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PubMed2000

Urinary fluoride excretion in children drinking fluoridated school milk.

OBJECTIVE: To determine fluoride excretion under various conditions of fluoride intake and to estimate the fractional urinary excretion of fluoride in individual children participating in a school milk fluoridation scheme. DESIGN: In the first part of the study, individual urine samples were collected from each of eight 4 to 5-year-old children for a continuous period of 55 h. For each child (n = 8) and for each day (n = 3) the maximum urinary fluoride concentration (p.p.m.F), the maximum fluoride excretion rate (microgram F/h) and the total daily fluoride excretion (mg) were calculated. The second part of the study was carried out to determine the 24 h fractional percentage of fluoride excreted following administration of a known dose of fluoride in the absence of other sources. RESULTS: Under usual conditions of fluoride intake (i.e. milk containing 0.5 mg fluoride, customary diet and toothbrushing with fluoride toothpaste) the children's daily fluoride excretion was 0.33 mg. The fractional urinary fluoride excretion of a 0.5-mg fluoride tablet was 30%. CONCLUSIONS: It is concluded that the children's mean 24 h fluoride excretion was somewhere between that reported in low fluoride conditions and that reported in optimally fluoridated areas. The fractional urinary fluoride excretion was found to be in agreement with the findings of other workers.

Animals↗
PubMed1998

Quantitative studies of human urinary excretion of uropontin.

Uropontin is the urinary form of osteopontin, an aspartic acid-rich phosphorylated glycoprotein. Uropontin has been previously shown to be a potent inhibitor of the nucleation, growth and aggregation of calcium oxalate crystals and the binding of these crystals to renal epithelial cells. Quantitative data defining the excretion of this protein are necessary to determine its role in urinary stone formation. In the present studies, we determined uropontin excretion rates of normal humans. Urine samples were obtained under conditions of known dietary intake from young adult human volunteers with no history, radiographic or laboratory evidence of renal disease. Urinary concentrations of uropontin were measured by a sensitive ELISA employing an affinity purified polyclonal antiserum to uropontin. Thirteen normal subjects ingested a constant diet providing 1 gram of calcium, 1 gram of phosphorus, 150 mEq of sodium and 1 gram of protein per kilogram of body wt per day during an eight day study period. The relationship of urinary volume to uropontin excretion was assessed by varying fluid intake on the last four days of the study to change the mean urine volume/24 hr by > 500 ml. Urine collected in six hour aliquots for eight days was analyzed for uropontin by ELISA, and for calcium, and creatinine. Daily uropontin excretion of 13 individual subjects was 3805 +/- 1805 micrograms/24 hr (mean +/- 1 SD). The mean urinary levels (1.9 micrograms/ml) detected in the present study are sufficient for inhibition of crystallization; our previous studies have demonstrated that the nucleation, growth and aggregation of calcium oxalate crystals and their binding to renal cells in vitro are inhibited by this concentration of purified uropontin. In contrast to the regular pattern of diurnal variation of calcium excretion seen in most subjects, uropontin excretion showed no regularity of diurnal variation and was not directly related to either calcium or creatinine excretion or changes in urinary volume. However, uropontin concentration varied inversely with urine volume (P < or = 0.001), so that the highest uropontin concentrations occurred when urine volume was the lowest. We conclude that the physiologic characteristic of an inverse relationship of uropontin concentration to urine volume favors protection from urinary crystallization of calcium oxalate by uropontin. Our quantitative definition of urinary uropontin excretion of normal adults provides the basis for the evaluation of uropontin excretion by individuals who have formed urinary stones.

Adult↗
PubMed2001

Plasma concentration and urinary excretion of N-terminal proatrial natriuretic peptides in patients with kidney diseases.

BACKGROUND: Biologically active N-terminal fragments such as proANP(1-30), proANP(31-67), and proANP(1-98) derive from the prohormone of alpha-human atrial natriuretic peptide [proANP(99-126) or alpha-ANP]. No systematic data are available for patients with different kidney diseases. METHODS: Specific immunoassays were developed to determine plasma and urine concentrations of these fragments in 121 patients with different degrees of kidney function and urinary protein excretion, respectively. RESULTS: In patients with kidney disease and normal renal function without proteinuria, circulating proANP(1-30) and proANP(31-67) increased 2.8-fold and 6.5-fold, respectively. Urinary excretion of proANP(31-67) increased by a factor of 7.7 in these patients, whereas proANP(1-30) was not affected. Patients with impaired renal function had a dramatic increase of urinary proANP(31-67) excretion even before serum creatinine levels started to rise. The progression of renal failure caused a significant rise of circulating proANP(1-30) (4.3-fold) and proANP(31-67) (3.0-fold) compared with patients with normal renal function. Urinary excretion of proANP peptides significantly increased, particularly when the serum creatinine level was> 5.0 mg/dL [proANP(1-30) 26-fold, proANP(31-67) 8.4-fold]. Urinary excretion of proANP(1-30) increased up to 4.4-fold and urinary excretion of proANP(31-67) increased up to 2.4-fold in patients with proteinuria in excess of 3 g/24 h. CONCLUSIONS: Plasma concentrations and urinary excretion of proANP(1-30) and proANP(31-67) are affected by kidney disease and function, but not by proteinuria per se. It is proposed that the diseased kidney increases early urinary excretion of proANP fragments to participate in the regulation of renal function as well as sodium and water excretion.

Adolescent↗
PubMed2001

Long-acting natriuretic peptide, vessel dilator, and kaliuretic peptide enhance urinary excretion rate of albumin, total protein, and beta(2)-microglobulin in patients with congestive heart failure.

BACKGROUND: Albumin excretion is increased in persons with congestive heart failure (CHF), but the mechanism of this increase is unknown. Atrial natriuretic peptide (ANP) does not correlate with this albumin excretion, but the other 3 cardiac hormones derived from the ANP prohormone have never been investigated as to whether they can enhance albumin and/or protein excretion in persons with CHF. METHODS AND RESULTS: Long-acting natriuretic peptide (LANP), vessel dilator, and kaliuretic peptide (100 ng/kg body weight/min) given intravenously for 60 minutes to NYHA Class III CHF patients (n = 24) increased the albumin excretion rate 2- to 7-fold (P <.001) and total protein excretion rate 2- to 5-fold (P <.001). These peptide hormones similarly enhanced beta(2)-microglobulin, a specific marker of proximal tubular reabsorption, excretion rate 25- to 40-fold (P <.0005) at the end of their respective infusions. Three hours after stopping their respective infusions, the beta(2)-microglobulin excretion rate was still 11- to 33-fold (P <.0005) increased. CONCLUSIONS: LANP, vessel dilator, and kaliuretic peptide each enhance albumin and total protein excretion in persons with CHF. Part of the mechanism of this enhanced protein excretion is the inhibition of proximal tubular reabsorption of protein as shown by the beta(2)-microglobulin data.

Adult↗
PubMed1978

Effect of parathyroid extract on renal cyclic AMP excretion in patients with normocalciuric nephrolithiasis.

It is uncertain whether normocalcemic, normocalciuric patients with calcium nephrolithiasis have a disorder of calcium metabolism. We studied the effect of a parathyroid extract (PTE) INFUSION (1.4 U/kg body weight) on the urinary cyclic AMP excretion in 16 such patients. For comparison, we investigated groups of normal individuals and patients with primary hyperparathyroidism, renal insufficiency and different gastrointestinal diseases. The increase of cyclic AMP above basal excretion in patients with nephrolithiasis was only 1.2 +/- 0.3 mumol/h (mean +/- SEM), versus 2.5 +/- 0.5 mumol/h in normal subjects (p less than 0.05) although the basal excretion was similar. Patients with renal insufficiency had low basal excretion of cyclic AMP and little stimulation of excretion by PTH (increase, 0.3 +/- 0.06 mumol). Patients with primary hyperparathyroidism had high baseline cyclic AMP excretion but sub-normal stimulation by PTE (increase, 0.46 +/- 0.13); in contrast, patients with different gastrointestinal disease had high baseline excretion and supranormal stimulation of cyclic AMP excretion (increase, 5.2 +/- 0.6). We speculate that an impaired response to PTH might be involved in the slightly increased urinary calcium excretion in normocalcemic stone formers suggested by others.

Adolescent↗
PubMedDate not supplied

[Thyroid gland ultrasound and urinary iodine excretion in children and adolescents with type I diabetes mellitus].

BACKGROUND: Date, studies on thyroid volume and urinary iodide excretion in patients with diabetes mellitus are not available. Sonographically determined parameters of the thyroid size are correlated to other anthropometrous data and the urinary iodide excretion is correlated to glucosuria, the HbA1c value and the diabetes duration. METHOD: In this prospective study we evaluated sonographically the thyroid volume in 107 patients with type I diabetes mellitus and 112 healthy children. The urinary iodide excretion was measured photometrically by using a modified ceric ion arsenious acid method for spontaneous urinary specimen and if available for the 24 h collected urin. RESULTS: The thyroid volume depended on site and age. A positive correlation of the thyroid volume and age, body weight and height, could be demonstrated. Referring to reference data a goitre prevalence of 30% in juvenile patients with diabetes mellitus type I was detected. Interestingly, juvenile type I diabetics presented with an average urinary iodide excretion of 183.0 micrograms iodide/g creatinine. Even the urinary iodide excretion of 162.5 micrograms iodide confirmed this increased level. The urinary iodide excretion in 24 hours correlated with glucosuria and the HbA1c level. The healthy children presented with an average urinary iodide excretion of 42.6 micrograms iodide/g creatinine. The mean value was clearly below the WHO recommendation of 150-300 micrograms iodide/g creatinine. Only 2.8% of the healthy children examined exceeded the lower limit of this range. CONCLUSION: In addition to the existing distinct under supply of iodide we assume an increased urinary iodide excretion in context with the osmotic diuresis in juvenile diabetics. Contrary to current opinion, that these data are correlated to the daily intake of iodide, which was calculated from urinary excretion rate, this thesis could not be affirmed for juvenile diabetics. Therefore it seems reasonable to frequently control thyroid volume and thyroid function in children and adolescents with diabetes mellitus.

Adolescent↗
PubMed2001

Difference in solute excretion during correction of hyponatremic patients with cirrhosis or syndrome of inappropriate secretion of antidiuretic hormone by oral vasopressin V2 receptor antagonist VPA-985.

VPA-985 is an orally active, competitive vasopressin V(2) receptor antagonist that in normal human beings increases water excretion without affecting solute excretion. Whether solute excretion is affected in patients with hyponatremia resulting from inappropriate secretion of antidiuretic hormone (SIADH) or from cirrhosis treated with VPA-985 is unknown. Six hyponatremic patients with SIADH and 5 hyponatremic patients with cirrhosis with ascitis (CWAs) were treated with 50 or 100 mg VPA-985 twice daily. Evolution of creatinine, urea, uric acid, sodium, potassium, and osmotic clearance were determined. Volume hormones (plasma renin [PR], aldosterone, antidiuretic hormone [ADH], atrial natriuretic factor [ANF]) were also determined before and after treatment. In patients with SIADH, serum sodium concentration (SNa) was generally corrected in 1 day (SNa: 126 +/- 4.5 mmol/L at t = 0 hours and 133 +/- 5.6 mmol/L at t = 24 hours) and associated with a decrease in sodium excretion (from 82 +/- 22 mmol/24 hours to 45 +/- 21 mmol/24 hours; P < 0.05) without modification in potassium excretion. Despite an increase in diuresis (from 0.84 +/- 0.2 ml/min to 1.46 +/- 0.4 ml/min) urea and uric acid clearances decreased. Urine osmolality decreased from 414 +/- 148 mOsm/kg H(2)O to 209 +/- 55 mOsm/kg H(2)O. Volume hormones did not change. In the CWAs the rise of SNa was more progressive (SNa: 126 +/- 2.8 mmol/L at t = H0 to 133 +/- 4.9 mmol/L at t = 48 hours) and parallel to an augmentation in sodium excretion (from 23 +/- 18 mmol/24 hours to 65 6 60 mmol/24 hours the second day of VPA administration). The higher sodium excretion was also connected with a progression in potassium excretion (from 22 6 7 mmol/24 hours to 36 +/- 18 mmol/24 hours). The increase in diuresis under VPA from 0.42 +/- 0.2 mL/min to 1.7 +/- 0.9 mL/min resulted in a higher urea clearance. Urine osmolality decreased from 509 +/- 142 mOsm/kg H(2)O before VPA to 194 +/- 106 mOsm/kg H(2)O after VPA. ADH increased in CWAs treated with VPA, from 1.9 +/- 1.2 pg/mL to 5.3 +/- 2.8 pg/mL (P <.05) while other volume hormones did not change. VPA-985 is a highly effective drug in the short-term management of hyponatremic patients with SIADH or CWAs. SNa correction is associated with urinary sodium retention in SIADH, whereas in CWAs a mild increase in sodium excretion is observed.

Antidiuretic Hormone Receptor Antagonists↗
PubMed2005

Urinary 6-hydroxymelatonin sulfate excretion in intellectually disabled subjects with sleep disorders and multiple medications: validation of measurements in urine extracted from diapers.

The aim of this study was to examine the applicability of urinary 6-hydroxymelatonin sulfate (MT6s) measurements in the evaluation of melatonin secretion in intellectually disabled patients with sleep disorders. All 17 patients received drugs with potential interactions with melatonin metabolism. Serum melatonin 24-h profiles were determined at hourly intervals. The area under the curve (AUC) value, peak amplitude, half-rise time, and half-decline time were calculated individually. Urinary MT6s excretion was determined from samples collected from disposable diapers during three consecutive days at varying intervals. The average excretion rate for each hour of the day was calculated. The excretion profiles were characterized by total amount of MT6s excretion/24 h/kg body mass, amount of excreted MT6s during 6 h of maximum excretion (MAX 6h), and start time of the maximum excretion (start MAX 6h). There were significant positive correlations between serum melatonin AUC value and total excretion of MT6s/body mass, between serum melatonin amplitude and urinary MAX 6h, and between melatonin half-rise time and start MAX 6h; one patient on phenobarbital medication was out of line. The serum melatonin profiles of the patients were classified by comparing them with those of matched healthy volunteers (low-, normal-, or high secretors, normal or delayed rhythm). Similarly, the parameters of MT6s profiles were compared with those obtained from healthy controls, and the patients were reclassified as normal or aberrant. The classifications based on serum melatonin and urinary MT6s measurements were mostly concordant. The daily pattern of urinary MT6s excretion reliably reflected the phase of the serum melatonin rhythm irrespective of the medications, but in some cases, the total amount of excreted MT6s was lower than expected based on serum melatonin measurements.

Adolescent↗
PubMed1981

Catecholamine and cortisol excretion patterns in three-year-old children and their parents.

Urinary catecholamine and cortisol excretion was studied in a group of three-year-olds, their mothers and fathers during night rest, one day at home and one day at hospital. The stay in the hospital, which was part of a longitudinal study of the families, induced a pronounced rise in adrenaline excretion and a moderate increase in noradrenaline excretion in relation to the at-home level. Although the catecholamine excretion in relation to body weight was much higher in the children, the magnitude of the increase at the hospital was about the same in all the family members. The adrenaline excretion was also affected by the diverse conditions at the hospital and showed, for example, a marked decrease during lunch hour. The cortisol excretion at the hospital tended to be elevated only in fathers. On the average, mothers excreted about the same amount of adrenaline as the fathers at the hospital, but significantly more noradrenaline. In earlier studies males have shown a greater adrenaline output than females during achievement-demanding situations. The findings of this study were interpreted within the context of the specific challenge that the situation represented to the mothers. The mothers also excreted more noradrenaline in the at-home condition. Catecholamine and cortisol excretion levels within family members tended to be positively correlated, but the correlations were generally low.

Adult↗
PubMedDate not supplied

A prospective longitudinal study of urinary excretion of a bone resorption marker in adolescents.

In growing subjects, the rates of bone resorption and bone deposition are substantially larger than in non-growing individuals. The purpose of this study was to measure the urinary excretion of a specific bone resorption marker in function of adolescent growth stages in a prospective longitudinal study. A cohort of 60 adolescents (28 male and 32 female) was followed for 3.4 years (range 1.7-4.6 years). Monthly measurements of height, weight and urinary excretion of a bone resorption marker, collagen type I N-telopeptides (NTx), were made. Changes in standing height were used to classify the adolescents into one or more of six adolescent growth stages: pre-pubertal growth (continuous moderate growth rate), ascending growth spurt (increasing growth rate), peak growth spurt (growth rate higher than 7 cm/year for at least 6 months), descending growth spurt (continuous decrease in growth rate), end of growth (growth rate between 0 and 2 cm/year), and no growth. An increase in NTx excretion from the pre-pubertal to peak growth spurt of about 33% was found (44% and 27% for females and males respectively). The decreasing growth rate after the pubertal growth spurt coincided with a clear decrease in NTx excretion. These differences were statistically significant, except between the prepubertal and ascending growth stage. Individual mean NTx excretion during each growth stage was correlated with the individual's growth rate during that time (r = 0.81). There was large inter-and intra individual variability. In non-growing adolescents (growth rate 0 cm/y) NTx excretion levels were 4-7 times greater than in adults. In all females, menarche was followed by a decrease in NTx excretion. In conclusion, the excretion of a specific bone resorption marker, NTx, was correlated with the changes in growth rate during adolescence, both for males and females. There were large inter and intra-individual differences in NTx excretion during the different growth stages. In adolescents who reached their adult height at the end of the pubertal growth spurt. bone resorption decreased dramatically but remained 4-7 fold higher than in adults.

Adolescent↗
PubMed1982

The effect of sodium intake on zinc excretion in patients with sickle cell anemia.

Urinary zinc excretion is known to be elevated in subjects with sickle cell anemia. Sodium intake has been suggested to influence zinc excretion in normal subjects. In order to assess the effect of sodium on zinc excretion in subjects with sickle cell anemia, urinary zinc excretion was measured in thirteen children and adolescents with sickle cell anemia on both a high (140 mEq/day) and low (20 mEq/day) sodium intake. Urinary zinc excretion was elevated on both diets. The mean urinary zinc excretion on the high sodium diet (775 +/- 238 micrograms/24 h) was significantly lower (P less than .005) than that on the low sodium diet (947 +/- 344 micrograms/24 h). The zinc excretion did not correlate with calcium or magnesium excretion or aldosterone secretion rates or plasma renin activity. Although elevated, the urinary zinc excretion in patients with sickle cell anemia is still significantly lowered by increasing sodium intake.

Adolescent↗
PubMed1998

Oxidative DNA damage in vivo: relationship to age, plasma antioxidants, drug metabolism, glutathione-S-transferase activity and urinary creatinine excretion.

Oxidative DNA modification has been implicated in development of certain cancers and 8-oxodG, the most abundant and mutagenic DNA modification, has for some time been considered a biomarker of this activity. Urinary excretion of 8-oxodG over 24h has been used to estimate the rate of damage to DNA, and animal studies have supported this rationale. Reported determinants include tobacco smoking, heavy exercise, environmental pollution and individual oxygen consumption. Samples from three published studies were used to determine the association of urinary 8-oxodG excretion with age, plasma antioxidants, the glutathione-S-transferase phenotype and the activity of the xenobiotic metabolising enzyme CYP1A2. In the age range 35-65 years, age was not related to urinary 8-oxodG excretion, and there were no relations to either the glutathione-S-transferase phenotype or to the plasma antioxidants: vitamin C, alpha-tocopherol, beta-carotene, lycopene or coenzyme Q10. The activity of CYP1A2 showed a significant correlation in two of the three studies, as well as a significant correlation of 0.26 (p < 0.05) in the pooled data set. Regression analysis of CYP1A2 activity on 8-oxodG indicated that 33% increase in CYP1A2 activity would correspond to a doubling of 8-oxodG excretion. This finding needs to be confirmed in independent experiments. Spot morning urine samples can under certain circumstances be used to estimate 8-oxodG excretion rate provided that creatinine excretion is unchanged (in paired experiments) or comparable (in un-paired experiments), as evaluated from the correlation between 8-oxodG excretion in 24 h urine samples and in morning spot urine samples corrected for creatinine excretion (r = 0.50, p < 0.05). We conclude that 8-oxodG excretion is determined by factors like oxygen consumption and CYP1A2 activity rather than by factors like plasma antioxidant concentrations.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1999

The course of phosphorus excretion in growing pigs fed continuously increasing phosphorus concentrations after a phosphorus depletion.

A balance study was performed in order to quantify the effect of continuously increased phosphorus (P) intake on faecal and urinary P excretion. The aim was to quantify the level of intake where regulatory P excretion becomes relevant for comparative digestibility measurements on P, and when the pig adapts its urinary P excretion to increased P intake. Phosphorus intake of growing pigs was continuously increased on a daily basis starting at a marginal level and P excretion via faeces and urine was continuously followed for 92 days. Two semi-synthetic diets were prepared with different proportions of Na2HPO4 resulting in 2.4 (diet 1) and 6.3 (diet 2) g P/kg DM. Concentration of Ca was adapted to achieve a Ca supply approximately 3.1 fold the digestible P supply. Six castrated male crossbred pigs (31 kg BW) were kept individually in metabolism crates after they had undergone a 14 d P depletion period during which they were fed diet 1 solely. Pigs received 1.04kg of diet 1 per day throughout the experiment, and each day the amount of feed and P supplied to pigs from diet 2 was increased by 12 g and 69 mg, respectively. ME supply was approximately 2.4 fold maintenance and average daily BW gain of pigs during the entire experiment was 690 +/- 30 g. While intake increased linearly, faecal excretion of P and Ca increased non-linearly and could be best described by third order polynomial functions. The proportion of ingested P not excreted via faeces followed a quadratic type of curve with a maximum of 81% at 25 days on experiment and P intake of 4.0 g/d. Thereafter, the proportion decreased continuously. The digestibility of P from diet 2, determined by the slope ratio technique, was constant and not affected by P intake up to a P intake of 5 g/d. Renal P excretion did not exceed inevitable losses until day 60 and increased exponentially thereafter when body P reserves were restored. It is concluded, that an adaptation to surplus P supply occurred earlier on the intestinal than on the renal level. While faecal P excretion appeared regulated depending on the actual requirement for P retention, the regulation via urine depended on the P status of the pig. Once the renal P excretion of growing pigs exceeds a level of 25 mg/d, intake of digestible P cannot be regarded sufficiently low to measure P digestibility as a capacity of the feedstuff.

Absorption↗
PubMedDate not supplied

Are hummingbirds facultatively ammonotelic? Nitrogen excretion and requirements as a function of body size.

Most birds are uricotelic. An exception to this rule may be nectar-feeding birds, which excrete significant amounts of ammonia under certain conditions. Although ammonia is toxic, because it is highly water soluble its excretion may be facilitated in animals that ingest and excrete large amounts of water. Bird-pollinated plants secrete carbohydrate- and water-rich floral nectars that contain exceedingly little protein. Thus, nectar-feeding birds are faced with the dual challenge of meeting nitrogen requirements while disposing of large amounts of water. The peculiar diet of nectar-feeding birds suggests two hypotheses: (1) these birds must have low protein requirements, and (2) when they ingest large quantities of water their primary nitrogen excretion product may be ammonia. To test these hypotheses, we measured maintenance nitrogen requirements (MNR) and total endogenous nitrogen losses (TENL) in three hummingbird species (Archilochus alexandri, Eugenes fulgens, and Lampornis clemenciae) fed on diets with varying sugar, protein, and water content. We also quantified the form in which the by-products of nitrogen metabolism were excreted. The MNR and TENL of the hummingbirds examined were exceptionally low. However, no birds excreted more than 50% of nitrogen as ammonia or more nitrogen as ammonia than urates. Furthermore, ammonia excretion was not influenced by either water or protein intake. The smallest species (A. alexandri) excreted a significantly greater proportion (>25%) of their nitrogenous wastes as ammonia than the larger hummingbirds ( approximately 4%). Our results support the hypothesis that nectar-feeding birds have low protein requirements but cast doubt on the notion that they are facultatively ammonotelic. Our data also hint at a possible size-dependent dichotomy in hummingbirds, with higher ammonia excretion in smaller species. Differences in proportionate water loads and/or postrenal modification of urine may explain this dichotomy.

Ammonia↗
PubMed1981

Carnitine intake and excretion in neuromuscular diseases.

Free and total carnitine serum concentrations and urinary excretion were examined in patients with various neuromuscular diseases. On a measured, low carnitine diet and during fasting, the patients did not differ from controls. Carnitine excretion in patients (3.09 +/- 1.87 mumol/kg/day) and controls (2.99 +/- 1.12) exceeded carnitine intake (patients, 2.35 +/- 0.94 mumol/kg/day; controls, 1.33 +/- 0.70). Because of heterogeneity in the patient population, carnitine excretion was assessed according to creatinine excretion, chosen as an indicator of muscle mass. Those patients with daily creatinine excretion less than 1 g/day had significantly lower carnitine excretion (106 +/- 47 versus 205 +/- 95 mumol/day, p less than 0.05), and there was a positive correlation between creatinine excretion and carnitine excretion (r = 0.82) and between muscle carnitine and carnitine excretion (r = 0.67). Urinary clearances for acylcarnitine were 10 and 20 times higher than those for free carnitine. Two patients with carnitine palmityl transferase deficiency were similar to the other patients, but the carnitine-deficient patient lost excessive carnitine during fasting, probably secondary to elevated acylcarnitine fraction in the blood.

Adolescent↗
PubMed1997

Urinary sodium excretion and myocardial infarction in hypertensive patients: a prospective cohort study.

Reduced-sodium diets are frequently recommended for hypertensive patients. To determine the relation of sodium intake to subsequent cardiovascular disease, 24-h urinary excretion of sodium, potassium, and creatinine and plasma renin activity (PRA) were measured in 2937 mildly and moderately hypertensive patients unmedicated for > or = 3-4 wk. Morbidity and mortality in these treated subjects were ascertained. Subjects were stratified by sex-specific quartiles of urinary sodium excretion; race, cardiovascular status, and blood pressure before and during treatment were similar for each stratum. Patients with lower urinary sodium excretion were thinner, excreted less potassium, and had higher PRA. During an average 3.8-y follow-up, 55 myocardial infarctions (MIs) occurred. Incidence of MIs and urinary sodium excretion were inversely associated in the total population and in males but not in females. In males, age- and race-adjusted MI incidence in the lowest compared with the highest quartile of urinary sodium excretion was 11.5 compared with 2.5 (RR: 4.3; 95% CI: 1.7, 10.6). No association was observed between mortality from causes other than cardiovascular disease (n = 11) and urinary sodium excretion. There was a significant linear trend in proportions of MI by quartile of urinary sodium excretion, with a breakpoint after the lowest quartile. In Cox multivariate analysis, the logarithm of PRA, age, systolic blood pressure, and cholesterol as continuous variables, as well as left ventricular hypertrophy and smoking, had a direct association and urinary sodium excretion an inverse, independent association (P = 0.036) with incidence of MI.

Cardiovascular Diseases↗
PubMed1994

Urinary albumin and N-acetyl-beta-D-glucosaminidase excretions in mild hypertension.

Renal effects of mild hypertension and therapy have not been established. Since urinary albumin and N-acetyl-beta-D-glucosaminidase excretions reflect renal effects of hypertension, they were related to blood pressure, other cardiovascular risk factors, cardiac target organ effects, and response to therapy in mild hypertension (diastolic blood pressure 85-99 mm Hg). Participants were from two clinics of the Treatment of Mild Hypertension Study (TOMHS), a multicenter randomized, double-blind, controlled trial. Participants received nutritional-hygienic therapy and one of five active drugs or placebo. Urinary albumin and N-acetyl-beta-D-glucosaminidase excretions were assessed prospectively using office "spot" collections from one clinic (n = 213) and retrospectively using overnight collections from the other clinic (n = 210). Relationships were determined between protein excretions and blood pressure, age, gender, race, blood glucose, cholesterol concentrations, and indices of body mass and left ventricular mass and function at baseline. Treatment effects were assessed after 3 to 12 months. Spot and overnight albumin excretions related positively to baseline systolic blood pressure by univariate analyses. Spot albumin excretion related positively to systolic blood pressure, age, creatinine clearance, and left ventricular function while overnight albumin excretion related positively to left ventricular mass and female gender by multiple regression analyses. Spot, but not overnight, albumin excretion declined significantly with active drug therapy. N-acetyl-beta-D-glucosaminidase excretion did not relate to blood pressure or decline with therapy. The combined results suggest albumin excretion correlates with blood pressure, decreases with antihypertensive drug therapy, and is associated with greater left ventricular function and mass, as well as glomerular filtration rate, even at mild levels of hypertension.

Acetylglucosaminidase↗
PubMed1997

Excretion of DNA adducts of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine and 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline, PhIP-dG, PhIP-DNA and DiMeIQx-DNA from the rat.

The heterocyclic aromatic amines, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) and 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline (4,8-DiMeIQx) are formed during frying of meat. PhIP and 4,8-DiMeIQx have, after metabolic activation, been shown to form adducts with DNA at the C8 of guanine both in vitro and in vivo. In order to investigate possible urinary biomarkers for estimation of the genotoxic dose of PhIP and 4,8-DiMeIQx, [3H]PhIP-dG, [3H]PhIP-DNA and [14C]4,8-DiMeIQx-DNA were injected i.p. to rats and the excretion of radioactivity in urine and faeces were measured. For all three [3H]PhIP-dG, [3H]PhIP-DNA and [14C]4,8-DiMeIQx-DNA 15-20% of the dose were excreted in the urine and 80-85% of the dose were excreted in the faeces. Urinary excretion showed maximum to 24 h (90%) with a rapid decline, 10% to 48 h and 0% to 72 h. Faecal excretion also showed maximum to 24 h (60%) with a slower decline, 30% to 48 h and 10% to 72 h. HPLC analysis of samples of urine and extracts from faeces, from rats dosed with [3H]PhIP-dG, showed that approximately 90% of the radioactivity co-eluted with PhIP-dG, indicating that PhIP-dG is excreted unmetabolized. HPLC analysis of samples of urine and extracts from faeces, from rats dosed with [3H]PhIP-DNA, showed that approximately 85% of the radioactivity co-eluted with PhIP-dG, indicating that PhIP-DNA adducts is mainly excreted as nucleoside adducts. Approximately 5% of the radioactivity excreted in the urine co-eluted with PhIP-G, indicating loss of deoxyribose. HPLC analysis of samples of urine and extracts from faeces, from rats dosed with [14C]4,8-DiMeIQx-DNA, showed that approximately 90% of the radioactivity co-eluted with 4,8-DiMeIQx-dG, indicating that 4,8-DiMeIQx-DNA adducts is mainly excreted as nucleoside adducts. Man is able to eliminate compounds of a higher mol. wt in the urine than the rat, the percentage of PhIP-dG and 4,8-DiMeIQx eliminated in the urine of man would therefore be expected to be higher than in the rat. Measurement of urinary nucleoside adducts of PhIP and 4,8-DiMeIQx could therefore provide a basis for the development of a biomonitoring strategy for the genotoxic dose of these food derived HAA.

Animals↗