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PubMed1999

Human parathyroid hormone (1-34) increases urinary excretion of lysosomal enzymes in rats.

The kidney is the major target of parathyroid hormone (PTH), and PTH influences the urinary excretion of calcium, phosphate and hydrogen ions. It was previously reported that the urinary, excretion of N-acetyl-beta-D-glucosaminidase (NAG), a lysosomal enzyme, transiently increases after human PTH (hPTH) (1-34) infusion in normal subjects and idiopathic hypoparathyroidism patients, but not in pseudohypoparathyroidism type I patients. Here we report that intravenous infusion of hPTH(1-34) to rats transiently increased the urinary excretion of various lysosomal enzymes, such as beta-glucuronidase and acid phosphatase as well as NAG. However, it did not affect the urinary excretion of tubular brush border membrane enzymes, i.e. alkaline phosphatase, leucine aminopeptidase and gamma-glutamyl transpeptidase. Human PTH(1-34) dose-dependently increased the urinary excretion of NAG in rats with a peak at 30 min, which returned to a baseline within 60 min. The increase in the urinary NAG excretion caused by hPTH(1-34) positively correlated with the increase in the urinary cAMP excretion (r = 0.844, p < 0.01), and infusion of dibutyryl cAMP at a dose of 20 mg/kg similarly increased the urinary excretion of NAG. These results suggested that the increase in the urinary excretion of lysosomal enzymes caused by hPTH(1-34) may be a functional response to hPTH(1-34) occurring in the renal tubules via PTH signaling pathway.

Acetylglucosaminidase↗
PubMed2000

CO2 transport and excretion in rainbow trout (Oncorhynchus mykiss) during graded sustained exercise.

A quantitative analysis of CO2 transport and excretion was conducted in seawater acclimated rainbow trout (Oncorhynchus mykiss) swimming at different sustained swimming velocities. CO2 excretion increased linearly with cardiac output during exercise but arterial P(CO2) (Pa(CO2)) and total CO2 levels also increased indicating a diffusion limitation to CO2 excretion. The elevated Pa(CO2) was not accompanied by a decrease in pH, indicating that the acid-base compensation was rapid. Mixed-venous P(CO2) increased to a greater extent than Pa(CO2) resulting in a large increase in the venous arterial difference in P(CO2) (Pv(CO2) - Pa(CO2)). The Pv(CO2) - Pa(CO2) difference was used to calculate the proportion of total CO2 excreted comprised of dissolved CO2 which accounted for less than 1% of total CO2 excreted in fish swimming at 11 cm sec(-1) but increased to about 9% at the greatest swimming velocity indicating that the pattern of CO2 excretion changes during exercise. There was no effect of exercise on the proportion of CO2 excreted which was dependent upon HCO3-/Cl- exchange (54%) or that which was dependent upon the dehydration of HCO3- that resided within the red cell prior to gill blood entry (42%). The large proportion of total CO2 excreted that was dependent upon HCO3-/Cl- exchange is significant because this is thought to be the rate limiting step in CO2 excretion.

Animals↗
PubMed1986

gamma-Glutamyl transpeptidase excretion in cisplatin-induced acute renal failure.

Cisplatin (cisdiamminedichloroplatinum), an important antineoplastic agent, possesses nephrotoxicity as its major side effect. A mild partially reversible nonoliguric form of acute renal failure (ARF) is generally the most common form of nephrotoxicity and occurs in experimental animals following a single dose. gamma-Glutamyl transpeptidase (gamma GT) is an enzyme with maximal activity located in the brush border of proximal renal tubular epithelium. To test the relationship between cisplatin nephrotoxicity and urinary gamma GT excretion, rats received a single 5.5 mg/kg dose of cisplatin and gamma GT excretion was evaluated and compared to anatomic and functional damage. Twenty-four hours following cisplatin administration, there was a marked enhancement of urinary gamma GT excretion, prior to the onset of azotemia. Urinary gamma GT excretion peaked at day 4, then returned to baseline, and decreased to values below baseline on days 8 through 10. By days 11 through 12, renal function and urinary gamma GT excretion had returned to normal. The correlation between nephrotoxicity, changes in urinary gamma GT excretion, and anatomic damage was excellent. Morphologically, increased gamma GT excretion was associated with loss of microvilli, and the return of urinary gamma GT excretion to normal correlated with their regeneration. We conclude that cisplatin administration results in increased urinary gamma GT excretion. This early enhancement, prior to the onset of azotemia, may provide a useful noninvasive marker of early cisplatin nephrotoxicity.

Acute Kidney Injury↗
PubMed1997

Effect of chelating agents on the excretion of copper, zinc and iron in the bile and urine of sheep.

The effect of tetrathiomolybdate (TM), disodium calcium ethylenediamine tetraacetate (EDTA), D-penicillamine (PEN), 2-3 dimercapto-1-propanol (BAL) and dimethyl dithiocarbamate (DDC) administration on biliary and urinary excretion of copper (Cu), zinc (Zn) and iron (Fe) was investigated in sheep on a low Cu diet (Group A) and a high Cu diet (Group B). Only biliary Cu excretion increased significantly (P<0.01) with TM treatment. Urinary Cu excretion increased (P<0.01) following PEN treatment. TM, EDTA, PEN, BAL and DDC adminstration increased Cu excretion via bile and urine by 254, 11, 266, 46 and 16%, respectively in Group A sheep, and by 354, 13, 196, 20 and (-) 31% in Group B sheep. Urinary Zn excretion increased (P<0.01) following EDTA and PEN treatments. Only urinary Fe excretion increased (P<0.01) with EDTA treatment. The results show that TM and PEN are the most efficient decoppering agents, but PEN unlike TM also removes Zn. The major routes of excretion of Cu chelates by TM and PEN are different. TM increases Cu excretion significantly (P<0.05 in Group A and P<0.01 in Group B) in bile with only a slight increase in urinary Cu whereas PEN increases Cu excretion significantly (P<0.01) in urine. Therefore from a therapeutic view, a combination therapy of TM and PEN would be useful to maximize Cu removal from the body.

Animals↗
PubMed2003

Liquid chromatography-based determination of urinary free and total N(epsilon)-(carboxymethyl)lysine excretion in normal and diabetic subjects.

We propose a specific, reproducible and sensitive HPLC method for the determination of N(epsilon)-(carboxymethyl)lysine (CML) excreted in urine. Total CML was measured in acid hydrolysates of urine samples, while free CML was measured in acetonitrile-deproteinised urine samples using a RP-HPLC method with ortho-phtaldialdehyde (OPA)-derivatisation and fluorescence detection suited for automation. We compared the CML excretion of 51 non-proteinuric patients with diabetes mellitus (DM) (age 57+/-14 years, HbA1c 8.0+/-1.8%) to 42 non-diabetic controls (C) (age 45+/-17 years). The urinary excretion of total CML in diabetic patients was increased by approximately 30% (DM: 0.58+/-0.21; C: 0.45+/-0.14 microM/mmol creatinine; P<0.001). While urinary excretion of free CML was not significantly different, excretion of bound CML was increased (DM: 0.36+/-0.17; C: 0.27+/-0.14; P<0.05) in diabetic patients. CML excretion was correlated with protein and albumin excretion, but did not correlate with HbA1c, duration of DM or diabetic complications such as neuropathy or retinopathy. Furthermore, no age-dependent change of total CML excretion was found, while free CML excretion was lower in younger subjects. The specific and sensitive determination of CML by RP-HPLC of its OPA-derivative is well suited for automation and better than that of less defined glycoxidation products (AGEs).

Adult↗
PubMed2003

Renal excretion of galactose and galactitol in patients with classical galactosaemia, obligate heterozygous parents and healthy subjects.

The age dependence of galactose and galactitol excretion was assessed in overnight-fasted galactose-1-phosphate uridyltransferase-deficient patients under dietary treatment (ages 4-34 years; n = 51), obligate heterozygous parents (ages 25-71 years; n = 49) and healthy subjects (ages 3-58 years; n = 215). Urine concentrations were analysed by stable-isotope dilution gas chromatography mass spectrometry. There was considerable interindividual variability. The intraindividual variation, however, was not age-dependent and was rather low. Excretion estimates were calculated from the creatinine-related concentrations using weight-, age- and sex-related creatinine excretion rates. Experimental evidence is presented underscoring the problems inherent in random sampling and substantiating the primary endogenous origin of galactose and galactitol in postabsorptive urine samples. Age-dependent excretion estimates were best fitted to a simple growth-related model assuming an exponential decrease with age until adulthood. According to the model, mean postabsorptive galactose and galactitol excretion in healthy subjects was similar and decreased exponentially from about 1.2 micromol/kg body weight per day in infants to about 0.2 micromol/kg body weight per day in adults. Excretion in heterozygotes was normal. In galactosaemic patients, galactose excretion was in the normal range. Galactitol excretion, however, was enhanced over 50-fold and decreased from a mean estimate of about 64 micromol/kg body weight per day in infants to about 23 micromol/kg body weight per day in adults. The results are discussed with respect to the significance of galactose and galactitol excretion for whole-body galactose removal and with respect to the applicability of urinary galactitol analysis for metabolic monitoring in galactosaemia.

Adolescent↗
PubMed2000

Biliary excretion of bile acids and organic anions in zone 1- and zone 3-injured rats.

AIMS: Hepatocytes in zone 1 of the hepatic lobule play a role in the uptake and biliary excretion of bile acids and organic anions under physiological conditions, and those in zone 3 may play a role only with a high-dose load. To further elucidate the role of hepatic zonation on the handling of bile acids and organic anions, biliary excretion of these compounds was studied in zone 1- and zone 3-injured rats. METHODS: Biliary excretion of bile acids and organic anions was studied in zone 1- and zone 3-injured rats, caused by allyl alcohol and bromobenzene, respectively. RESULTS: Biliary excretion of a tracer dose of taurocholate was unchanged in the injury in both zones, but that of leukotriene C4 was decreased in zone 1 injury. The excretory maximum of taurocholate was decreased with zone 1 and the zone 3 injuries. Biliary excretion of deoxycholate metabolites was decreased in zone 3 injury, although the profile of metabolites in the bile was unchanged. Sulfobromophthalein excretion was decreased in zone 1 injury, but unchanged in zone 3 injury. CONCLUSIONS: These findings indicate that zone 1 is very important for biliary excretion of both organic anions and bile acids. In contrast, zone 3 is considered not to have a role in biliary excretion of organic anions, but to play a role in the excretion of bile acids.

Alanine Transaminase↗
PubMed1981

Mechanism by which enhanced ammonia production reduces urinary potassium excretion.

To determine the mechanism whereby an increase in ammonia production decreases urinary potassium excretion, we perfused isolated rat kidneys at a pH of either 7.0 or 7.4. After 45 min of perfusion at either pH, glutamine or ammonium chloride was added to the perfusate to result in concentration of 5 and 0.8 mM, respectively and observations were continued for 50 min. Control kidneys were perfused at both pH's without further additions to the perfusate. At pH 7.0 glutamine increased ammonia production and increased urinary ammonium excretion strikingly; whereas the addition of ammonium chloride did not change ammonia production but increased urinary ammonium excretion to a comparably degree. Both maneuvers resulted in a reciprocal fall in urinary potassium excretion in comparison with control perfusions. The decreases in potassium excretion could not be accounted for by differences in perfusate or urinary acid-base parameters, or by changes in urinary sodium, water, or chloride excretion. At pH 7.4, glutamine also significantly increased ammonia production and perfusate ammonia concentration. In contrast to the studied at pH 7.0 in which the urine pH was acid (5.9), the urine remained alkaline (pH 7.2), and both urinary ammonium excretion and urinary potassium excretion were unaltered. Thus, potassium sparing is not a nonspecific effect of glutamine, its metabolism to ammonia, or perfusate ammonia concentration but is directly related to an increase in urinary ammonium excretion.

Ammonia↗
PubMed1989

Urinary excretion of C5b-9 reflects disease activity in passive Heymann nephritis.

Passive Heymann nephritis (PHN) is a model of membranous nephropathy in rats in which glomerular injury is mediated by the terminal C5b-9 membrane attack complex of complement. This model has been shown to be associated with markedly elevated urinary excretion of C5b-9, compared to other experimental models of glomerulonephritis To determine if urinary C5b-9 excretion could serve as an index of disease activity by correlating with the formation and quantity of glomerular subepithelial immune deposits in PHN, we measured urinary excretion of C5b-9 in PHN under several experimental conditions. In the heterologous phase a direct correlation was demonstrated between levels of urinary C5b-9 excretion and the amount of anti-Fx1A IgG deposited in glomeruli (r = 0.85). In the autologous phase, C5b-9 excretion correlated with the amount of deposit forming antibody present in the serum and resolved when antibody disappeared, despite persistence of glomerular deposits of antigen, antibody, C5b-9 and heavy proteinuria. Glomerular C3 deposits paralleled urinary C5b-9 excretion. Re-initiation of active deposit formation by a second injection of anti-Fx1A produced new C3 deposits and a marked rise in C5b-9 excretion. Finally, complete abrogation of deposit formation by transplanting PHN kidneys into normal recipients also halted C5b-9 excretion. Our findings demonstrate that urinary excretion of C5b-9 is a sensitive index of on-going immunologic disease activity in the PHN model of membranous nephropathy.

Animals↗
PubMed1991

Potassium administration reduces and potassium deprivation increases urinary calcium excretion in healthy adults [corrected].

This study was undertaken to evaluate the effects of dietary K intake, independent of whether the accompanying anion is Cl- or HCO3-, on urinary Ca excretion in healthy adults. The effects of KCl, KHCO3, NaCl and NaHCO3 supplements, 90 mmol/day for four days, were compared in ten subjects fed normal constant diets. Using synthetic diets, the effects of dietary KCl-deprivation for five days followed by recovery were assessed in four subjects and of KHCO3-deprivation for five days followed by recovery were assessed in four subjects. On the fourth day of salt administration, daily urinary Ca excretion and fasting UCa V/GFR were lower during the administration of KCl than during NaCl supplements (delta = -1.11 +/- 0.28 SEM mmol/day; P less than 0.005 and -0.0077 +/- 0.0022 mmol/liter GFR; P less than 0.01), and lower during KHCO3 than during control (-1.26 +/- 0.29 mmol/day; P less than 0.005 and -0.0069 +/- 0.0019 mmol/liter GFR; P = 0.005). Both dietary KCl and KHCO3 deprivation (mean reduction in dietary K intake -67 +/- 8 mmol/day) were accompanied by an increase in daily urinary Ca excretion and fasting UCaV/GFR that averaged on the fifth day +1.31 +/- 0.25 mmol/day (P less than 0.005) and +0.0069 +/- 0.0012 mmol/liter GFR (P less than 0.005) above control. Both daily urinary Ca excretion and fasting UCaV/GFR returned toward or to control at the end of recovery. These observations indicate that: 1) KHCO3 decreases fasting and 24-hour urinary Ca excretion; 2) KCl nor NaHCO3, unlike NaCl, do not increase fasting or 24-hour Ca excretion and 3) K deprivation increases both fasting and 24-hour urinary Ca excretion whether the accompanying anion is Cl- or HCO3-. The mechanisms for this effect of K may be mediated by: 1) alterations in ECF volume, since transient increases in urinary Na and Cl excretion and weight loss accompanied KCl or KHCO3 administration, while persistent reductions in urinary Na and Cl excretion and a trend for weight gain accompanied K deprivation; 2) K mediated alterations in renal tubular phosphate transport and renal synthesis of 1.25-(OH)2-vitamin D, since KCl or KHCO3 administration tended to be accompanied by a rise in fasting serum PO4 and TmPO4 and a fall in fasting UPO4 V/GFR, a fall in serum 1,25-(OH)2-D and a decrease in fasting UCa V/GFR, while dietary KCl or KHCO3 deprivation were accompanied by a reverse sequence.

Adult↗
PubMed1993

Role of glucocorticoid in excretion of an acute potassium load in patients with Addison's disease and panhypopituitarism.

Glucocorticoid (GC) has been shown to stimulate potassium (K) excretion in various conditions, but it is still incompletely resolved whether its presence is essential for the normal K homeostasis. We addressed this question in patients with selective GC deficiency (panhypopituitarism) and with combined GC and mineralocorticoid deficiency (Addison's disease), studied 24 hours after withdrawal of their regular substitution therapy. Compared to data in healthy subjects, both basal K excretion and the kaliuresis after a KCl load (1 mmol/kg body wt orally) were impaired in either patient group (P < 0.05). Physiological cortisol supplementation (20 mg 3 hr prior to test, and 1 mg/hr during test) increased basal K excretion (from 10.6 +/- 1.8 to 19.2 +/- 1.9 mmol/5 hr, P < 0.01) and KCl stimulated kaliuresis (from 47.9 +/- 6.1 to 54.8 +/- 4.7 mmol/5 hr, P = 0.06) to normal levels in panhypopituitarism. Cortisol also improved basal K excretion (from 10.2 +/- 1.5 to 16.9 +/- 3.5 mmol/5 hr, P < 0.05) and KCl-stimulated K excretion (from 31.6 +/- 2.5 to 45.2 +/- 3.8 mmol/5 hr, P < 0.05) in Addison's disease, although KCl-stimulated K excretion remained below normal (P < 0.01). The effects of cortisol on sodium excretion differed between the two patient groups (P < 0.05) in that only in Addison's disease the improved K excretion was associated with sodium retention. Additional experiments with the purely GC compound dexamethasone (0.5 mg 3 hr prior to test, and 0.03 mg/hr during test) in the patients with Addison's disease also improved K excretion (P < 0.05), but without the concomitant sodium retention observed after cortisol.(ABSTRACT TRUNCATED AT 250 WORDS)

Addison Disease↗
PubMed1996

Urinary oxalate excretion increases with body size and decreases with increasing dietary calcium intake among healthy adults.

Increasing dietary calcium intake decreases urinary oxalate excretion by increasing intestinal precipitation of dietary oxalate as calcium oxalate. This mechanism was speculated to account for the decreased prospective incidence of kidney stones as estimated dietary calcium intake, adjusted for caloric intake, increased among men in a recent large epidemiological study. To further assess the relationship between estimated diet calcium and urinary oxalate, we studied 94 health adults, 50 women and 44 men, ages 20 to 70 years with weights ranging form 47 to 104 kg while they ate their customary diets. Each subject completed a semiquantitative food frequency questionnaire and collected three 24-hour urines preserved with HCl. The urines were collected accurately as judged by a mean intrasubject CV for creatinine excretion of 9.8% and direct relations between urinary creatinine excretion and body wt (r = 0.62; P < 0.0001), or predicted urine creatinine content for sex, age and weight using the Cockcroft and Gault formulas (r = 0.76; P < 0.0001). Estimated diet calcium intake ranged from 6.8 to 68 mmol/day (272 to 2720 mg/day) and averaged 29.5 mmol/day (1180 mg/day). Individual mean urinary oxalate excretion ranged from 0.079 go 0.332 mmol/day (7 to 29 mg/day) and averaged 0.198 mmol/day (17 mg/day). Among all subjects, daily oxalate excretion was directly related to creatinine excretion as an estimate of lean body mass (r = 0.61; P < 0.0001). Thus, oxalate excretion among men averaged 0.228 +/- 0.051 SD mmol/day, a value significantly higher than the average among women of 0.173 +/- 0.045 mmol/day (P < 0.001). Daily urine oxalate excretion/creatinine decreased curvilinearly as estimated dietary Ca intake increased (r = -0.30; P = 0.0035) and as the ratio of estimated dietary calcium to dietary oxalate increased (r = -0.39; P = 0.0001). We conclude that body size is the major determinant of urinary oxalate excretion among healthy adults, presumably reflecting variations in endogenous oxalate synthesis with lean body mass. Increasing estimated diet calcium intake, especially up to the range of 15 to 20 mmol/day (600 to 800 mg/day) has an additional effect to decrease during oxalate excretion, presumably by limiting intestinal absorption of dietary oxalate.

Adult↗
PubMed1984

Dependence of urinary prostaglandin E2 excretion on urinary volume rather than solute handling or segmental nephron function in man.

Eight normal subjects underwent water loading alone and water loading plus 40 mg of frusemide IV, fluid intake ad libitum alone and fluid intake ad libitum plus frusemide, plus each of the preceding after pretreatment with indomethacin. After frusemide administration, increases in urinary sodium excretion paralleled increases in urinary volume, and urinary prostaglandin E2 (PGE2) excretion correlated closely with sodium excretion (y = 1.03x - 0.28; r = 0.940; P less than 0.0001). In the absence of the diuretic, urinary volume varied over a wide range with little change in sodium excretion. Again, urinary PGE2 excretion correlated with urinary sodium excretion (y = 0.12x + 0.05; r = 0.789; P less than 0.002). However, the correlation differed markedly from that observed in the studies with frusemide. Expressing urinary PGE2 excretion as a function of urinary volume for all of the studies resulted in a highly significant correlation (y = 10.7x - 0.70; r = 0.975; P less than 0.0001). Multiple and stepwise regression analyses assessing the correlation of urinary PGE2 excretion with urinary flow rate and with indices of function of various nephron segments indicate that the correlation with urinary PGE2 could be predominantly accounted for by urinary volume. We conclude that in the condition of this study in man, urinary PGE2 excretion is a correlate of urinary volume.

Adult↗
PubMed1987

Amiloride inhibits the rise of urinary kallikrein excretion induced by frusemide administration in the rat.

The effect of amiloride administration on the urinary kallikrein response to the injection or continuous infusion of frusemide in normal Sprague-Dawley rats was investigated. Injections of frusemide induced repeatedly an increase in urinary kallikrein excretion. This effect was suppressed by amiloride. Amiloride also blocked the response to mannitol injection. A continuous infusion of frusemide lasting 100 min also induced an increase in urinary kallikrein excretion which persisted throughout the experiment. This response was completely blocked by the injection of amiloride. Urinary kallikrein excretion was directly and positively related to urine volume and urinary sodium excretion before and after amiloride injection. The regression lines had markedly decreased slopes after amiloride administration. The urinary kallikrein excretion was also positively related to the urine volume and urinary sodium excretion when frusemide was continuously infused. However, these relationships were abolished after amiloride injection. In both the injection and the infusion experiments, there was a direct relationship of urinary kallikrein excretion to urinary potassium excretion. Although this relationship persisted after amiloride injection, the regression line was shifted to the left. The suppression of the kallikrein stimulating effect of frusemide by the sodium channel blocker amiloride indicates that distal tubule sodium reabsorption is the triggering factor in urinary kallikrein excretion. The study suggests that the mechanism involved in the release of kallikrein by the distal tubular cells is linked to the renal mechanism affected by amiloride.

Amiloride↗
PubMed1991

Urinary excretion of nitrogenous and non-nitrogenous compounds in the chronic ethanol-fed rat.

1. The metabolic consequences of chronic ethanol feeding was investigated by assay of urinary metabolites. Male Wistar rats were fed a liquid diet containing 35% of total energy as ethanol or isovolumetric, isocaloric and isonitrogenous amounts of the same diet in which ethanol was substituted by isocaloric glucose (controls). 2. At 6 weeks the entire skeletal muscle mass was reduced by approximately 20%. The urinary excretion of nitrogen, urea and uric acid increased by between 23 and 128%. Urinary creatinine excretion was not significantly altered. 3. Urinary excretion of magnesium was significantly increased by 43%. Urinary excretion of sodium, potassium, calcium and phosphate was increased slightly (i.e. 5-22%), but this change was not statistically significant. 4. Proton n.m.r. spectroscopic analysis showed that ethanol feeding reduced the urinary excretion of citrate and 2-oxoglutarate (by approximately 50%), suggesting decreased citric acid cycle activity. There was an increased excretion of alanine (44%), but excretion of succinate and acetate was not significantly altered. Ethanol in the urine of ethanol-fed rats comprised approximately 2% of total ethanol intake and less than 1% of total energy intake. 5. Lactose was detectable in urine of ethanol-fed rats, but not in control rats, reflecting the reported decreased intestinal lactase activity and increased gut permeability in alcoholics. Urinary galactose excretion decreased by 41%, but relatively large increases in lactate excretion (50%) did not achieve statistical significance. 6. It was concluded that chronic ethanol feeding causes disturbances in whole-body nitrogen homoeostasis and alterations in intermediary metabolism.

Alanine↗
PubMed1992

2,3-Dinor metabolites of thromboxane A2 and prostacyclin in urine from healthy human subjects: diurnal variation and relation to 24h excretion.

1. Urinary levels of the 2,3-dinor metabolites of thromboxane A2 (2,3-dinor-thromboxane A2, Tx-M) and prostacyclin (2,3-dinor-6-keto-prostaglandin F1 alpha, PGI-M) are frequently analysed as indices of platelet and endothelial activity and interaction in vivo. Despite this, little is known about the possible diurnal variations in urinary Tx-M and PGI-M in healthy human subjects, and how the urinary levels of Tx-M and PGI-M in single samples reflect their respective 24 h excretion rates. We addressed this by determining Tx-M, PGI-M and creatinine in consecutive portions of urine collected during 24 h in 15 healthy non-smoking subjects. 2. The total 24 h excretion of Tx-M and PGI-M did not differ between men (223 +/- 31 and 132 +/- 27 ng, respectively) and women (215 +/- 44 and 127 +/- 29 ng, respectively). Neither the excretion of Tx-M nor that of PGI-M displayed any significant diurnal variation. 3. The excretion of Tx-M during a 3 h period and the Tx-M/creatinine ratio in a urine sample accurately reflected the 24 h excretion of Tx-M (correlation coefficient ranges 0.74-0.94 and 0.74-0.86, respectively). The excretion of PGI-M during a 3 h period and the PGI-M/creatinine ratio in a urinary sample were accurate measures of 24 h excretion of PGI-M (correlation coefficient ranges 0.76-0.94 and 0.72-0.83, respectively). Urinary Tx-M and PGI-M expressed as simple concentrations were poor indices of their respective 24 h excretion. 4. We conclude that time-related excretions of Tx-M and PGI-M may be the best indices ex vivo of the cardiovascular formation of thromboxane A2 and prostacyclin, but that urinary creatinine-related concentrations of Tx-M and PGI-M in a urine sample are accurate measures as well.

6-Ketoprostaglandin F1 alpha↗
PubMed1993

Effect of posture and acute glycaemic control on the excretion of retinol-binding protein in normoalbuminuric insulin-dependent diabetic patients.

1. It has been suggested that tubular damage may precede glomerular damage at the onset of diabetic nephropathy. This may be reflected by increased urinary excretion of low-molecular-mass proteins, such as retinol-binding protein. 2. We have measured the urinary excretion rate of retinol-binding protein overnight, during orthostasis and during a hyperinsulinaemic euglycaemic clamp (blood glucose concentration 7.0 mmol/l) with stable diuresis in 34 normotensive, normoalbuminuric insulin-dependent diabetic patients and in 10 normal control subjects. Normal control subjects were not clamped. A further four normoalbuminuric insulin-dependent diabetic patients were rendered euglycaemic without a water load. 3. Overnight retinol-binding protein excretion rate was 58 (16-157) [median(range)] ng/min in patients with insulin-dependent diabetes and 32 (15-72) ng/min in control subjects (P < 0.01). The excretion rate did not change during orthostasis [patients with insulin-dependent diabetes, 67 (3-173) ng/min; control subjects, 23 (5-78) ng/min]. During the euglycaemic clamp retinol-binding protein excretion rate increased to 383 (78-4897) ng/min in patients with insulin-dependent diabetes (P < 0.01). An average increment in retinol-binding protein excretion rate of greater than 4000% was noted after acute euglycaemia in those patients with insulin-dependent diabetes who were not water-loaded. 4. In insulin-dependent diabetes, both overnight and orthostatic retinal-binding protein excretion was not correlated with fasting blood glucose concentration, HbA1, fructosamine or duration of diabetes. The absolute and incremental excretion rates of retinol-binding protein during the clamp were, however, correlated with both fasting blood glucose concentration and glucose excretion rate (rs = 0.41-0.48, P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2004

Low melatonin excretion during mechanical ventilation in the intensive care unit.

Biochemical markers for the circadian rhythm were studied in patients treated at the ICU (intensive care unit) of two regional hospitals. A normal rhythm is characterized by a relatively higher melatonin and a lower cortisol excretion at night. Disturbances affect sleep, mood and cognitive performance. All urine excreted between 07:00 and 22:00 hours (day) and between 22:00 and 07:00 hours (night) was collected and sampled throughout the entire ICU period (median, 10 days) in 16 patients for the excretion of 6-SMT (6-sulphatoxymelatonin), which is a metabolite of melatonin, and free cortisol. The overall excretion of 6-SMT was slightly lower and the cortisol excretion higher than reported for healthy reference populations. Mechanical ventilation was associated with a markedly lower 6-SMT excretion (median, 198 ng/h) compared with periods without such help (555 ng/h; P<0.0001), whereas infusion of adrenergic drugs increased the 6-SMT excretion (P<0.01). Five patients (31%) showed a virtually absent melatonin excretion for 24 h or more. The diurnal rhythms were consistently or periodically disturbed in 65% and 75% of the patients. These alterations cannot be explained by excessive exposure to light at night. In conclusion, there was hyposecretion of melatonin during mechanical ventilation, an overall high cortisol excretion and a disturbed diurnal rhythm of both of these hormones in most patients treated in two ICU departments.

Adult↗