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PubMed2002

Identification and chromosomal localization of ecogenetic components of electrolyte excretion.

OBJECTIVE: To determine to what extent urinary excretion of blood pressure-modulating electrolytes is genetically determined, and to identify their chromosomal localization. DESIGN AND METHODS: Twenty-six rat recombinant inbred strains (RIS) originating from reciprocal crosses of normotensive Brown Norway (BN.Lx) and spontaneously hypertensive rats (SHR) were used. A pilot experiment on a subset of strains determined that fasting decreases the impact of environmental noise and increases that of heritability. Twenty-four-hour urinary collections were obtained from fasting rats aged 6-12 weeks (3-8 rats per strain). Sodium (Na), potassium (K) and calcium (Ca) excretions were measured, and the Na/K ratio calculated. These phenotypes served as quantitative traits for the search of quantitative trait loci (QTLs) by scanning the RIS genome that was mapped with 475 polymorphic markers. RESULTS: Constant Na intake resulted in a low heritability for Na excretion, reflecting the environmental impact (intake = excretion), whereas fasting revealed a gradient among RIS indicative of the genetic component of the traits. In the fasting state, a locus on chromosome 14 was found to be significantly associated with K excretion (Alb, P = 0.00002, r = -0.69, logarithm of the odds score (LOD) 3.9), whereas another locus on chromosome 10 (D10Cebrp97s5, P = 0.0003, r = -0.69, LOD 3.0) and one on chromosome 6 (D6Cebrp97s14, P = 0.0007, r = -0.65, LOD 1.9) were more significantly associated with Na excretion and the Na/K ratio respectively. The observed correlations were all negative for Na, K and Na/K, indicating a higher excretion of Na and K and a greater Na/K ratio in rats bearing BN.Lx alleles at these loci, i.e. salt retention in fasting SHR. These three loci accounted for 47-55% of variance of their associated trait, suggesting that they are the main genetic determinants for these phenotypes in basal fasting conditions. Rats bearing the Y chromosome of SHR origin had significantly higher K excretion that, in turn, led to a significantly lower Na/K ratio. Finally, a locus on chromosome 7 was linked to Ca excretion, explaining 46% of the trait variance (D7Mit10, LOD score 3.0). CONCLUSION: RIS enabled us to determine QTLs for environmentally modulated traits such as Na, K and Ca excretions. We demonstrated that whereas urinary electrolytes are determined mainly by intake (environment) in a steady state, their excretion in an adaptive state (fasting) is predominantly genetically determined by distinct QTL on autosomes as well as the Y chromosome. Furthermore, the loci responsible for Na and K excretions act independently of the locus governing the relative excretion of Na/K. Thus, the salt-retaining aspects of some hypertensives may be, in large part, determined by genes responsible for renal excretion, the impact of which is predominant over the environment under acute challenge.

Age Factors↗
PubMed1987

Effect of urinary pH and urine flow rate on prostaglandin E2 and kallikrein excretion by the conscious dog.

1. The effects of urine flow rate and urinary pH on renal prostaglandin E2 (PGE2) and kallikrein excretion were investigated in conscious dogs during water deprivation followed by rehydration and under conditions which altered urine pH, but caused similar change in salt and water excretion. 2. When water-restricted dogs were rehydrated in two steps by gavage giving the animals tap water, urine flow increased by 22- and 63-fold with a concomitant increase in PGE2 excretion by 100 and 318%, respectively; whereas urinary kallikrein excretion and urine pH did not change significantly. 3. Oral administration of isotonic sodium chloride solution increased urine flow as well as electrolyte excretion without altering urine pH (6.90 +/- 0.26) and PGE2 excretion. 4. When urine was made alkaline (pH 7.79 +/- 0.09) by oral sodium bicarbonate, urine flow and electrolyte excretion were similar to those observed after oral sodium chloride, while renal PGE2 excretion increased by 66% (P less than 0.05). 5. When urine was made acidic (pH 5.31 +/- 0.14) by oral ammonium chloride, urine flow and electrolyte excretion were similar to the values seen after oral sodium chloride. Urinary PGE2 excretion, however, was reduced by 46% (P less than 0.05). 6. After oral fluid loads a positive correlation could be detected between urine pH and urinary PGE2 excretion (r = 0.854, P less than 0.001). 7. Urinary kallikrein excretion was not significantly altered by any of the three interventions mentioned above. 8. The present results suggest that, in conscious dogs, urine flow as well as urine pH are important determinants of urinary PGE2 excretion rates, but not of kallikrein excretion.

Ammonium Chloride↗
PubMed1986

Aldosterone excretion rates in children and adults during sleep.

The present study undertook to examine aldosterone excretion during sleep as an integrated measurement of aldosterone production. A 24-hour urine collection was divided into awake and sleep fractions. Urinary aldosterone and electrolyte excretion were measured in 26 healthy children (mean age, 8.9 +/- 1.9 [SD] years) and 28 adults (mean age, 29.9 +/- 9.5 years). Aldosterone excretion in children was 5.6 +/- 3.9 (SD) micrograms/g creatinine during the awake period, which was significantly different from the 3.9 +/- 4.1 micrograms/g creatinine value recorded during sleep (p less than 0.002). In adults, awake aldosterone excretion was significantly greater than that during sleep; 4.9 +/- 2.7 versus 3.2 +/- 1.6 micrograms/g creatinine (p less than 0.001). Sleep aldosterone excretion values were highly correlated with the corresponding 24-hour aldosterone excretion values (r = 0.85, p less than 0.001) in children and in adults (r = 0.64, p less than 0.001). Sleep aldosterone excretion was correlated with 24-hour potassium excretion (p less than 0.02) only in children. Sleep aldosterone excretion correlated with neither sleep nor 24-hour sodium excretion in children or adults. Sleep electrolyte excretion rates were highly correlated with 24-hour excretion rates in both children and adults. Dexamethasone, 1 mg, administered the night before to suppress the normally high morning levels of endogenous adrenocorticotropic hormone, had no discernible effect on sleep aldosterone excretion. These results indicate that measurement of aldosterone excretion in an easily collected sleep urine sample provides a reliable index of aldosterone production in children and adults.

Adrenocorticotropic Hormone↗
PubMed2007

Renal albumin excretion: twin studies identify influences of heredity, environment, and adrenergic pathway polymorphism.

Albumin excretion marks early glomerular injury in hypertension. This study investigated heritability of albumin excretion in twin pairs and its genetic determination by adrenergic pathway polymorphism. Genetic associations used single nucleotide polymorphisms at adrenergic pathway loci spanning catecholamine biosynthesis, storage, catabolism, receptor action, and postreceptor signal transduction. We studied 134 single nucleotide polymorphisms at 46 loci for a total of >51,000 genotypes. Albumin excretion heritability was 45.2+/-7.4% (P=2x10(-7)), and the phenotype aggregated significantly with adrenergic, renal, metabolic, and hemodynamic traits. In the adrenergic system, excretions of both norepinephrine and epinephrine correlated with albumin. In the kidney, albumin excretion correlated with glomerular and tubular traits (Na(+) and K(+) excretion; fractional excretion of Na(+) and Li(+)). Albumin excretion shared genetic determination (genetic covariance) with epinephrine excretion, and environmental determination with glomerular filtration rate and electrolyte intake/excretion. Albumin excretion associated with polymorphisms at multiple points in the adrenergic pathway: catecholamine biosynthesis (tyrosine hydroxylase), catabolism (monoamine oxidase A), storage/release (chromogranin A), receptor target (dopamine D1 receptor), and postreceptor signal transduction (sorting nexin 13 and rho kinase). Epistasis (gene-by-gene interaction) occurred between alleles at rho kinase, tyrosine hydroxylase, chromogranin A, and sorting nexin 13. Dopamine D1 receptor polymorphism showed pleiotropic effects on both albumin and dopamine excretion. These studies establish new roles for heredity and environment in albumin excretion. Urinary excretions of albumin and catecholamines are highly heritable, and their parallel suggests adrenergic mediation of early glomerular permeability alterations. Albumin excretion is influenced by multiple adrenergic pathway genes and is, thus, polygenic. Such functional links between adrenergic activity and glomerular injury suggest novel approaches to its prediction, prevention, diagnosis, and treatment.

Adolescent↗
PubMed2004

[Associations between dietary intake and urinary excretion of sodium, potassium, phosphorus, magnesium, and calcium].

OBJECTIVES AND METHODS: The associations between dietary intake and urinary excretion of sodium (Na), potassium (K), calcium (Ca), magnesium (Mg), and phosphorus (P), and the major dietary sources derived from the urinary minerals were studied in a nutritional survey of 219 Japanese females aged 27-84 years, who completed anthropometric measurements, a one-day dietary record, and a 24 hr urine collection. RESULTS: The minerals excreted in the urine were significantly and positively correlated with each other, in which Na excretion was correlated with K and Ca excretion (r = 0.490 and r = 0.482, respectively, p < 0.01) and Ca excretion was correlated with Mg excretion (r = 0.526, p < 0.01). The ratios of urinary exertion to dietary intake of Na, K, Ca, Mg, and P were 81.5%, 62.7%, 24.5%, 21.7%, and 56.1%, respectively. The dietary intake and the urinary excretion of the minerals expressed per body weight (kg) were significantly and positively correlated (Na, r = 0.267; K, r = 0.460; Ca, r = 0.181; Mg, r = 0.245; P, r = 0.351, p < 0.01). Further examinations using chief component analysis for food intake showed several significant positive correlations, including between Na intake and the intake of vegetables, noodles, and seasonings (r = 0.332-0.381, p < 0.01); between K, Mg and P intake and the intake of vegetables, fruits, and potatoes (r = 0.332-0.533, p < 0.01); and between Ca intake and the intake of bread and dairy foods (r = 0.428, p < 0.01). In addition, significant positive associations were found between Na excretion and the intake of confectionaries, nuts, and seeds (r = 0.223, p < 0.01). Weak correlations were also found between K excretion and the intake of vegetables (r = 0.296, p < 0.01); between Ca and P excretion and the intake of meat, oil, and fats (r = 0.135, P < 0.05; r = 0.193, P < 0.01, respectively), and between Mg excretion and the intake of bread and dairy foods (r = 0.137, P < 0.05). CONCLUSIONS: Findings from this study indicate that, while urinary excretion of Ca and Mg is unlikely to be a reliable biochemical marker of dietary intake, the levels of urinary excretion of Na, K, and P can be reflective of the intake of salt, vegetables, and meats, respectively. The urinary excretion of the minerals, particularly Na, K, and Ca, may be highly linked to salt intake in Japanese females.

Adult↗
PubMed1992

Urinary protein excretion and renal function in young people with diabetes mellitus.

To detect early renal involvement in young diabetic patients (IDDM), urinary protein excretion and renal function were examined in 110 patients aged 5.9-25.0 years. Clearances of inulin and PAH were determined as well as albumin (Alb), IgG, N-acetyl-beta-D-glucosaminidase (NAG) and creatinine (Cr) excretion rates (UV). The patients were grouped according to IDDM duration (2- less than 5, 5-10 and greater than 10 years) and albumin excretion rate (non-albuminuria less than 20, microalbuminuria 20-200, and albuminuria greater than 200 micrograms/min per 1.73 m2). Four patients had overt albuminuria, 17 microalbuminuria (equally distributed among the duration groups). Grouped according to albumin excretion rate, the mean GFR was increased in those without albuminuria but 'normalized' in patients with microalbuminuria/albuminuria. Grouped according to albumin excretion rate and the duration of the disease, the non-albuminuric patients with IDDM for greater than 10 years had a lower GFR than those with a shorter duration of IDDM. The patients with microalbuminuria/albuminuria and IDDM for less than 5 years had a reduced GFR. Patients with increased NAG excretion rate had lower Na excretion rate, lower fractional Na excretion and greater creatinine excretion than those with normal NAG excretion. Albumin excretion correlated with IgG excretion, but also with NAG excretion. Our results suggest that early albuminuria in IDDM is of both glomerular and tubular origin. The hyperfiltration declines with increasing albumin excretion but also with the duration of the disease.

Acetylglucosaminidase↗
PubMed1994

[Estimation of 24-h excretion of some promotors and inhibitors of crystallization and degree of urine saturation with calcium oxalate in calcium urinary calculi].

UNLABELLED: The aim of the study was to estimate the renal citrate excretion in basal condition and to find out the relationship between their excretion and excretion of calcium, oxalate, magnesium and phosphate in patients with calcium stone disease and in control group. In 93 patients with urolithiasis and 46 healthy subjects 24-h excretion of calcium, magnesium, oxalate, phosphate and citrate as well as the degree of urine saturation with calcium oxalate was evaluated. 24-h renal excretion of calcium was significantly higher in patients with urolithiasis than in control group (p < 0001). Excretion of magnesium, phosphate and oxalate were'nt significantly different between patients with urolithiasis and healthy subjects. Daily excretion of citrate was significantly lower in patients with calcium stone disease (p < 0.01) and the degree of urine saturation with calcium oxalate was significantly higher in this group (p < 0.001). Hypocitraturia was observed in 61.3% stone-formers. A significant positive correlation was observed between excretion of citrate and calcium (r = 0.2760 p < 0.01) as well as citrate and oxalate (r = 0.5310 p < 0.001) in patients with urolithiasis. CONCLUSIONS: 1. In 61.3% of patients with urolithiasis the daily citrate excretion was reduced. In 50% of patients with urolithiasis and reduced citrate excretion "idiopathic" hypocitraturia was recognized. The daily citrate excretion was reduced in 70.2% of stone-formers with infected urine. 2. The positive correlation between 24-h excretion of calcium and citrate suggests that high excretion of lithogenic factor is accompanied by high excretion of this inhibitor of crystallization.

Adult↗
PubMed1994

Comparative effects of nabumetone, sulindac, and indomethacin on urinary prostaglandin excretion and platelet function in volunteers.

Nonsteroidal antiinflammatory drugs differ with respect to their effects on prostaglandin metabolism in various tissues, a property that may be partly responsible for some of the differences in the pharmacologic activities and side-effect profiles that are associated with their use. The effects of nabumetone on urinary prostaglandin excretion have not been reported. Fourteen healthy females, age 21-43 years, were treated with nabumetone (NAB) 1000 mg daily, sulindac (SUL) 200 mg every 12 hours, and indomethacin (IND) 50 mg every 12 hours for 7 days in a randomized period-balanced crossover study. The effects of drug treatment on urinary prostaglandin excretion (PGE2, 6-keto-PGF1 alpha, PGF2 alpha, thromboxane [TX] B2) and platelet function (collagen-induced whole blood platelet aggregation [CIPA] and template bleeding time) were determined on day 1 and day 7. For each treatment regimen, mean baseline urinary PG excretion values were comparable for each prostanoid, but the pattern of excretion differed in response to each drug. Treatment with NAB significantly increased the urinary excretion rates of PGE2 and PGF2 alpha, but 6-keto-PGF1 alpha and TXB2 excretion were unchanged. IND treatment did not result in a significant change in PGE2 excretion but did significantly reduce urinary 6-keto-PGF1 alpha and TXB2 excretion rates. Reduced excretion of PGF2 alpha was observed on both study days during treatment with IND and SUL. SUL treatment also resulted in increased urinary PGE2 excretion while significantly reducing 6-keto-PGF1 alpha excretion on day 7. Significant differences were observed between the NAB and SUL regimens with respect to PGF2 alpha excretion and between the NAB and SUL regimens for PGE2, PGF2 alpha, 6-keto-PGF alpha 1 (on day 1 only) and TXB2 (on day 1 only). Neither NAB nor SUL caused inhibition of CIPA or bleeding time although platelet aggregation was inhibited during IND treatment. That NAB treatment was neither associated with alterations in platelet function nor decreases in the urinary excretion of the vasodilatory prostaglandins, PGE2 and 6-keto-PGF1 alpha, suggests that NAB possesses renal sparing properties.

Adult↗
PubMedDate not supplied

[Urinary excretion of fluorides in inhabitants of the Canton Vaud who consume fluoridated salt as compared with that of the inhabitants of neighboring cantons who consume nonfluoridated salt].

In the Swiss canton of Vaud (512000 inhabitants) the salt available for human consumption has been fluoridated since 1969 by adding 250 mg F- per kg of salt. The urinary excretion of fluoride has been investigated in large samples of the population in 1970 and in 1974. The present study reports the results of the 1974 study, in which the urinary fluoride excretion of persons living in the canton of Vaud was compared to that of a smaller sample of people living in small townships across the border of the canton, in which neither edible salt nor water are fluoridated. The concentration of fluoride in 444 single samples of urine from adult persons living in the canton of Vaud was 1.06 +/- 0.03 mg/l, in 40 subjects living two townships across the border 0.62 +/- 0.06 mg/l. The excretion of fluoride per 24 hrs has been evaluated by measuring simultaneously the creatinine concentration in the urine samples under the assumption of constant creatinine and fluoride excretion within 24 hour periods. The calculated fluoride excretion in 366 subjects living in the canton of Vaud was 1.14 +/- 0.03 mg/24 hrs, that of 40 subjects living outside of the canton 0.60 +/- 0.05 mg/24 hrs when the figure inserted for the excretion of creatinine within 24 hours was taken from a study of Rowe [9]. A few data reported suggest that the mean excretion of creatinine in the urine of normal subjects living in Switzerland was only 67% of that measured in the U.S. by Rowe. Total fluoride excretions calculated under this assumption were 0.76 +/- 0.02 mg/24 hrs for persons living in Vaud vs. 0.40 +/- 0.04 mg/24 hrs in the subjects living outside of Vaud. The concentrations of fluoride found in the urine of the adult subjects of the present study did not differ significantly from those found in school children aged 7-15 living in the same communities. Concentrations of fluoride in urine appear to have increased since 1970 in subjects living in the canton of Vaud. This fact may indicate that a steady state equality between intake and urinary excretion of fluoride had not yet been reached in 1970. In 366 urine samples of subjects living in Vaud in 1974, the concentration of fluoride in urine could be represented as a linear regression on the concentration of creatinine. The slope of this regression was smaller than unity indicating an enhanced fluoride excretion at higher rates of urine flow and a depressed excretion at low rates of urine flow. The occurrence of diurnal variations in the urinary excretion of fluoride or of creatinine could not be excluded in the present study. The urinary excretion of fluoride exceeded 2.5 mg/24 hr in approximately 2% of the subjects living in the canton of Vaud but was smaller than 0.8 mg/24 hr in approximately 18%. It was concluded that fluoridation of salt at the level indicated should be an effective measure for the prevention of dental caries. It was, furthermore, concluded that salt fluoridation at the level indicated does not present any risk of toxicity.

Adult↗
PubMed1980

Influence of indomethacin on cation excretion after acute unilateral nephrectomy in dogs.

Acute unilateral nephrectomy (AUN) causes functional changes in the remaining kidney. Since renal prostaglandins (PGs) may participate in this response, we investigated the effect of the PG synthetase inhibitor, indomethacin (INDO), on the function of the remaining kidney after AUN. Glomerular filtration rate (GFR), effective renal plasma flow (ERPF), filtration fraction (FF), sodium excretion, and potassium excretion were measured for 1 hr prior to and 3 hr after AUN in dogs anesthetized with sodium pentobarbital. Group I and II animals underwent AUN. A third group was sham-operated (Group III). Group I received INDO (2 mg/kg) before and 2 hr after AUN, while Groups II and III received a buffered saline vehicle. AUN alone (Group II) had no effect on GFR, ERPF, FF, or sodium excretion, while potassium excretion was increased. In animals administered INDO prior to AUN (Group I), the increase in potassium excretion was abolished, FF rose and sodium excretion, while potassium excretion was increased. In animals administered INDO prior to AUN (Group I), the increase in potassium excretion was abolished, FF rose and sodifore and 2 hr after AUN, while Groups II and III received a buffered saline vehicle. AUN alone (Group II) had no effect on GFR, ERPF, FF, or sodium excretion, while potassium excretion was increased. In animals administered INDO prior to AUN (Group I), the increase in potassium excretion was abolished, FF rose and sodium excretion was decreased. Results suggest that renal PGs participate in the compensatory response of the remaining kidney to AUN and may specifically play a role in increased cation excretion following AUN.

Animals↗
PubMed1999

Day-to-day and within-day variation in urinary iodine excretion.

OBJECTIVE: To examine the day-to-day and within-day variation in urinary iodine excretion and the day-to-day variation in iodine intake. DESIGN: Collection of consecutive 24-h urine samples and casual urine samples over 24h. SETTING: The study population consisted of highly motivated subjects from our Institute. SUBJECTS: Study 1: Ten healthy subjects (seven females and three males) aged 30-46 y. Study 2: Twenty-two healthy subjects (9 males and 13 females) aged 30-55 y. METHODS: Study 1: 24-h urine samples were collected for four consecutive days. Study 2: Each urine voided over 24 h was collected into separate containers. In both studies dietary records were kept. MAIN OUTCOME MEASURES: Twenty-four-hour urinary iodine excretion, 24-h urinary iodine excretion estimated as I/Cr*24 h Cr and as a concentration in casual urine samples. RESULTS: Study 1: Both iodine excreted in 24-h urine and iodine intake varied from day-to-day. Iodine excretion correlated with iodine intake (=-0.46, P=0.01). Iodine intake (mean 89 +/- 6.5 microg/d) was not significantly different from iodine excretion (mean 95 +/- 5.3 microg/d). Study 2: Twenty-four hour iodine excretion estimated as I/Cr*24 h Cr from the morning urine sample was significantly lower than actual 24-h iodine excretion, whereas 24-h iodine excretion estimated as I/Cr*24 h Cr from the first sample after the morning sample and the last sample before the subjects went to bed was not significantly different from actual 24-h iodine excretion. Twenty-four-hour urine excretion estimated as a concentration was lower than actual 24-h iodine excretion in casual urine taken at any time of the day. CONCLUSIONS: For determination of iodine status in an individual, more than one 24-h urine sample must be used. The use of the I/Cr ratio in casual urine samples is a usable measure of iodine status if corrected for the age- and sex-adjusted 24-h creatinine excretion. Further, the study suggests that fasting morning urine samples would underestimate iodine status in this population.

Adult↗
PubMed1975

Urinary noradrenaline excretion and renal function in normal and hypertensive 50-year-old men.

1. Sympathetic nervous system activity, measured by urinary noradrenaline excretion, was determined in a group of untreated hypertensive subjects (n = 35), a reference group (n = 80) and a normotensive group (n = 51), all derived from a random population sample of 50-year-old men. It was compared with casual and resting blood pressure, urinary sodium excretion, urinary cretinine concentration and glomerular filtration rate. Hypertension was defined as systolic pressure greater than 175 or diastolic greater than 115 mmHg on two separate occasions. Normotension was defined as systolic pressure less than 160 and diastolic pressure less than 95 mmHg. 2. There was no difference in the average excretion of noradrenaline during the day or night between the reference, normotensive and hypertensive groups. None of the hypertensive patients had values for urinary noradrenaline excretion during the day above the range found in normotensive subjects, indicating that hypertension with increased sympathetic nervous system activity is uncommon when hypertension in defined as above. 3. No correlation between urinary noradrenaline excretion during the day and blood pressure was found in the reference group or in the normotensive group. In the hypertensive group, there was a negative correlation between urinary noradrenaline excretion and blood pressure after rest. This finding might indicate that factors other than sympathetic nervous system activity determine the level of blood pressure in hypertensive subjects. 4. In the hypertensive group, urinary noradrenaline excretion during the day was positively correlated with both urinary sidium excretion during the day and glomerular filtration rate. Urinary noradrenaline excretion per 24 h was positively correlated with urinary sodium excretion during the same time. High resting blood pressure, low urinary sodium excretion, low glomerular filtration rate and a reversed diurnal rhythm of urinary excretion characterized hypertensive patients with low urinary noradrenaline excretion, indicating more severe hypertension in these hypertensive patients with reduced sympathetic nervous system activity.

Blood Pressure↗
PubMed1992

Oxidative DNA damage estimated by 8-hydroxydeoxyguanosine excretion in humans: influence of smoking, gender and body mass index.

Oxidative DNA damage may be implicated in ageing, carcinogenesis and other degenerative diseases. Oxidative DNA damage can be assessed in humans in vivo from the urinary excretion of the DNA-repair product 8-hydroxydeoxyguanosine (8OHdG). We investigated factors influencing the excretion of 8OHdG in 24 h urine from 83 randomly selected healthy subjects (52 women) aged 40-64 years. For 2 weeks prior to urine collection the subjects kept a weighed diet record. 8OHdG was quantified by an automatic three-dimensional HPLC analysis with electrochemical detection. The 8OHdG excretion was 252 +/- 103 (mean +/- SD) pmol kg body weight/24 h with a range from 78 to 527. Multiple regression analysis identified three factors, smoking, body mass index (BMI) and gender, as significant predictors of the 8OHdG excretion. In 30 smokers the 8OHdG excretion was 320 +/- 99 pmol/kg/24 h opposed to 213 +/- 84 pmol/kg/24 h in 53 non-smokers. According to multiple regression analysis smokers excreted 50% (31-69%; 95% confidence interval) more 8OHdG than non-smokers. In 52 women the 8OHdG excretion was 240 +/- 106 pmol/kg/24 h opposed to 271 +/- 96 pmol/kg/24 h in 31 men. According to the multiple regression analysis men excreted 29% (10-48%) more 8OHdG than women. According to multiple regression analysis the 8OHdG excretion decreased with 4% (2-6%) per increment in BMI measured in kg/m2. The dietary distribution of energy demonstrated no important predictive value with respect to 8OHdG excretion. The intake of the antioxidant vitamins C and E and of vitamin A equivalents, including beta-carotene, was not associated with 8OHdG excretion. The results suggest that smoking increases oxidative DNA damage by approximately 50%. This effect implies potential serious health effects adding to the other well-known health hazards of smoking. The higher 8OHdG excretion in men and lean subjects may be related to a higher rate of metabolism with increased availability of reactive oxygen species. The apparent 7-fold individual variation in oxidative DNA damage carries implications regarding the rate of ageing and the risk of cancer and other degenerative diseases. The excretion of 8OHdG into urine offers a valuable tool for testing such hypotheses in humans.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1990

Increased urinary excretion of transferrin in children with type 1 diabetes mellitus.

Urinary transferrin excretion was measured by radioimmunoassay in 74 children with Type 1 diabetes mellitus and in 40 normal children, and compared with urinary excretion of albumin, alpha-1-microglobulin, and N-acetyl-beta-D-glucosaminidase. Urinary transferrin excretion was significantly elevated in diabetic (median (range) 186 (18-1671) mg mol-creatinine-1) compared with normal (85 (27-668) mg mol-creatinine-1) children (p less than 0.001). Seventeen diabetic children had transferrin excretion above the 95th centile for normal children. In contrast there was no significant increase in urinary albumin excretion in the diabetic children although 8 had urinary albumin excretion which exceeded the 95th centile for normal children (6 of these 8 patients having coexistent urinary hyperexcretion of transferrin). Urinary transferrin excretion correlated significantly with urinary albumin excretion in both normal (rs = 0.62, p less than 0.001) and diabetic (rs = 0.61, p less than 0.001) children. The indices of proximal renal tubular function (urinary excretion of alpha-1-microglobulin and N-acetyl-beta-D-glucosaminidase) correlated significantly with transferrin excretion in both diabetic (rs = 0.43 and rs = 0.41, p less than 0.001) and normal (rs = 0.40, p less than 0.02 and rs = 0.53, p less than 0.001) children, but not with albumin excretion (rs = 0.20, p greater than 0.05 and rs = 0.22, p greater than 0.05). In addition urinary transferrin excretion significantly correlated with urinary glucose concentration (rs = 0.34, p less than 0.007) in Type 1 diabetic children. The discrepancy in urinary excretion of transferrin and albumin may reflect impaired proximal renal tubular reabsorption of transferrin and/or altered glomerular basement membrane selectivity for the two proteins.

Acetylglucosaminidase↗
PubMedDate not supplied

Urinary transferrin excretion in type 1 (insulin-dependent) diabetes mellitus.

Urinary excretion of transferrin and albumin was studied by radioimmunoassay in 47 adult patients with Type 1 diabetes and 28 control subjects. Median (range) urinary transferrin excretion rate was significantly elevated in the diabetic group 0.58 (0.02-2663.3) micrograms min-1 compared with the control group 0.04 (0.01-0.28) micrograms min-1, p less than 0.001. Urinary transferrin:creatinine ratios (x 10(2)) were different in diabetic 47 (0.6-958.0) micrograms mmol-1 and control groups 0.7 (0.06-2.3) micrograms mmol-1, p less than 0.001). There were correlations between urinary transferrin and albumin excretion rates in diabetic (r = 0.78, p less than 0.001) and control groups (r = 0.81, p less than 0.05). Forty (85%) diabetic patients had elevated transferrin excretion rates, 18 (38.3%) had elevated albumin excretion rates. All diabetic patients with elevated albumin excretion rates had elevated transferrin excretion rates. Twenty-one (77.8%) of the patients with normal albumin excretion rates had elevated transferrin excretion rates. Urinary excretion of N-acetyl-beta-D-glucosaminidase was greater in diabetic patients than control subjects (142 vs 58 mumol h-1 l-1, p less than 0.001). There were correlation between transferrin and N-acetyl-beta-D-glucosaminidase excretion (r = 0.67, p less than 0.01) and albumin and N-acetyl-beta-D-glucosaminidase excretion (r = 0.63, p less than 0.01) in the diabetic group. Elevated urinary transferrin excretion rate may be a marker for renal dysfunction in diabetes mellitus.

Acetylglucosaminidase↗
PubMed1987

Urinary 18-hydroxycortisol and its relationship to the excretion of other adrenal steroids.

The urinary excretion of 18-hydroxycortisol was recently reported to be increased in patients with primary aldosteronism who have an adrenal adenoma and in those with glucocorticoid-suppressible aldosteronism. A direct RIA for 18-hydroxycortisol in urine and plasma has been described, and we here report our experience using a similar direct RIA and a more elaborate RIA which includes a preliminary high pressure liquid chromatography (HPLC) purification step. The urinary excretion of 18-hydroxycortisol was compared with that of other adrencorticoids. The urinary excretion of 18-hydroxycortisol in 37 normal subjects using the direct RIA was 112 +/- 49 (+/- SD) microgram/24 h, and that with the HPLC-RIA method was 63 +/- 36 micrograms/24 h. The accuracy and specificity of the HPLC-RIA assay method were confirmed by measuring the steroid after the HPLC step as the glycolic acid ester derivative. The urinary excretion of 18-hydroxycortisol correlated with that of cortisol (r = 0.36; P less than 0.01), 18-oxocortisol (r = 0.42; P less than 0.01), and 19-nordeoxycortisosterone (r = 0.71; P less than 0.001), but did not correlate with the excretion of aldosterone 18-oxoglucuronide (r = 0.25; P = 0.15942). Dexamethasone administration to five normal subjects significantly decreased 18-hydroxycortisol excretion from 81 +/- 47 to 23 +/- 8 micrograms/24 h. ACTH infusion in these subjects receiving dexamethasone significantly raised 18-hydroxycortisol excretion to 147 +/- 37 micrograms/24 h. Five days of a sodium-restricted diet (10 mmoles/day) resulted in a significant (P less than 0.02) increase in 18-hydroxycortisol excretion, but two of eight subjects had decreased excretion, although urinary aldosterone excretion increased, as expected. These studies demonstrate that the direct RIA significantly overestimates urinary 18-hydroxycortisol excretion. These studies also demonstrate that the major factor resulting 18-hydroxycortisol excretion is ACTH. However, since 18-hydroxycortisol excretion may increase during sodium depletion, angiotensin or other factors may also regulate its secretion.

Adrenal Cortex Hormones↗
PubMed1993

Racial differences in aldosterone excretion: a longitudinal study in children.

Aldosterone production, estimated from urinary excretion of aldosterone and the plasma aldosterone level, was found in a previous cross-sectional study to be lower in black children than white children. The present study examined aldosterone excretion longitudinally to determine whether the aldosterone excretion rate changed with time and if the racial difference in aldosterone excretion persisted. Urine samples were collected every 6 months for up to 5.5 yr in 351 white and 170 black children for measurements of aldosterone, sodium (Na+), and potassium (K+) excretion. Results were expressed per mumol urinary creatinine. Mean values for excretion rates for the total longitudinal period were determined. Na+ excretion was not significantly different in the two groups, whereas K+ excretion was 18% lower in blacks than whites (P = 0.0001). Body weight and urinary Na+ and K+ excretion were significantly related to aldosterone excretion. After adjusting for these variables, the aldosterone excretion rate was 35% lower in blacks than whites (P = 0.0001), a racial difference that did not change with age. Aldosterone excretion rates showed no longitudinal trend to either increase or decrease. The physiological relevance of the lower aldosterone excretion rate in black children remains unknown.

Adolescent↗
PubMed1999

Urinary excretion of aquaporin-2 in rat is mediated by a vasopressin-dependent apical pathway.

Clinical studies have shown that aquaporin-2 (AQP2), the vasopressin-regulated water channel, is excreted in the urine, and that the excretion increases in response to vasopressin. However, the cellular mechanisms involved in AQP2 excretion are unknown, and it is unknown whether the excretion correlates with AQP2 levels in kidney or levels in the apical plasma membrane. The present study was undertaken to clarify these issues. Immunoblotting of rat urine samples revealed significant excretion of AQP2, whereas AQP3, being a basolateral aquaporin in the same cells, was undetectable. Thus, there was a nonproportional excretion of AQP2 and AQP3 (compared with kidney levels), indicating that AQP2 is excreted predominantly via a selective apical pathway and not by whole cell shedding. Urinary AQP2 was associated with small vesicles, membrane fragments, and multivesicular bodies as determined by immunoelectron microscopy and negative staining techniques. In rats with normal water supply, daily urinary excretion of AQP2 was 3.9+/-0.9% (n = 6) of total kidney expression. Treatment with desmopressin acetate subcutaneously caused a fourfold increase in urinary excretion of AQP2 during 8 h. Forty-eight hours of thirsting, known to increase endogenous vasopressin secretion, resulted in a three-fold increase in kidney AQP2 levels but urinary excretion increased ninefold to 15+/-3% (n = 6) of AQP2 in kidney of thirsted rats. Moreover, rats that were thirsted for 48 h and subsequently allowed free access to water for 24 h produced a decrease in urinary AQP2 excretion to 38+/-15% (n = 6) of that during thirsting. In Brattleboro rats or lithium-treated normal rats completely lacking vasopressin action, and hence having extremely low levels of AQP2 in the apical plasma membrane, AQP2 was undetectable in urine. Thus, conditions with known altered vasopressin levels and altered levels of AQP2 in the apical plasma membrane were associated with corresponding major changes in AQP2 urine excretion. In contrast, in such conditions, kidney AQP2 levels and urinary AQP2 excretion did not show a proportional relationship.

Animals↗