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PubMed1998

The effects of eprosartan, an angiotensin II AT1 receptor antagonist, on uric acid excretion in patients with mild to moderate essential hypertension.

The effects of antihypertensive agents, including angiotensin II receptor antagonists, on urine uric acid excretion may have important clinical consequences. Therefore, the effects of single and repeated doses of eprosartan on uric acid excretion were evaluated in 57 male patients with mild-to-moderate essential hypertension in a double-blind, randomized, placebo-controlled, repeated dose, dose-rising, two-period, period-balanced, crossover study conducted in two parts. In part 1 (n = 33), the effects of eprosartan dose regimens of 50 mg, 100 mg, and 350 mg once daily and 150 mg every 12 hours on uric acid excretion were assessed. In part 2 (n = 24), the effects of eprosartan dose regimens of 600 mg, 800 mg, and 1,200 mg once daily on uric acid excretion were assessed. Eprosartan was well tolerated. There were no appreciable changes from predose values in fractional excretion of uric acid (FEua), urine uric acid excretion, urine uric acid to creatinine (Uua/Ucr) ratios, or serum uric acid concentrations after single or repeated doses of eprosartan. Mean Uua/Ucr ratios for eprosartan doses of 50 mg, 100 mg, or 350 mg daily or 150 mg every 12 hours were comparable to those for placebo. Mean FEua values and Uua/Ucr ratios for eprosartan doses of 600 mg, 800 mg, or 1,200 mg daily also were comparable to those for placebo. Single and repeated oral doses of eprosartan ranging from 50 mg to 1,200 mg daily had no effect on serum uric acid concentrations or urine uric acid excretion in patients with mild-to-moderate essential hypertension.

Acrylates↗

PubMed1990

Urinary fluoride excretion in responders and nonresponders after fluoride therapy in osteoporosis.

The aim of the study was to investigate the usefulness of urinary fluoride excretion in evaluating fluoride therapy. In a prospective study, 35 patients with osteoporosis were treated for about 44 months with a mean dosage of 31.4 mg fluoride ion per day. Urinary fluoride excretion and serum alkaline phosphatase activity were measured at 3-month intervals. Bone mineral content (BMC) was measured in L2-L4 with dual-photon absorptiometer. The mean number of BMC measurements was 5.7 per patient. The interindividual reproducibility for measurements in 10 patients was 2.1%. For each individual, the regression coefficient of BMC for the period of treatment was calculated. Responders were defined as those who had a positive value and nonresponders had 0 or a negative value. The percentage responders was 83%. Between responders and nonresponders no differences were found for age, fluoride dosage, duration of treatment, or changes in serum alkaline phosphatase activity. Urinary fluoride excretion was higher in responders than in nonresponders (p less than 0.001) and a positive correlation (p less than 0.001) was obtained between the changes in BMC and urinary fluoride excretion. In the responders, 90% had a urinary fluoride excretion greater than 8 mg/24 h. All nonresponders had a urinary fluoride excretion less than 8 mg/24 h. Urinary fluoride excretion is a valuable predictor of BMC response during fluoride therapy for osteoporosis.

Aged↗

PubMed1992

Urinary excretion of taurine as a function of taurine intake: potential for estimating taurine bioavailability in the adult cat.

Urinary taurine excretion increases markedly when excess taurine is consumed. Experiments were designed to characterize this response in an attempt to develop an assay system for taurine bioavailability in common cat foods using an adult cat model. Initial studies investigated the time course of changes in urinary taurine excretion in response to alterations in taurine intake. The rate of urinary taurine excretion decreased rapidly when cats were switched from a casein diet supplemented with 0.2% crystalline taurine to a diet containing no supplemental taurine, reaching steady-state in 2 d. In contrast, urinary taurine excretion by cats switched from low to high taurine did not plateau until 6 to 7 d. Subsequently, cats (n = 18) were fed a casein diet containing graded levels of crystalline taurine (0, 0.025, 0.05, 0.10, 0.15 or 0.20%). After a 7-d adjustment period, urinary taurine excretion was quantified over a 5-d collection period and also by cystocentesis, and blood taurine levels were measured on d 6. Plasma taurine increased linearly (r = 0.88) as taurine intake increased, while whole-blood taurine increased asymptotically, reaching 95% of maximum concentration at a taurine intake of 93 mu mole/(kg body weight.d). The rate of urinary taurine excretion increased only slightly as taurine intakes increased to 96 mu mol/(kg body weight.d), but increased markedly (15-fold) thereafter. The same pattern was observed whether urinary taurine excretion was expressed as mu mole/(kg body weight.d) from total urine collection or as mu mole/g creatinine from cystocentesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

PubMed1989

The effect of cyclosporine on urinary kallikrein excretion in patients with rheumatoid arthritis.

The effect of cyclosporine (6 to 8 mg/kg/24 hr) on urinary kallikrein excretion is summarized for 9 patients with rheumatoid arthritis using a specific kallikrein radioimmunoassay. Baseline serum creatinine and BUN values were within the normal range for all patients, and baseline kallikrein excretion rates were either normal (n = 5) or more than two S.D. below the mean of the normal group (n = 4). The patients with normal baseline values excreted significantly less urinary kallikrein three and six months after cyclosporine therapy was started, but all of them completed the six-month protocol. Patients in the subgroup with low baseline values also decreased their kallikrein excretion in response to cyclosporine therapy, and two of the four in this group experienced elevations of BUN such that therapy was terminated. In a low-dose (3 mg/kg/24 hr) open extension that followed the initial trial, kallikrein excretion decreased by almost 50% at least one month before any change in serum creatinine was observed. The data suggest that changes in urinary kallikrein excretion rates may be an indicator or predictor of cyclosporine nephrotoxicity. Decreased kallikrein excretion rates could also be a factor in the diminished renal blood flow reported in patients treated with cyclosporine.

Arthritis, Rheumatoid↗

PubMed1985

Intestinal excretion of toxic substances.

Chemicals can be eliminated from body via feces by two major mechanisms, namely biliary and intestinal excretion. The relative importance of these processes in the elimination of a highly lipophilic xenobiotic such as hexachlorobenzene (HCB) has been studied. It has been demonstrated that fecal (90%) rather than urinary (10%) excretion is the major route of elimination of HCB in most species. It has been shown also that the bile of HCB dosed animals contained HCB metabolites only whereas fecal excretion consisted primarily of the parent compound. These findings suggested that the bile could not be the source of fecal HCB. Indeed, bile duct ligation in rats increased rather than decreased the fecal excretion of HCB. Experiments in rhesus monkeys with complete biliary bypass confirmed the conclusion that the source of fecal HCB is not the bile, suggesting that most of the fecal HCB originated from intestinal excretion. Exfoliation of intestinal epithelium and exudation across the intestinal mucosa are the two major nonbiliary mechanisms whereby xenobiotics can enter the intestinal lumen. The contribution of desquamation and exudation to fecal excretion of HCB was estimated in jejunectomized and hemicolectomized rats. Removal of 50% of the jejunum did not influence fecal excretion of HCB, whereas excision of 50% of the large intestine reduced it by 40%. These data suggest that the source of fecal HCB is nonbiliary, intestinal transfer (exudation) from blood into the intestinal contents, which occurs primarily in the large intestine. Fecal elimination of HCB is significantly enhanced by dietary treatments with mineral oil or hexadecane.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

PubMed1992

Feeding but not salt loading is the dominant factor controlling urinary dopamine excretion in conscious rats.

We studied urinary dopamine excretion in three different groups of rats after the following treatment regimens: normal chow and tap water (controls, CON), normal chow and 1% NaCl as drinking water (high salt, HS), and chow with low sodium content plus tap water (low salt, LS). On days 5 and 7 of the respective dietary treatment, rats were placed in metabolic cages. Using a cross over design, chow was given (fed) or withheld (fasted). Urine was collected for 24 h and analyzed for sodium, creatinine, and dopamine. Urinary dopamine excretion did not change in proportion to large differences in sodium excretion in fasted animals. Sodium excretion was enhanced (45%) due to feeding only in the CON group but not in HS and LS rats. However, there was a striking increase in renal dopamine excretion in fed compared to fasted animals, irrespective of their sodium diet: 2.5-fold in CON, 2-fold in HS, and 1.8-fold in LS rats. Urinary creatinine excretion was significantly elevated during the feeding condition compared to fasted animals in all treatment groups. Our results demonstrate that urinary dopamine excretion is dominantly influenced by feeding but not by oral sodium intake in conscious rats. We conclude that 1) the dietary state of the animals should be controlled in experiments on renal dopamine production, 2) renally formed dopamine could be involved in the functional response of the kidney to oral food intake.

Animals↗

PubMed1992

Adaptation to soil pollution by cadmium excretion in natural populations of Orchesella cincta (L.) (Collembola).

Population differentiation in Orchesella cincta (L.) (Collembola) populations, from various heavy metal contaminated sites, was studied by comparing cadmium excretion efficiency in first generation (F1) laboratory individuals. Animals from sites with high metal concentrations in the litter and with a long history of contamination showed significantly higher excretion efficiencies than animals from low pollution, or reference sites. Differences found in the F1 laboratory animals suggest evidence for genetic differences between the populations. Beneficial and detrimental effects of cadmium excretion were studied in relation to body growth and cadmium concentrations. In chronically exposed animals from an unpolluted site, no physiological acclimation was observed. Excretion efficiency was negatively correlated with body concentrations of cadmium. No detrimental effects were found. Whole-body equilibrium concentrations of cadmium and lead were similar in F1 animals from the reference site and polluted sites. Significant differences in excretion efficiencies imply that the distribution of toxic metals over body compartments differs, tolerant populations having a higher proportion deposited in the gut. Body concentrations of zinc were consistently higher in animals from the polluted site, during both cadmium and zinc exposure. No detrimental effects of increased cadmium excretion on body concentrations of zinc were observed. Population comparisons of cadmium excretion efficiency data and growth reduction in F1 laboratory animals showed that both parameters were inversely related. Cadmium and lead contamination were not the sole factors determining tolerance differentiation.

Adaptation, Physiological↗

PubMed1980

Intravenous insulin decreases urinary albumin excretion in long-term diabetics with nephropathy.

The effect of intravenous injection of insulin on heart rate, plasma noradrenaline and urinary excretion rates of albumin and beta-2-microglobulin was examined in 10 long-term diabetics, 5 of whom had albuminuria. --In patients without albuminuria intravenous injection of insulin resulted in changes similar to but less pronounced than those previously observed in short-term diabetics: albumin excretion, plasma noradrenaline and heart rate increased, creatinine excretion decreased significantly. --Intravenous injection of insulin increased heart rate but not plasma noradrenaline in long-term diabetics with albuminuria. Arterial blood pressure did not change after insulin. Contrary to expectation insulin decreased urinary albumin excretion (from 418 to 312 micrograms/min, 27 per cent) in these patients. There was a marked decrease in urinary excretion rates of beta-2-microglobulin and creatinine (55 and 17 per cent, respectively) after insulin. --The decrease in albumin excretion after insulin in diabetics with albuminuria is most likely due to renal vasoconstriction. The absence of a rise in albumin excretion after insulin may be due to severe morphological changes in glomeruli in these patients.

Adult↗

PubMed1988

Urinary protein excretion rates in experimentally diabetic dogs and experimentally galactosaemic dogs.

The relationship between urinary protein excretion and control of diabetes was evaluated in alloxan-diabetic dogs prospectively assigned to poor, moderate, or good glycaemic control. Protein excretion rate increased with the duration of insulin deficiency, and was significantly greater than normal in the poor control group by the fourth year of diabetes. Appreciable differences in the severity of the proteinuria were observed among animals of the poor and moderate glycaemic control groups; some of the animals excreted in excess of 500 mg protein/24 h while others excreted no more than normal throughout the 5 years of study. Differences in glycaemic control among these insulin-deficient animals seem not sufficient to account for the observed differences in protein excretion. Immunoassay for albumin indicated that the defect resulting in supranormal protein excretion was at least partly glomerular in origin. Good glycaemic control prevented the protein loss from exceeding normal. A potential role of hyperglycaemia in the development of proteinuria was examined in nondiabetic dogs made experimentally hyperglycaemic with galactose. Consumption of a 30% galactose diet for up to 5 years duration had little influence on protein excretion.

Animals↗

PubMed1989

Urinary albumin excretion in diabetic pregnancy.

We have analysed the results of urinary albumin excretion in timed overnight urine samples once every two weeks during pregnancy and post-natally in 25 non-diabetic women and 14 women with Type 1 (insulin-dependent) diabetes who were Albustix negative and had urinary albumin excretion less than 15 micrograms.min-1 at conception. Urinary albumin excretion did not vary significantly in the first two trimesters in either group and at 28 weeks was 2.73 micrograms.min-1 (0.32-251.68) (median and range) in the diabetic women and 2.53 micrograms.min-1 (0.90-13.37) in control patients (not significant). During the third trimester urinary albumin excretion increased, and levels were significantly higher in diabetic patients from 36 weeks (9.37 (0.9-31.78) vs 3.52 (0.19-33.74) micrograms.min-1, p less than 0.01) until delivery. In both groups, urinary albumin excretion reached a peak within the week following delivery - diabetic 17.42 micrograms.min-1 (2.03-46.64), control subjects 16.29 micrograms.min-1 (1.53-35.56), but six weeks after delivery, levels were similar to those in early pregnancy. The effect of pregnancy on urinary albumin excretion in these diabetic women would appear to be an exaggeration of the normal pattern, with levels returning to normal post-delivery. It is not possible to know if this has significance for future renal function, but it would be important to investigate this phenomenon in patients who already have raised urinary albumin excretion at conception.

Adult↗

PubMed1988

Coronary heart disease and urinary albumin excretion rate in type 2 (non-insulin-dependent) diabetic patients.

Associations between overnight urinary albumin excretion rate and prevalent coronary heart disease and its major risk factors were examined in a cross-sectional study of 141 Type 2 (non-insulin-dependent) diabetic patients. Mean albumin excretion rate was higher in men (geometric mean 13.5 micrograms/min; 95% confidence interval 10.3-17.6) than women (7.5 micrograms/min; 5.7-9.8, p less than 0.01). In diabetic men and women mean albumin excretion rate was higher in those with electrocardiographic and/or symptomatic evidence of coronary heart disease than in those without (men, 23.1 micrograms/min; 95% confidence interval 13.7-39.0 versus 10.6 micrograms/min; 7.9-14.2, p less than 0.01, women, 13.7 micrograms/min; 8.0-23.5 versus 5.4 micrograms/min; 4.2-6.8, p less than 0.01). Multiple logistic regression analysis was used to allow for confounding between variables. In the diabetic group as a whole, raised albumin excretion rate (p less than 0.001), gender (p less than 0.05) and systolic blood pressure (p = 0.06) entered the "best" model for coronary heart disease prediction. In women, albumin excretion rate alone (p less than 0.01) and in men albumin excretion rate (p less than 0.01) and age (p = 0.05) entered the "best" models. We conclude that albumin excretion rate is significantly associated with coronary heart disease morbidity after taking into account the confounding effects of raised blood pressure and other cardiovascular risk factors.

Adult↗

PubMed1986

Urinary polyamine excretion by tumor-bearing and tumor-free mice exposed to cyclophosphamide, 5-fluorouracil and 6-mercaptopurine.

The effects of cytostatic treatment on urinary polyamine excretion have been investigated in tumor-bearing (either Ehrlich carcinoma of S 180 sarcoma) and in tumor-free mice. The animals were exposed to single or multiple treatment with various doses of cyclophosphamide, 5-fluorouracil, or 6-mercaptopurine. Treatment invariably enhanced polyamine excretion dependent on dose and effectiveness of the cytostatic drug. The most pronounced increases were observed in the excretion of spermine and putrescine, with peak excretion usually occurring after 1-2 and 3-4 days, respectively. The urinary excretion of spermidine was relatively modest in untreated mice, but the increases observed following drug treatment were high in proportion. Significant differences in urinary polyamine excretion were observed between tumor-free and tumor-bearing animals following treatment with all cytostatic agents. Peak values were invariably higher in tumor-bearing mice even in those with small, barely detectable tumors. After discontinuation of treatment polyamine excretion returned to normal values and stabilized in groups in which regression predominated, whereas in those groups of animals which showed little or no tumor regression urinary polyamine levels gradually increased again during a 2-week observation period.

Animals↗

PubMed1988

Pharmacokinetics of biliary excretion in man. VI. Indocyanine green.

The pharmacokinetics of Indocyanine Green (ICG) has been studied in 15 patients given 0.5, 1.0 and 2.0 mg.kg-1. The plasma disappearance and biliary excretion rate were measured in patients with tightly fitting catheters under slight negative pressure in order to achieve complete collection of bile. Recovery of unchanged ICG in bile over 18 h after the i.v. injection was 80% of the dose in all three dose groups. Plasma disappearance in all 3 groups was biphasic, showing an initial phase with a t1/2 of 3-4 min and a secondary phase with a dose-dependent apparent t1/2 of 67.6, 72.5 and 88.7 min, respectively. After 0.5 and 1.0 mg.kg-1 the biliary excretion rate curves showed an ascending phase with a mean t1/2 of 5 min and a descending phase with a mean t1/2 of 72 min. It was inferred that the secondary component of the plasma-decay mainly reflected the biliary excretion rate. After 2.0 mg.kg-1 in some patients the biliary excretion curve showed features of saturation; the t1/2 of the descending phase ranged from 73 to 440 min, and the time of maximal excretion was increased from 1.3 to 2.7 h after injection, whilst the mean maximal excretion rate was in the same range as the excretion rate after the 1.0 mg.kg-1 dose. The non-linear pharmacokinetics was only moderately reflected in the measured plasma disappearance patterns. Two compartment analysis of the plasma levels indicated a clearance of 230-260 ml.min-1, whereas the clearance conventionally calculated from the initial t1/2 was 475 ml.min-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1977

Paradoxical potassium excretion in response to aldosterone antagonists.

The activity of two aldosterone antagonists in reversing the urinary electrolyte changes induced by the mineralocorticoid fludrocortisone was examined in healthy subjects. Between 2-10 h after treatment there were dose-related increases in sodium excretion and the urine log 10 Na/K ratio, but no significant changes in urine volume, potassium concentration, or potassium excretion. Between 12-16 h after treatment there were dose-related increases in urine sodium excretion and the log 10 Na/K ratio. Unexpectedly, there were significant dose-related increases in potassium excretion despite significant dose-related reductions in urinary potassium concentration. The paradoxical increases in potassium excretion were attributed to dose-related increases in urine volume in the same period. These observations may explain the increased potassium excretion occasionally observed during clinical use of aldosterone antagonists and suggest that potassium excretion in man is influenced by the urine flow rate.

Adult↗

PubMed1981

The effects upon urinary excretion of distension of the isolated pulmonary arteries in anaesthetized dogs.

1. The experiments were carried out to determine whether localized pulmonary arterial distension caused changes in the renal excretion of water and solutes. 2. When pulmonary arterial pouch pressure was maintained constant at low pressure 0.5-1.6 KPa (4-12 mm Hg) urinary excretion of sodium remained relatively constant over a period of 110 min. 3. Increasing pulmonary arterial pouch pressure by 3.6 KPa (27 mm Hg) did not cause changes in systemic pressure or solute excretion. Increasing pulmonary arterial pouch pressure by 6.7 KPa (50 mm Hg) increased systemic arterial pressure and caused a small increase in sodium excretion. 4. In dogs prepared in similar fashion but with one kidney totally isolated and perfused at constant pressure, increasing pulmonary arterial pouch pressure by 9.3 KPa (70 mm Hg), increased systemic arterial pressure, osmolal clearance and solute excretion from the intact kidney. There were no changes in urinary excretion from the isolated perfused kidney. 5. The increase in solute excretion associated with pulmonary arterial distension is most likely to be due to haemodynamic effects on the kidney possible accompanied by changes in renal nerve activity.

Anesthesia, General↗

PubMed1994

The differential diagnostic value of urinary enzyme and amino acid excretion in children with nephrotic syndrome.

Urinary enzymes N-acetyl-beta-D-glucosaminidase (NAG) and gamma-glutamyl transpeptidase (gamma-GT) are sensitive markers of specific renal cell damage. Excessive urinary amino acid excretion may also be an indicator of renal tubular damage. We have evaluated urinary excretion of NAG, gamma-GT and 37 amino acids, phospholipids and dipeptides in 30 children (aged 2.3-18.1 years) with nephrotic syndrome (NS), 23 with minimal change nephrotic syndrome (MCNS), 7 with focal segmental glomerulosclerosis (FSGS) and 16 healthy age-matched controls. Nine MCNS patients were in relapse and 14 in remission. Enzyme activity is expressed as micromoles per milligram urinary creatinine. In FSGS, NAG excretion correlated with the following: blood urea nitrogen (BUN) (r = 0.8), serum protein (r = 0.57), serum cholesterol (r = 0.85), serum albumin (r = -0.68) and proteinuria (r = 0.56). In FSGS the gamma-GT excretion was not significantly different from MCNS in remission or in relapse. In FSGS, gamma-GT excretion correlated with the following: BUN (r = 0.48), serum creatinine (r = -0.66), serum protein (r = -0.54), serum albumin (r = -0.68) and serum cholesterol (r = 0.87). Compared with controls, the urinary excretion of 5 amino acids was increased in FSGS patients as a possible indicator of tubular damage. The value for 7 amino acids was reduced in MCNS patients. Urinary amino acid excretion was not different from controls for the other amino acids in either FSGS or MCNS.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylglucosaminidase↗

PubMed1994

Urinary mineral excretion among normal Taiwanese children.

Prompted by a large population of children with renal stones seen in 20 of our country's teaching hospitals over the past 10 years, this study of urinary mineral excretion in normal children was performed. Fasting urine from 1,072 normal Taiwanese school children and 24-h urine collections from 125 children separated into three age groups were analysed for calcium (Ca), phosphate, magnesium (Mg), uric acid, sodium (Na) and creatinine (Cr). Fasting Ca/Cr ratios were not different between the sexes. Ca/Cr ratios were higher in the 17- to 18-year age group as were 24-h urinary Ca excretions. Urinary Mg/Cr ratios were higher in girls than boys and 24-h urinary Mg excretion was highest in the younger age groups. Urinary Mg excretion in Taiwanese children is 54%-86% lower than previously reported in Caucasian children. Both uric acid/Cr ratios and 24-h urinary uric acid excretion were highest in the youngest children. Urinary Na/Cr ratios and 24-h urinary Na excretion were higher in the two younger age groups. There was no correlation between 24-h urinary Ca and Na excretion.

Adolescent↗

PubMed1991

Inhalation exposure to 1,3-dichloropropene in the Dutch flower-bulb culture. Part II. Biological monitoring by measurement of urinary excretion of two mercapturic acid metabolites.

A biological monitoring study was carried out in the Dutch flower-bulb culture to determine the relationship between respiratory occupational exposure to Z- and E-1,3-dichloropropene (Z- and E-DCP) and urinary excretion of two mercapturic acid metabolites, N-acetyl-S-(Z- and E-3-chloropropenyl-2)-L- cysteine (Z- and E-DCP-MA). Urinary excretion of Z- and E-DCP-MA, either based on excretion rates or on creatinine excretion, followed first order elimination kinetics after exposure. Urinary half-lives of elimination were 5.0 +/- 1.2 hr for Z-DCP-MA and 4.7 +/- 1.3 hr for E-DCP-MA and were not statistically significantly different. Calculated coefficients of variation indicated that the half-lives of elimination of Z- and E-DCP-MA were quite consistent inter- and intra-individually. Strong correlations (r greater than or equal to 0.93) were observed between respiratory 8-hr time weighted average (TWA) exposure to Z- and E-DCP and complete cumulative urinary excretion of Z- and E-DCP-MA. Z-DCP yielded three times more mercapturic acid than E-DCP, probably due to differences in metabolism. Z- and E-DCP were excreted 45 and 14% as their respective mercapturic acid metabolites. A respiratory 8-hr TWA exposure to the Dutch occupational exposure limit of 5 mg.m-3 DCP would result in a complete cumulative excretion of 14.4 mg (95% confidence interval: 11.7-17.0 mg) Z-DCP-MA and 3.2 mg (95% confidence interval: 2.3-4.1 mg) E-DCP-MA.

Adult↗