These changes were the result of decreased rate constants governing 4MUG and 4MUS biliary excretion. In vitro assays and perfused livers from Bcrp and P-glycoprotein gene-knockout mice indicated that 4MUS did not interact with P-glycoprotein but was transported by Bcrp in a GF120918-sensitive manner. In the rat liver, Mrp2 mediates the biliary excretion of 4MUG, whereas both Mrp2 and Bcrp contribute almost equally to the transport of 4MUS into bile.

ATP Binding Cassette Transporter, Subfamily G, Mem↗
PubMed2005

Involvement of BCRP (ABCG2) in the biliary excretion of pitavastatin.

Pitavastatin, a novel potent 3-hydroxymethylglutaryl coenzyme A reductase inhibitor, is distributed selectively to the liver and excreted into bile in unchanged form in rats. We reported previously that the hepatic uptake is mainly mediated by organic anion transporting polypeptide (OATP) 1B1, whereas the biliary excretion mechanism remains to be clarified. In the present study, we investigated the role of breast cancer resistance protein (BCRP) in the biliary excretion of pitavastatin. The ATP-dependent uptake of pitavastatin by human and mouse BCRP-expressing membrane vesicles was significantly higher compared with that by control vesicles with Km values of 5.73 and 4.77 microM, respectively. The biliary excretion clearance of pitavastatin in Bcrp1-/- mice was decreased to one-tenth of that in control mice. The biliary excretion of pitavastatin was unchanged between control and Eisai hyperbilirubinemic rats, indicating a minor contribution of multidrug resistance-associated protein (Mrp) 2. This observation differs radically from that for a more hydrophilic statin, pravastatin, of which biliary excretion is largely mediated by Mrp2. These data suggest that the biliary clearance of pitavastatin can be largely accounted for by BCRP in mice. In the case of humans, transcellular transport of pitavastatin was determined in the Madin-Darby canine kidney II cells expressing OATP1B1 and human canalicular efflux transporters. A significant basal-to-apical transport of pitavastatin was observed in OATP1B1/MDR1 and OATP1B1/MRP2 double transfectants as well as OATP1B1/BCRP double transfectants, implying the involvement of multiple transporters in the biliary excretion of pitavastatin in humans. This is in contrast to a previous belief that the biliary excretion of statins is mediated mainly by MRP2.

ATP Binding Cassette Transporter, Subfamily G, Mem↗
PubMed2006

The important role of Bcrp (Abcg2) in the biliary excretion of sulfate and glucuronide metabolites of acetaminophen, 4-methylumbelliferone, and harmol in mice.

The role of Mrp2, Bcrp, and P-glycoprotein in the biliary excretion of acetaminophen sulfate (AS) and glucuronide (AG), 4-methylumbelliferyl sulfate (4MUS) and glucuronide (4MUG), and harmol sulfate (HS) and glucuronide (HG) was studied in Abcc2(-/-), Abcg2(-/-), and Abcb1a(-/-)/Abcb1b(-/-) mouse livers perfused with the respective parent compounds using a cassette dosing approach. Biliary clearance of the sulfate conjugates was significantly decreased in Bcrp-deficient mouse livers, resulting in negligible biliary excretion of AS, 4MUS, and HS. It is noteworthy that the most profound decrease in the biliary clearance of the glucuronide conjugates was observed in Bcrp-deficient mouse livers, although the biliary clearance of 4MUG was also approximately 35% lower in Mrp2-deficient mouse livers. As expected, biliary excretion of conjugates was not impaired in P-glycoprotein-deficient livers. An appreciable increase in perfusate recovery due to a shift in the directionality of metabolite excretion, from bile to perfusate, was noted in knockout mice only for conjugates whose biliary clearance constituted an appreciable (> or =37%) fraction of total hepatic excretory clearance (i.e., 4MUS, HG, and HS). Biliary clearance of AG, AS, and 4MUG constituted a small fraction of total hepatic excretory clearance, so an appreciable increase in perfusate recovery of these metabolites was not observed in knockout mice despite markedly decreased biliary excretion. Unlike in rats, where sulfate and glucuronide conjugates were excreted into bile predominantly by Mrp2, mouse Bcrp mediated the biliary excretion of sulfate metabolites and also played a major role in the biliary excretion of the glucuronide metabolites, with some minor contribution from mouse Mrp2.

ATP Binding Cassette Transporter, Subfamily G, Mem↗
PubMed1980

Biliary excretion of cephalosporins in rats: influence of molecular weight.

The biliary excretion of 18 cephalosporin derivatives with varying 3- and 7-substituents was examined in cannulated rats. In spite of the widely differing physical chemical properties imparted by the different structures, the dominant influence on the degree of biliary excretion was the molecular weight of the compound. Above a threshold molecular weight of about 450, biliary excretion increased in a generally progressive way, becoming the principal route of excretion of the higher-molecular-weight derivatives. Examples were found in which the molecular weight influence was modified but not abolished by specific substituents. Biliary excretion varied from less than 5% to greater than 90% of the dose. Interruption of bile flow resulted in an increase in urinary excretion. Biliary excretion may influence the evaluation of new cephalosporins in rodent models. Such influence must be considered when selecting candidate compounds intended for eventual use in humans, where the excretion pattern may be different from that in rodents.

Animals↗
PubMed1988

Effect of ursodeoxycholate on the biliary excretion of cefotiam and sulbenicillin in patients with percutaneous transhepatic biliary drainage.

The effects of ursodeoxycholate administration on the biliary excretion of the antibiotics cefotiam and sulbenicillin were studied in five patients with stable hepatic function receiving percutaneous transhepatic biliary drainage for obstructive jaundice. Cefotiam (I g) and sulbenicillin (2 g) were administered intravenously before and after ursodeoxycholate administration, and the maximum concentrations of the antibiotics in the bile and total amounts excreted in the bile during the 4 h after administration were determined. After ursodeoxycholate administration, both the maximum concentration of cefotiam in the bile and the amount excreted increased significantly. Ursodeoxycholate also increased the peak concentration and total excretion of sulbenicillin. For both cefotiam and sulbenicillin, the amount of antibiotic excreted in the bile during the 4 h after administration showed a significant correlation with the amount of bile acids excreted in the bile. This strongly suggests a common mechanism for the biliary excretion of these antibiotics and bile acids. Ursodeoxycholate administration is a benign way to increase both the concentration and the total amount of antibiotic excreted in the bile. Therefore, it may be useful in the treatment of serious biliary tract infections, especially in patients receiving biliary drainage.

Aged↗
PubMed1971

Physiological studies of biosynthetic indole excretion in Bacillus alvei.

Bacillus alvei excretes indole during early exponential growth in acid-hydrolyzed casein medium. l-Threonine is the amino acid responsible for "early" indole excretion, and the amount of indole excreted is directly related to the amount of l-threonine in the medium. "Early-indole" excretion can be prevented by the continuous addition of serine (3.1 mumoles per ml per hr) or by substituting a mutant with an impaired ability to degrade serine. The addition of serine to a culture during the period of indole excretion halts the excretion and stimulates indole utilization. Threonine is a competitive inhibitor of serine (K(i) = 0.6 m) in the tryptophan synthetase B reaction. The internal tryptophan concentration increases during the period of indole excretion, suggesting that threonine acts by increasing the activity of the tryptophan pathway. This view is supported by experiments demonstrating that anthranilic acid and indoleacrylic acid also stimulate indole excretion. A metabolic explanation is offered and discussed.

Acrylates↗
PubMed1989

Characterization of the precursor of Serratia marcescens serine protease and COOH-terminal processing of the precursor during its excretion through the outer membrane of Escherichia coli.

The Serratia marcescens serine protease, which is directed by the gene encoding a precursor composed of a typical NH2-terminal signal sequence, a mature enzyme domain, and a large COOH-terminal domain, was excreted through the outer membrane of Escherichia coli. The precursor, with the expected molecular size (110 kilodaltons), was detected in an insoluble form in the periplasmic space of E. coli cells after induction with isopropyl-beta-D-thiogalactopyranoside of the expression of the gene under the control of the tac promoter. Upon membrane fractionation of the disrupted cells by sucrose density gradient centrifugation, the precursor was recovered from a fraction slightly heavier than the outer membrane fraction but not from the inner membrane fraction. Conversion of the precursor into the mature form, which was accompanied by its excretion into the medium, was observed even in the absence of de novo protein synthesis caused by the addition of chloramphenicol. The mutated gene product lacking all of the COOH-terminal domain was localized in the periplasmic space only and was not excreted into the medium. Additional mutant genes were generated by site-directed mutagenesis to test the role of some amino acids in the excretion of this protease in E. coli. The mutant protein with no protease activity because of the change of the catalytic residue Ser-341 to Thr was still excreted into the medium but with abnormal processing. Both self-processing and host-dependent processing of the precursor seem to be involved in the excretion of the mature enzyme. Replacement of the four Cys residues, two in the mature enzyme and two in the COOH-terminal domain, with Ser in different combinations caused a distinct or complete loss of excretion, suggesting that a certain conformation possibly formed via disulfide bonding was important for the excretion of the S. marcescens protease.

Base Sequence↗
PubMed2000

Oxalate and calcium excretion in cystic fibrosis.

BACKGROUND: A patient with cystic fibrosis (CF) and repeated calcium oxalate renal stones prompted us to investigate other children for risk factors for this recognised complication of CF. METHODS: Twenty four hour urinary excretion of calcium, oxalate, and glycolate was measured in children with CF and no symptoms of renal tract stones. Normal diet and treatments were continued. RESULTS: In 26 children (aged 5-15.9 years) oxalate excretion was correlated with age; 14 of 26 children had oxalate excretion above an age appropriate normal range. There was a positive correlation between oxalate excretion and glycolate excretion. Mean calcium excretion was 0.06 mmol/kg/24 h with 21 of 24 children having calcium excretion below the normal range. CONCLUSIONS: Hyperoxaluria may reflect malabsorption although correlation between excretion of oxalate and glycolate suggests a portion of the excess oxalate is derived from metabolic processes. The hypocalciuria observed here may protect children with CF from renal stones.

Adolescent↗
PubMed1987

Patterns of urinary excretion of gold in patients with rheumatoid arthritis undergoing chrysotherapy.

Thirty patients receiving gold therapy for rheumatoid arthritis (RA) were studied for the urinary excretion of gold. Statistical analysis of all the urine specimens passed over a period of four days by each patient showed that a definite rhythm of gold excretion exists for each patient which is possibly related to water excretion but not to creatinine excretion. The study indicates possible reasons for the inability of earlier workers to relate gold excretion to the general body gold status of patients and suggests that as the study of 24 hour excretions of gold may be an insensitive marker of gold excretion, closer examination of individual patient rhythms of gold excretion could possibly provide a more useful method of analysis.

Adolescent↗
PubMed1983

Seminal fluid excretion of cytomegalovirus related to immunosuppression in homosexual men.

Seminal fluid samples from 84 Danish homosexual men were successfully cultured to determine the prevalence of cytomegalovirus excretion. Ten (15%) out of 66 men positive for the antibody were found to be excreting the virus. Although the proportion excreting was inversely related to age (p less than 0.01), three men aged over 30 and with many years of homosexual experience excreted the virus. In addition, a 50 year old man with Kaposi's sarcoma excreted the virus. A further study of the ratio of T cell helpers to suppressors in the men aged over 30 and a series of age matched non-excreting homosexual control or heterosexual men showed that those excreting cytomegalovirus in their seminal fluid had statistically lower ratios (all less than 0.77) than the controls (p less than 0.05). Excretion of cytomegalovirus may be related to re-emergence of latent infection in immunosuppressed homosexual men.

Adolescent↗