Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “EXCRETION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 541 records · Page 30Linked to original sources
PubMed2003

Urinary chiro-inositol and myo-inositol excretion is elevated in the diabetic db/db mouse and streptozotocin diabetic rat.

Inositol phosphoglycan molecules containing either D-chiro-inositol or myo-inositol have been isolated from various mammalian tissues and are putative mediators of insulin action. Urinary excretion of inositols appears to be altered in diabetes mellitus; however, the relationships with different types of diabetes are unclear. The objective of this study was to determine the urinary excretion of chiro- and myo-inositol in diabetic animal models, including streptozotocin (STZ) rats, db/db mice, and fa/fa Zucker rats. In STZ rats (type 1 diabetes), 12-hr urinary excretion of chiro-inositol was elevated 336-fold and myo-inositol excretion was elevated 47-fold compared with their nondiabetic counterparts. When corrected for creatinine, chiro-inositol excretion was 259-fold higher and myo-inositol excretion was 36-fold higher in STZ rats than in normal rats. The same pattern was observed in db/db mice (type 2 diabetes), where 12-hr urinary chiro-inositol excretion was elevated 247-fold compared with normal mice. When corrected for creatinine, chiro-inositol excretion was 2455-fold higher and urinary myo-inositol excretion was elevated 8.5-fold in db/db mice compared with normal mice. The fa/fa Zucker rats (impaired glucose tolerance) had a pattern of urinary inositol excretion that was similar to the nondiabetic animals (lean Zucker rats, C57BL/6 mice, and Sprague-Dawley rats). In summary, urinary chiro-inositol and myo-inositol excretion was elevated in animal models of type 1 and type 2 diabetes mellitus, concomitant with hyperglycemia and glucosuria.

Animals↗
PubMed1984

Urinary kallikrein excretion in insulin-dependent diabetes mellitus and its relationship to glycemic control.

The renal kallikrein-kinin system is thought to be involved in vasoregulatory and epithelial ion-transporting processes. Renal kallikrein has not been studied in patients with diabetes mellitus, a disease in which abnormalities of renal hemodynamics and electrolyte handling occur. The urinary excretion of this kallikrein was measured in 20 type I diabetic patients and 10 normal subjects. On a 120-meq Na diet, daily kallikrein excretion, determined by both esterase activity and direct RIA, in 12 poorly controlled diabetic patients [hemoglobin A1c (HbA1c) = 14.2 +/- 0.5% (mean +/- SEM)] was significantly greater (P less than 0.05) than excretion in 8 diabetic patients in good to moderately good control (HbA1c = 9.4 +/- 0.5%) or in 10 normal subjects. In these groups, urinary esterase activities were 9.4 +/- 1.0, 6.1 +/- 1.4, and 6.7 +/- 0.5 esterase units/24 h, respectively. Corresponding excretion values of immunoreactive kallikrein were 171 +/- 14, 118 +/- 26, and 123 +/- 11 micrograms/24 h. Creatinine clearances were similar in the three groups. Urinary kallikrein was also measured in 8 diabetic and 8 normal subjects during 7 subsequent days of 10 meq Na intake. It increased less in diabetic patients than in normal subjects during Na depletion (P less than 0.02). The increase in urinary kallikrein in the diabetic patients was inversely related to their HbA1c levels (r = 0.88; P less than 0.01). The effect of glycemic control on urinary kallikrein excretion was determined in nine diabetic patients. Initial glycemic control was achieved using an artificial endocrine pancreas (Biostator) and was maintained by continuous sc insulin infusion with a portable pump. Before glycemic control, urinary kallikrein was 190 +/- 30 micrograms/24 h (by RIA). After 8-12 days of glycemic control, excretion fell to 144 +/- 23 micrograms/24 h (P less than 0.02). The abnormalities in kallikrein excretion in diabetic patients were not correlated with differences in water, electrolyte, protein, glucose, or aldosterone excretion in any of the studies. These results show that kallikrein excretion was increased in patients with poorly controlled insulin-dependent diabetes, and excretion rose less in diabetic subjects with low Na intake than in normal subjects. Strict glycemic control decreased urinary kallikrein excretion. These findings suggest that the renal kallikrein-kinin system is functioning abnormally in diabetes mellitus.

Adult↗
PubMed1998

Urinary equol excretion with a soy challenge: influence of habitual diet.

Equol is an isoflavonoid phytoestrogen produced from the soy isoflavone daidzein by gut microflora. Not all humans produce equol from daidzein, presumably due to differences in colonic bacterial populations among individuals. Previously, smaller studies reported that approximately 30% of participants excreted equol when consuming soy. The purpose of our study was to determine the prevalence of equol excreters in a larger sample and to examine what dietary components might influence the tendency to be an equol excreter. Thirty men and thirty women consumed a soy protein beverage containing 22 mg genistein and 8 mg daidzein for 4 days as a supplement to their habitual diets. The mean daily nutrient content of their habitual intakes was determined from 4-day food records. On Day 4, participants provided a 24-hour urine collection. Urinary isoflavonoid (genistein, daidzein, equol, and O-desmethylangolensin) excretion was measured by gas chromatography-mass spectrometry. Twenty-one of the 60 participants (35%) excreted equol (> 2000 nmol/day) after 3 days of consuming the soy supplement. Daily equol excretion ranged from 2,134-20,301 nmol/day in the excreters and 21-233 nmol/day in the nonexcreters. There was no difference in equol excreter prevalence between men (43%) and women (27%). Daily excretion of daidzein, genistein, and O-desmethylangolensin was similar between equol excreters and nonexcreters and between men and women. Among the women, equol excreters consumed a significantly higher percentage of energy as carbohydrate and greater amounts of plant protein and dietary fiber, both as soluble and insoluble fiber compared to nonexcreters. Such differences were not observed in the men, who overall had significantly higher fiber intakes than the women. These data suggest that, among women, dietary fiber or other components of a high-fiber diet may promote the growth and/or the activity of bacterial populations responsible for equol production in the colon.

Adult↗
PubMed1978

Studies on the metabolism and toxicity of dinitrotoluenes--on the absorption and excretion of tritium-labelled 2,4-dinitrotoluene (3H-2, 4-DNT) in the rat.

In order to investigate the detailed absorption and excretion of 2, 4-DNT in the rat, after the single oral administration of 3H2, 4-DNT, the time-course of radioactivity level in blood, liver and digestive organ contents, and of biliary, faecal and urinary excretion were observed. Radioactivity level in blood reaches a peak at 6 hr after the administration and its half-life was about 22 hr. Maximum level of radioactivity in the liver was observed at 6 hr after the administration as well as in the blood. In contrast with the radioactivity levels in blood and liver, amount of radioactivity in small intestine content is markedly decreased for 6 hr after administration. In the biliary excretion, about 10 per cent of the radioactivity administered was excreted in bile within 24 hr. The excretion rate is rising steadily from 6 hr after administration and its peak time was 9-10 hr. In the faecal excretion, the most of the excretion radioactivity was concentrated on 6-9 hr. In the faecal excretion, the most of the excretion radioactivity was concentrated on 6-9 hr faeces as reflected with the biliary excretion pattern. On the other hand, the most of the urinary excretion radioactivity was concentrated on 0-6 hr urine.

Absorption↗
PubMed1999

Urea and osmotic excretion in rats exposed to chronic centrifugation.

BACKGROUND: A reduction in vasopressin was attributed to the initial diuresis reported in rats exposed to chronic centrifugation. However, it was suggested that urea may also contribute an osmotic component to this observed diuresis. HYPOTHESIS: Increased urea excretion will contribute to osmotic excretion during chronic centrifugation, which may be partly responsible for the initial diuresis previously observed. METHODS: Eight Sprague-Dawley rats were centrifuged (12 d at -2Gx) and eight were used as a control group. Daily urine samples were collected and an aliquot measured for excreted solutes and aldosterone. RESULTS: Urine volume was elevated over the first 7 d of centrifugation with a peak on day 4. Urea and osmotic excretion were elevated over the first 5 d. Excreted Na+ was elevated on days 1 and 2, which coincided with an increase in excreted aldosterone over the first 3 d of centrifugation. Urea excretion accounted for up to 54% of the increase in osmotic excretion during the initial portion of centrifugation suggesting that urea was, in part, responsible for the observed increase in urine output despite a reduction in water consumption. Following the first day of centrifugation, aldosterone appears to regulate Na+ as suggested by the reduction in Na+ excretion between days 2 and 3 when aldosterone excretion was elevated. CONCLUSIONS: It would appear that centrifugation induced an acute increase in protein catabolism as indicated by the increase in urea excretion which resulted in an increase in obligatory water loss. This increased diuresis may have acute consequences on the hydration state of centrifuged rats.

Aldosterone↗
PubMedDate not supplied

A population-specific formula predicting creatinine excretion in continuous peritoneal dialysis.

OBJECTIVE: The Cockroft-Gault formula was shown to systematically overestimate the decline in creatinine excretion with age in continuous peritoneal dialysis (CPD) patients and is, therefore, not suitable for studying creatinine excretion. The purpose of the present study was to develop and test a population-specific formula predicting average creatinine excretion in CPD. METHODS: Creatinine excretion in urine plus dialysate was measured in 925 CPD patients. Forty patients were excluded because of evidence of noncompliance. The remaining 885 subjects were randomly grouped into a derivation group (n = 432) and a validation group (n = 453). Stepwise multiple linear regression models were used to predict creatinine excretion in the derivation group. The candidate variables, chosen because they were previously shown to be predictors of creatinine excretion in CPD, included weight (W), age (A), gender (G), diabetes (D), and interaction terms between these four variables. Estimates of creatinine excretion from the best-fit regression formula (CrExcr1) and from the Cockroft-Gault formula (CrExcr2) were compared to creatinine excretion (CrExcr) in the validation group. RESULTS: The best-fit regression model in the derivation group included all four candidate variables (W, A, G, D), but no interaction terms. This model was as follows: CrExcr1 = 302.150 - 4.380A + 171.234G - 39.041D + 11.730W (r2 = 0.477, p < 0.001). In the validation set, CrExcr = -15.795 + 0.988CrExcr1 (r2 = 0.447, p < 0.001), and CrExcr = -303.823 + 0.732CrExcr2 (r2 = 0.340, p < 0.001). When the differences between measured and predicted creatinine excretion did not take into account the sign of each individual difference, CrExcr - CrExcr1 = 201 +/- 156 mg/24 hours, and CrExcr - CrExcr2 = 235 +/- 174 mg/24 hr (p < 0.001) in the validation group. When the sign of the difference was taken into account, CrExcr - CrExcr1 = -28 +/- 149 mg/24 hr, and CrExcr - CrExcr2 = 63 +/- 295 mg/24 hr (p < 0.001). CONCLUSIONS: A population-specific formula predicting creatinine excretion in CPD was derived. This formula has greater accuracy than the Cockroft-Gault formula and can be used in studies of creatinine excretion in CPD.

Adult↗
PubMed1976

Effect of bile acid on hepatic excretion and storage of bilirubin in ponies.

Endogenous bilirubin uptake from plasma and biliary bilirubin excretion were determined in ponies with chronic biliary T-tube fistulas. Excreted bile was quantitatively recovered. Uptake was calculated from the plasma disappearance of 14C-labeled bilirubin. Biliary bilirubin excretion was determined directly in excreted bile. When bile acid excretion was low (during continuous drainage without bile acid replacment), bilirubin excretion was 37% less than uptake. Uptake and excretion were essentially identical when taurocholic acid was infused to replace bile acids. After depletion of the bile acid pool, replacement of bile acids (by taurocholic acid infusion) greatly increased both bilirubin excretion and its biliary concentration for approximately 1 hour. After this initial increase, bilirubin excretion was maintained at a rate approximately 30% greater than the preinfusion rate. Bile acid excretion was found to be essential for normal, endogenous bilirubin excretion.

Animals↗
PubMed1975

Anion excretion pattern following infusion of hyperoncotic human serum albumin into dogs.

The effects of hyperoncotic human serum albumin on the excretion rates of several electrolytes and cyclic-AMP were measured in mongrel dogs and the results were compared with those obtained after the infusion of saline. Hyperoncotic albumin increased the excretion rates of sodium, potassium, bicarbonate, and phosphate. There was a small increase in chloride excretion after albumin, while there was a significant decrease in the rate of excretion of cyclic-AMP. Saline, on the other hand, caused a marked increase in the rate of of excretion of all the measured ions. Like albumin, saline was associated with a decrease in the rate of excretion of cyclic-AMP. The marked increase in bicarbonate and phosphate excretion suggests that the response to albumin which includes decreased isotonic reabsorption in the proximal tubule and increased urinary sodium excretion could result from decreased reabsorption in the proximal tubule accompanied by distal sodium and chloride reabsorption. Saline, on the other hand, caused a greater increase in sodium excretion and, although phosphate and bicarbonate excretion also increased, a much greater effect on the excretion of chloride was observed, suggesting that saline may also decrease sodium and chloride reabsorption in the distal nephron.

Animals↗
PubMedDate not supplied

Circadian and seasonal variations in iodine excretion in children with and without endemic goiter.

The urinary iodine excretion was measured in 193 children 11 +/- 1.5 years of age living in the endemic goiter area of Dîmboviţa, Romania. One hundred and thirty four of the children showed some degree of endemic goiter, 59 showed none. All children followed a diurnal activity pattern with rest during the night. They received their usual iodine supplement of 1 gm potassium iodide once a week during the school year (which included the time of all measurements made). Urine was collected in six 4-hour samples over a 24-hour span. The examinations were conducted during the months of March, June, September and December. Iodine was determined by an automated ceric ion arsenic acid method using a Technicon Autoanalyzer. Circadian and seasonal variations of urine volume and iodine excretion were statistically verified by the cosinor technique and the seasonal variations also by one way analysis of variance using the circadian means as input. A comparable circadian rhythm of iodine excretion was found in the children with and without endemic goiter, with an acrophase during the evening (20:16 with a 95% C.I., from 19:32 to 21:04). The circadian rhythm in iodine excretion has to be taken into account whenever an estimate of the 24-hour excretion is attempted from a sample covering less than the entire 24-hour span. There was a statistically significant seasonal variation of the 24-hour iodine excretion in the boys with and without endemic goiter and in the group as a whole. The 24-hour iodine excretion during March was 102 +/- 6 mcg, during June 81 +/- 4 mcg, during September 79 +/- 3 mcg and during December 102 +/- 7 mcg. The average 24-hour iodine excretion pooled over all seasons was 91 +/- 3 mcg/24 hrs in the children with and 91 +/- 5 mcg/24 hrs in the children without endemic goiter. During March and December the iodine excretion indicates an iodine intake not usually associated with a high prevalence of endemic goiter. However, during the months of June and September (and presumably even more during the months of July and August when during summer vacation no iodine supplementation was given in school) the 24-hour iodine excretion indicates some degree of iodine deficiency. The seasonal variation in urinary iodine excretion thus points to a time when increased iodine prophylaxis may be of value.

Child↗
PubMed1987

Effect of inhibition of gamma-glutamyltranspeptidase on biliary and urinary excretion of glutathione-derived thiols and methylmercury.

Acivicin (AT-125; 6.25-200 mumol/kg i.v.) inhibited hepatic, biliary and renal gamma-glutamyltranspeptidase (GGT) activity up to 88, 99 and 97%, respectively, in 4-week-old rats. This inhibition of GGT by acivicin resulted in a 10- to 12-fold increase in the biliary excretion of reduced (GSH) and oxidized glutathione. Because the biliary excretion of cysteinylglycine (Cys-Gly), Cys-Gly disulfide, cysteine (Cys) and cystine concomitantly decreased (63-99%), the biliary excretion rate of total glutathione-derived thiols and disulfides did not change. In contrast, acivicin treatment dramatically elevated the urinary excretion rate of glutathione-derived thiols in a dose-dependent fashion, resulting in a 390-fold increase at the highest dosage. This mainly originated from enhancement of urinary excretion of GSH (up to 7200-fold), although the excretion of Cys and Cys-Gly into urine was also increased. Acivicin treatment did not affect hepatic and renal levels of GSH but, at high dosages, reduced the concentration of Cys in these organs. GSH and oxidized glutathione concentrations in serum were increased, whereas cystine was diminished in acivicin-treated rats. Inhibition of GGT by acivicin (100 mumol/kg i.v.) failed to influence the biliary excretion of methylmercury but increased urinary excretion 34-fold. Even though the urinary thiol excretion was much higher than the biliary thiol excretion in the acivicin-treated rats, methylmercury was preferentially excreted into bile rather than urine, indicating the importance of the liver as an excretory organ for methylmercury.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Effects of long-term aurothiomalate and D-penicillamine treatments on renal function and urinary excretion of prostanoids in patients with rheumatoid arthritis.

The effects of long-term aurothiomalate and D-penicillamine treatments on renal function and the urinary excretion of prostanoids were studied in 20 patients with classic or definite rheumatoid arthritis. Twelve-hour urine was collected overnight, on the following day blood samples were taken in the morning and 12-hour urine was collected during the following day. Albumin excretion into the urine was determined by a sensitive quantitative method. Beta-2-microglobulin (B2MIGLO) and N-acetyl-beta-glucosaminidase (NAG) serum concentrations and excretions into the urine were measured to detect possible tubular or glomerular damage, respectively. The excretions of prostaglandin E2 (PGE2), thromboxane B2 and 6-keto-PGF1 alpha into urine were determined. In the aurothiomalate group, albumin excretion ranged 1-16 mg/12 h, and in the penicillamine group 0.8-31 mg/12 h. In the penicillamine group, but not in the aurothiomalate group, total protein, B2MIGLO and PGE2 excretions were higher (p less than 0.05) during the daytime than during the night. The daytime excretion of PGE2 was higher (p less than 0.01) in the penicillamine than in the aurothiomalate group. In the penicillamine group B2MIGLO excretion into urine correlated (p less than 0.01) with PGE2 excretion in the daytime. According to the results, not even long-term aurothiomalate treatment affects renal prostanoid excretion, while penicillamine increases urinary PGE2 excretion. This could be related either to the cofactor-like activity of penicillamine in the prostanoid synthesis or to damage in tubular cells. The role of prostanoids in maintaining blood flow and filtration may be more important in patients with renal damage than in normal conditions.

Adult↗
PubMed1983

Systemic excretion of benzo(a)pyrene in the control and microsomally induced rat: the influence of plasma lipoproteins and albumin as carrier molecules.

In vitro studies have previously indicated that benzo(a)pyrene distributes primarily into the plasma lipoprotein fraction when incubated with whole plasma. Hydroxylated metabolites of benzo(a)pyrene distribute increasingly into the albumin fraction as the degree of metabolite hydroxylation increases. This report assesses the influence of plasma lipoproteins and albumin as carriers for benzo(a)pyrene on carcinogen excretion in the control and microsomally induced rat. Male Sprague-Dawley rats cannulated in the bile duct received i.v. injections of radiolabeled benzo(a)pyrene noncovalently bound to the very-low-density, low-density, or high-density lipoproteins in equimolar amounts. Bile was collected and measured for radioactivity. Cumulative biliary excretions of benzo(a)pyrene complexed with rat lipoproteins were 39.6 +/- 9.7 (S.D.), 24.6 +/- 1.3, and 21.2 +/- 8.8% for very low-density, low-density, and high-density lipoprotein, respectively. Values for excretion of benzo(a)pyrene complexed with rat or human lipoproteins were comparable. These data suggest that the transport molecule can effect a 2-fold difference in benzo(a)pyrene excretion under conditions of the present study. We infer that metabolism of the plasma lipoprotein molecules determines, in part, the extent of benzo(a)pyrene excretion. Cumulative biliary excretions of albumin-bound benzo(a)pyrene, 3-hydroxybenzo(a)pyrene, benzo(a)pyrene 7,8-dihydrodiol, and benzo(a)pyrene-4,5-epoxide were 28.0 +/- 2.7, 39.8 +/- 0.5, 46.9 +/- 2.5, and 49.8 +/- 1.2%, respectively. Thus, excretion increased as the degree of benzo(a)pyrene hydroxylation increased. The effect of microsomal enzyme induction on excretion of lipoprotein-bound benzo(a)pyrene was also assessed. Contrary to expectation, excretion of benzo(a)pyrene bound to the very-low-density, low-density, or high-density lipoproteins in Aroclor-induced rats was not greater than that of control animals. Hence, under the conditions of the present study, 60 to 80% of the injected benzo(a)pyrene and 50 to 60% of the injected benzo(a)pyrene metabolites were not excreted immediately in control or microsomally induced animals. This benzo(a)pyrene may represent a carcinogen pool that is slowly excreted.

Animals↗
PubMed1981

Changes in the excretion of catecholamines and their metabolites in patients with essential hypertension during sodium intake restriction.

Excretion of noradrenaline (NA), adrenaline (A), dopamine (DA) and their metabolites vanillylmandelic acid (VMA), methoxycatecholamines (MNA + MA) as well as 3-methoxy-4-hydroxy-phenylglycol (MHPG) was studied in 95 patients with essential hypertension and in 25 normal subjects on normal and low sodium diets. The patients were divided into 3 groups according to NA excretion under basal conditions. NA excretion was increased during sodium intake restriction, the highest values of this increase being found in patients whose basal NA excretion was diminished. At low sodium intake the high and the low NA excretors responded with significant increases of DA excretion. The mean excretion of VMA increased significantly on low sodium diet in all 3 groups of patients. The MNA + MA excretion decreased significantly during sodium intake restriction in patients with normal NA excretion. At low sodium intake the excretion of MHPG was highest in patients with low basal NA excretion. These data suggest that in patients with essential hypertension subjected to sodium restriction the excretion and metabolism of catecholamines are related to basal sympathetic activity.

Adolescent↗
PubMed1993

[Experimental study of fecal excretion of nitrogen in different nutritional conditions].

Fecal nitrogen excretion in different nutritional conditions were studied in 32 adult Wistar rats, casually distributed in four groups: group A (12), with normal control rats; group B (6), with subcutaneous impalnt of Walker-256 carcinosarcoma, at the beginning of the experiment; group C (8), with tumor implant eight days before the experiment beginning; group D (6), with standard skin wound in 15th day. The animals were fed with normoproteic diet (25% casein content). Nitrogen ingestion and urinary and fecal excretion were daily measured. Evaluation selected parameters were: nitrogen ingestion and urinary, fecal and total excretion; nitrogen fecal excretion/ingestion, nitrogen fecal excretion/urinary excretion and nitrogen fecal excretion/total excretion ratios; nitrogen urinary excretion/ingestion and nitrogen urinary excretion/total excretion ratios. Adequate statistical analysis was done with p < 0.05 critical limit value. It was observed that in normal animals nitrogen fecal excretion was equal to 5.7% ingestion value, 12.0% urinary excretion and 10.8% total excretion. In presence of malignant tumor, nitrogen fecal excretion was equal to 79% of normal animals value. In rats with skin wound in cicatrization nitrogen fecal excretion was 70.5% of normal animals value.

Animals↗
PubMed1993

Excretion of catecholamines and metabolites in response to increased dietary phosphate intake.

The urinary excretion of free dopamine, norepinephrine, and epinephrine could reflect the contribution of the neural release and filtration of these catecholamines as well as the intrarenal tubular synthesis and metabolism of dopamine. Because these catecholamines are rapidly metabolized, the excretion of the free amines represents only a fraction of the total release and synthesis by the kidney. The present study determined the effect of increasing dietary phosphate intake on the excretion of free dopamine, norepinephrine, and epinephrine and their primary stable metabolites. Seven male rats were placed in metabolic balance cages and fed 12 gm/day of normal phosphate diet (NPD) (0.7% inorganic phosphorus [Pi]) for 4 days and then fed a high phosphate diet (HPD) (1.8% Pi) for 4 days. Twenty-four-hour urine samples were collected for determination of free catecholamines, their major stable metabolites, and electrolyte excretions. The urinary excretion data for the seven rats was combined for all 4 days of each dietary regimen. Increasing phosphate intake from 0.7% to 1.8% significantly increased free dopamine excretion by 23%, from 5.6 +/- 0.2 to 6.8 +/- 0.1 micrograms/day (n = 7, p < 0.05). This increase in free dopamine excretion was associated with similar increases in urinary excretion of dopamine glucuronide, 21.6 +/- 1.3 to 27.9 +/- 1.8 micrograms/day (32%) and the dopamine metabolite DOPAC, 9.4 +/- 0.5 to 12.1 +/- 0.6 micrograms/day (30%) and total dopamine excretion from 32.9 +/- 1.7 to 41.0 +/- 1.9 micrograms/day (27%). Plasma DOPA levels were unchanged by increased dietary phosphate intake; however, plasma norepinephrine levels decreased significantly. Excretion of free or sulfated norepinephrine was not changed by increased phosphate intake. However, excretion of MHPG, a metabolite of norepinephrine and epinephrine, decreased significantly, from 33.7 +/- 2.1 to 23.9 +/- 0.8 micrograms/day, n = 7, p < 0.05.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1977

Factors affecting bilirubin excretion in patients with cholesterol or pigment gallstones.

To identify factors affecting bilirubin excretion, the effects of bile flow and bile salt excretion on bilirubin output into bile have been examined in normobilirubinemic, cholecystectomized patients with balloon-occludable, reinfusion T-tubes, 8 patients with cholesterol (CS) and 2 with pigment (PS) gallstones. Another patient with pigment gallstones, sickle cell disease (SS), and stable jaundice was studied to examine the mechanism by which an increased bilirubin load was excreted. Total bilirubin was almost entirely conjugated and excretion was related linearly to bile salt excretion PS and CS subjects; one-third of bilirubin excretion was bile salt independent and two-thirds was bile salt associated. In the SS patient 90% of the bilirubin excretion was independent of bile salt output. In PS and CS patients, bilirubin output was linearly related to bile flow, but the SS patient showed significant bilirubin excretion at low flow rates. CS and PS patients had similar patterns of bilirubin excretion, but the increased bilirubin load in the SS patient was excreted independently of bile salts. In the SS patient, unconjugated bilirubin output was hyperbolically related to bile salts output and represented a maximum of 3% of the total bilirubin output. The bile salt-independent excretion of conjugated bilirubin suggests that micelles were not required for transport into bile; whereas the hyperbolic relationship for unconjugated bilirubin and bile salt output, similar to that of the micellar lipids. cholesterol, and phospholipids, suggests interaction with micelles.

Adult↗
PubMed1977

Excretion of 4-pyridoxic acid and oxalic acid in patients with urinary calculi.

Urinary excretion of 4-pyridoxic acid and oxalic acid was investigated in 75 patients with urinary calculi and in 50 normal subjects on regular diet. Mean excretion of 4-pyridoxic acid was 0.85 and 0.90 mg per day, respectively, and mean excretion of oxalic acid was 27.5 and 28.0 mg per day, respectively. Statistically there was no difference between the two groups in 4-pyridoxic acid excretion or in oxalic acid excretion. There was a weak positive correlation between the urinary excretion of 4-pyridoxic acid and oxalic acid. Patients who were on ascorbic acid supplementation during the urine collection period excreted increased amounts of oxalic acid. It was concluded from this investigation that most patients with urinary calculi had 4-pyridoxic acid excretion and oxalic acid excretion within normal limits. Low 4-pyridoxic acid values were not combined with high excretion values of oxalic acid, and the nutritional state of vitamin B6 in patients with urinary calculi was assumed to be satisfactory in order to control the endogenous oxalic acid production. The significance of high excretion values of 4-pyridoxic acid and oxalic acid is discussed.

Ascorbic Acid↗
PubMedDate not supplied

[Sodium excretion in children with lithogenic disorders].

INTRODUCTION: The causes of nephrolithisis are multifactorial and have not yet been enough investigated [1]. Hypercalciuria is the most common cause of metabolic nephrolithiasis [2-4]. Close relationship between urinary calcium and urinary sodium has been a subject of reported observations in the past, showing that high urinary sodium is associated with high urinary calcium [5-7]. Hyperoxaluria, hyperuricosuria and cystinuria are also metabolic disorders that can lead to nephrolithiasis. Recent studies have indicated that urinary elimination of cystine is influenced by urinary sodium excretion. Based on these observations it has been hypothesised that patients with high urinary sodium excretion are at high risk of urinary stone disease. The purpose of the study was to investigate sodium excretion in a 24-hour urine and first morning urine collected from children with lithogenic metabolic abnormalities (hypercalciuria, hyperoxaluria, hyperuricosuria, cystinuria), both with nephrolithiasis and without it, in order to determine its significance in urinary calculi formation. PATIENTS AND METHODS: Urinary sodium excretion was investigated in 2 groups of children: patients with lithogenic metabolic abnormalities, but without urinary stone disease (L group) and patients with nephrolithiasis (C group). Both groups were divided into 2 subgroups: patients with hypercalciuria and without it. There were 22 patients in group L (mean age 11.97 +/- 4.13 years), of whom 17 formed a hypercalciuric subgroup and 5 formed a non-hypercalciuric subgroup (3 patients with hyperuricosuria and 2 patients with hyperoxaluria). Group C consisted of 21 patients with nephrolithiasis (mean age 12.67 +/- 3.44 years), of whom 6 formed a hypercalciuric subgroup and 15 formed a non-hypercalciuric group (2 patients with cystinuria and 13 patients without lithogenic metabolic abnormalities). Control group consisted of 42 healthy age-matched children. All subjects had a normal renal function. A detailed history and clinical examination were done, and ultrasonography was performed in all patients. A 24-hour urine, first morning urine and serum specimen were analysed for sodium, potassium, calcium, uric acid, urea and creatinine. Fractional excretion of sodium, as well as urinary sodium to creatinin ratio and urinary sodium to potassium ratio, were calculated from the findings. Sodium and potassium levels were determined by flame photometry, calcium was measured by atomic absorption technique (Beckman Atomic Spectrophotometer, Synchron CX-5 model, USA), uric acid by carbonate method and creatinine by Jaffe technique. Cystine and dibasic amino acids were quantified by ion chromatography. Urinary oxalate excretion was determined by enzyme spectrophotometry. Hypercalciuria was defined by 24-hour calcium excretion greater than 3.5 mg/kg per day and/or calcium to creatinine ratio greater than 0.20 [8]. Uric acid excretion was expressed as uric acid excretion factored for glomerular filtration, according to Stapleton's and Nash's formula [9]. Normal values were lower than 0.57 mg/dl of glomerular filtration rate in 24-hour samples. Mean values were statistically analyzed by Pearson's linear correlation and analysis of variance (ANOVA). RESULTS: Urinary sodium concentration values including urinary sodium to potassium ratios, are shown in Table 1. We found that urinary sodium excretion was significantly increased in patients of both L and C groups when compared with controls (p < 0.05). Further analysis of the subgroups showed that urinary sodium excretion was significantly higher only in patients with hypercalciuria of both L and C groups in comparison to controls (p < 0.05) (Table 2). A significant positive correlation was found between 24-hour urinary sodium to creatinine ratio and urinary calcium to creatinine ratio (r = 0.31; p < 0.001) (Graph 1), as well as between urinary sodium to potassium ratio in 24-hour and first morning urine (r = 0.69; p < 0.001) (Graph 2). (A

Calcium↗