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PubMed2000

Decreased urinary excretion of vascular endothelial growth factor in idiopathic membranous glomerulonephritis.

BACKGROUND: Membranous glomerulonephritis (MGN) has, for unknown reasons, an unpredictable and highly variable clinical course. Vascular endothelial growth factor (VEGF) enhances endothelial cell proliferation, angiogenesis, microvascular permeability, and monocyte chemotaxis, and it activates proteinases. In normal kidneys, it is predominantly expressed by glomerular podocytes, where its physiological function and role in development of renal diseases are obscure. This study was designed to evaluate the urinary excretion of VEGF in MGN compared with several other glomerular disease and to asses its relationships to the clinical activity of MGN. METHODS: Urinary VEGF was studied during renal biopsy using a sandwich enzyme immunoassay from 30 patients with idiopathic MGN, 8 with minimal change glomerulonephritis, 10 with focal segmental glomerulosclerosis (FSGS), 8 with necrotizing glomerulonephritis associated with systemic vasculitis, and 12 with diabetic nephropathy. In addition, 33 healthy controls were examined. Fifteen patients with MGN were re-evaluated 12 months later, and the evolution of proteinuria was compared with changes in urinary VEGF excretion. RESULTS: In healthy control subjects, urinary VEGF excretion was 68 +/- 10 (95% CI, 49 to 88) ng/mmol creatinine (UCr). In MGN, the excretion was decreased to 16 +/- 3 (CI, 10 to 23) ng/mmol crea (P < 0.0001, ANOVA), whereas in minimal change glomerulonephritis and diabetic nephropathy, it was unchanged [55 +/- 14 (CI, 24 to 86) and 101 +/- 25 (CI, 45 to 156) ng/mmol UCr, respectively, P = NS]. In vasculitis and FSGS patients, the excretion was higher than normal [184 +/- 68 (CI, 24 to 344), P = 0.01, and 160 +/- 29 (CI 95 to 226), P = 0.002 ng/mmol UCr, respectively]. The excretion did not correlate with serum VEGF, renal function, or proteinuria. In the follow-up of 15 patients, improving MGN (decreasing proteinuria) was associated with increasing VEGF excretion, while persistent disease (no change or increase of proteinuria) was associated with constantly low urinary VEGF excretion. The change in urinary protein excretion over one year correlated inversely with the change in urinary VEGF (r = -0.57, P = 0.026). CONCLUSIONS: MGN is associated with decreased urinary VEGF compared with normal subjects, which is in contrast with other proteinuric diseases. Moreover, decreasing clinical activity (proteinuria) is accompanied by increasing VEGF excretion. Urinary VEGF may serve as an indicator of activity of MGN.

Adult↗
PubMed2003

Effect of triglyceride structure on fecal excretion of 13C-labeled triglycerides.

OBJECTIVE: The aim of this work was to determine the effects of specific changes in the structure of (13)C-labeled triglyceride (TG*) on its fecal excretion relative to total stool fat excretion determined simultaneously in patients with reduced exocrine pancreatic function. METHODS: A series of 47 studies were conducted in 26 young cystic fibrosis (CF) patients and 11 adult patients with chronic pancreatitis over a five year period. Each test consisted of ingesting a single high fat test meal containing both (13)C-labeled triglyceride (TG*) and dysprosium chloride (DyCl(3)) a nonabsorbable marker of intestinal transit; in most studies the food colorant brilliant blue (FD&C blue #1) was administered along with the DyCl(3). The TG*s tested were: P*P*P* = TRIPALMITIN-1,1,1-(13)C(3); SO*S = 2-OCTANOYL-1,3-DISTEARIN-2-octanoyl-1,2-(13)C(2); and P*LP* = 2-LAURYL-1,3-DIPALMITIN-dipalmitoyl-1,1,2,2-(13)C(4). Ingestion of the test meal was followed by collection of individual stools for at least 72 hours. Stools were analyzed for (13)C-Excess ((13)C*), total fat, and Dy. RESULTS: Excretion of P*LP* showed a high degree of linear correlation with stool fat (r(2) = 0.924) over a wide-range of fecal fat values. Excretion of SO*S was also significantly correlated with stool fat, but its excretion was less than 10% at all levels of steatorrhea and the slope of the regression line relating TG* excretion to stool fat was some four to five times smaller than observed for P*LP*. Fecal excretion of P*P*P* was highly correlated with stool fat (r(2) = 0.941) in patients with moderate steatorrhea (<25 g fat/24 hours) and the slope of the regression line (3.20) was considerably greater than for P*LP*. Only results from those studies in which stool collections were complete (Dy excretion >90%) were utilized in the statistical comparisons (36 of 47 studies). CONCLUSIONS: The observed highly significant linear correlation between P*LP* and stool fat over the entire range of steatorrhea suggests that P*LP* excretion may be a suitable surrogate for fecal fat in patients with reduced exocrine pancreatic function. Because fecal excretion of TG* administered as described can be accurately determined by sampling only two visually marked stools, development of a noninvasive test to replace the current 72-hour stool fat test using this approach is possible. Use of other engineered TG*s and/or labeled fatty acids, may provide a method for non-invasive in vivo assessment of the specific defect(s) leading to steatorrhea in other patient groups.

Adolescent↗
PubMed2000

Urinary excretion of trace elements in humans after sodium 2,3-dimercaptopropane-1-sulfonate challenge test.

OBJECTIVE: To evaluate the effects of intravenous sodium 2,3-dimercaptopropane-1-sulfonate (DMPS, Dimaval) on urinary excretion of essential trace elements in subjects who received this chelating agent as a mercury challenge test. SUBJECTS: Eleven subjects sought medical attention due to concern with the toxicity of mercury released from dental amalgam fillings. DESIGN: The subjects were given DMPS 3 mg/kg intravenously. Spot urine samples were collected 1 hour before and 1 hour after the DMPS dose for laboratory analysis. In addition to mercury, the urinary excretion of copper, zinc, selenium, magnesium, manganese, molybdenum, chromium, cobalt, and aluminum were measured. RESULTS: A significant increase in urinary excretion of mercury (3- to 107-fold) was observed after the DMPS dose. The DMPS treatment led to a 2- to 119-fold increase in copper excretion; 3- to 43.8-fold in selenium excretion; 1.6- to 44-fold in zinc excretion; and 1.75- to 42.7-fold in magnesium excretion. The excretion of manganese, chromium, cobalt, aluminium, and molybdenum remained unchanged. CONCLUSIONS: In this study, an intravenous DMPS challenge test produced a significant increase in mercury excretion and also led to an increased excretion of copper, selenium, zinc, and magnesium.

Chelating Agents↗
PubMed1981

Urinary oxalate excretion after large intakes of ascorbic acid in man.

The influence of high dose intake of ascorbic acid on the urinary excretion of oxalate was investigated in five healthy male volunteers. Oxalate was measured by a newly developed specific method using isotachophoresis. With intakes of 10 g ascorbic acid (5 X 2 g daily for 5 days; four subjects) mean urinary oxalate excretion was enhanced from about 50 mg to 87 mg (range 60 to 126 mg) per day. At least 25% of the ascorbic acid was absorbed and excreted with the urine. On discontinuing ascorbic acid administration, oxalate excretion returned to baseline values within 24 h. The time-course of oxalate excretion revealed that following the 3rd dose of 2 g ascorbic acid a plateau in urinary oxalate excretion was reached (0.6 microgram ml-1 min-1) which was not exceeded despite additional 2-g doses of ascorbic acid. On termination of ascorbic acid administration the oxalate excretion rate remained at this level for a further 6 h and then decreased to prestudy rates. No effect of high-dose ascorbic acid ingestion was found on the daily urinary excretion of creatinine, uric acid, and inorganic phosphate. Calcium excretion was slightly reduced. In comparison to the large amounts of ascorbic acid ingested, the increase in urinary oxalate excretion as measured by isotachophoresis in these healthy male volunteers was very low, and is thus similar to the change in urinary content of oxalate which results from consuming normal diets.

Ascorbic Acid↗
PubMed2002

Indicators of marginal biotin deficiency and repletion in humans: validation of 3-hydroxyisovaleric acid excretion and a leucine challenge.

BACKGROUND: The results of clinical studies have provided evidence that marginal biotin deficiency is more common than was previously thought. A previous study of 10 subjects showed that the urinary excretion of biotin and 3-hydroxyisovaleric acid (3HIA) are early and sensitive indicators of marginal biotin deficiency. OBJECTIVE: Marginal biotin deficiency was experimentally induced and corrected to assess the utility of 3 indicators of biotin status: urinary excretion of biotin and 3HIA and the increase in 3HIA excretion after leucine loading. DESIGN: Eleven healthy adults consumed an egg white diet for 28 d. Blood and 24-h urine samples were collected before the start of the diet and twice weekly thereafter. In 5 subjects, an oral leucine challenge was performed weekly for 4 wk. After depletion, biotin status was restored with a general diet with or without a supplement containing 80 micro g biotin. Urinary excretion of biotin, bisnorbiotin, and biotin sulfoxides was determined by avidin-binding assay after HPLC. Excretion of 3HIA, an indicator of reduced activity of the biotin-dependent enzyme methylcrotonyl-CoA carboxylase (EC 6.4.1.4), was measured by gas chromatography-mass spectrometry. RESULTS: 3HIA excretion increased significantly with time on the egg white diet (P < 0.0001), as did 3HIA excretion in response to the leucine challenge (P < 0.002); the excretion of both biotin and bisnorbiotin decreased significantly with time (P < 0.0001). In most subjects, biotin status returned to normal after 1 wk of a general diet. CONCLUSIONS: Excretion of 3HIA and of biotin are early and sensitive indicators of biotin deficiency. 3HIA excretion after a leucine challenge is at least as sensitive.

Adult↗
PubMed1993

Effect of intravenous calcium infusion on indices of activity of the parathyroid glands and on urinary calcium and sodium excretion in normotensive and hypertensive subjects.

The effect of an intravenous calcium gluconate load (10 mg/kg over 5 min) on plasma ionized calcium concentration, parathyroid hormone (PTH), and the rate of urinary excretion of calcium, sodium, and nephrogenous cyclic adenosine monophosphate (NcAMP) was examined in 26 patients with essential hypertension and 27 age- and sex-matched normotensive subjects. Prior to calcium administration hypertensives had lower plasma ionized calcium concentration (P < .01) and higher PTH levels (P < .001) and excreted more calcium (P < .05) and NcAMP (P < .001) in the urine compared to normotensives. Following calcium infusion, plasma ionized calcium did not differ significantly between the two groups, but PTH levels remained higher in the hypertensive subjects at both 60 min (P < .001), and at 120 min (P = .02) post-load. Post-load values for both urinary calcium excretion and urinary sodium excretion were significantly higher in the hypertensive subjects than in the control group. Both before and after calcium infusion, urinary calcium excretion was positively correlated with urinary sodium excretion in each of the two groups, but for the same level of sodium excretion, hypertensives excreted more calcium in the urine, compared to normotensives, both before (P < .05) and after calcium infusion (P < .001). A positive correlation between basal plasma renin activity (PRA) values and plasma ionized calcium values obtained before (r = 0.42, P = .03) or at 60 min (r = 0.41, P = .03) and 120 min (r = 0.42, P = .03) after calcium infusion existed only in the hypertensive subject group. Post-load urinary sodium excretion values were negatively correlated to basal PRA values in both groups (r = -0.55, P < .01 and r = -0.58, P < .01 for hypertensives and normotensives, respectively), but a similar negative correlation between post-load urinary calcium excretion values and basal PRA values existed only in the hypertensive subject group (r = -0.50, P < .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1975

Urea, citrate and orotate excretion in growing rats fed amino acid-deficient diets.

Male, weanling rats were fed a control purified amino acid diet or the same diet with lysine, phenylalanine, tryptophan, valine, or arginine omitted singly, or both arginine and lysine omitted. Blood urea reached three to four times that of control levels with all deficient diets. Urea excretion increased almost linearly with time during the first 3 days of amino acid deficiency. Rates of urea excretion on day 3 in decreasing order for various deficiencies were as follows: lysine and arginine combined are more than lysine is more than tryptophan equals valine is more that phenylalanine equals arginine. Urinary citrate was 26 and 21.8 times that of control values without arginine and 11.4 and 6.2 times that of control values without lysine on days 2 and 3, respectively. By day 8 citrate excretion had returned to control levels without lysine but not without arginine. Citrate excretion was unchanged with other deficiencies. Orotic acid excretion increased markedly only without arginine and slightly without tryptopahn. A deficiency of arginine and lysine increased urea and citrate excretions to a greater extent than either deficiency alone. Two injections of arginine or homoarginine (0.50 mmole/injection) given at 12-hour intervals to rats fed no lysine and arginine for 3 days decreased citrate excretion immediatedly and on the following day. Urea excretion decreased with injected homoarginine, but not with arginine. Orotic acid excretion increased more than four times on the day of homoarginine injection compared with that of the preceding day. Arginine injection returned orotic acid excretion to nearly control levels within 24 hours. Urea degradation in the gastrointestinal tract was increased in animals fed amino acid-deficient diets.

Amino Acids, Essential↗
PubMed1996

Gut endogenous nitrogen and amino acid excretions in adult domestic cats fed a protein-free diet or an enzymatically hydrolyzed casein-based diet.

Ileal and fecal gut endogenous nitrogen and amino acid excretions in adult domestic cats were determined. Ileal digesta were collected (10 cm of terminal ileum) from the cats fed either a protein-free diet or an enzymatically hydrolyzed casein-based diet (free amino acids and peptides < 10,000 Da) for 1 wk. Chromic oxide was included in each diet as an indigestible marker. The relative contribution of the hindgut to total endogenous gut excretion was investigated in a separate study by feeding cats a protein-free diet with or without added antibiotics for 10 d. Endogenous ileal nitrogen and amino acid nitrogen excretions of (mean +/- SEM 2.4 +/- 0.27 and 1.9 +/- 0.13 mg/g food dry matter intake, respectively, were found for the cats fed the protein-free diet, whereas higher excretions of 3.6 +/- 0.73 (P = 0.12) and 3.6 +/- 0.76 (P = 0.03) mg/g food dry matter intake were obtained in cats fed the enzymatically hydrolyzed casein. Significantly (P < 0.05) higher endogenous ileal amino acid excretions, for the enzymatically hydrolyzed casein-fed cats compared with those fed the protein-free diet, were found for methionine, aspartic acid, serine, glutamic acid, proline, valine and isoleucine, with the differences in excretions of glycine, alanine, leucine and histidine being significant at the 6% level. Most of the endogenous fecal amino acid excretions were unaffected by the inclusion of the antibiotics in the protein-free diet, although bacterial numbers were significantly lower (69%). Antibiotics addition led to significantly higher fecal endogenous excretions of nitrogen, taurine, threonine, serine and histidine but significantly lower excretions of methionine and lysine. Cats, like other simple-stomached mammals, excrete higher amounts of endogenous amino acids at the terminal ileum when the diet contains peptides.

Amino Acids↗
PubMed2005

Urinary excretions of lipocalin-type prostaglandin D2 synthase predict the development of proteinuria and renal injury in OLETF rats.

BACKGROUND: Otsuka Long-Evans Tokushima Fatty (OLETF) rats genetically develop diabetes which is associated with hypertension. In preliminary studies, urinary excretions of L-PGDS (lipocaline-type prostaglandin D synthase) increase before diabetic nephropathy obviously develops, and this may predict progression of renal injury following diabetes. In the present study, we attempted to define whether urinary excretions of L-PGDS behave as the predictor of development of diabetic nephropathy in OLETF rats. METHODS: We investigated alterations of urinary L-PGDS excretions during the establishment of diabetes and assessed the relationship between the L-PGDS excretions and renal function in OLETF rats. Furthermore, we treated OLETF rats with troglitazone and analysed the effects on L-PGDS metabolisms. Urinary L-PGDS was measured by immunoenzyme assay and the occurrence of L-PGDS and its mRNA in the kidney was assessed by immunohistochemistry and a PCR method. RESULTS: Urinary excretions of L-PGDS were significantly higher in OLETF rats than non-diabetic Long-Evans Tokushima Otsuka (LETO) rats. The excretions age-dependently increased in OLETF and this increase appeared to be due to increased glomerular permeability to L-PGDS. Messenger RNA and antigenicity of L-PGDS were demonstrated in renal tissue; however, the de novo synthesis of L-PGDS mRNA seemingly contributed to urinary L-PGDS excretions much less than glomerular filtration. Multiple regression analysis revealed that urinary L-PGDS was determined by urinary protein excretions, and not by high blood pressure per se. Conversely, urinary proteinuria in the established diabetic nephropathy was predicted by urinary L-PGDS excretions in the early stage of diabetes. CONCLUSIONS: Urinary excretions of L-PGDS are likely to reflect the underlying increase in glomerular permeability. This property may be useful to predict forthcoming glomerular damage following diabetes in OLETF rats.

Animals↗
PubMed1997

Relationship of diastolic blood pressure with cyclic GMP excretion among young adults (the CARDIA Study): influence of a family history of hypertension. Coronary Artery Risk Development in Young Adults.

BACKGROUND: Guanosine 3':5'-cyclic monophosphate (cGMP) is the second messenger of nitric oxide and atrial natriuretic factor, and mediates local vasodilatation. These vasodilatory factors are important in blood pressure regulation and possibly in the etiology of hypertension. Urinary cGMP levels among normotensive young adults have not previously been studied. SUBJECTS: A subset of normotensive participants from the CARDIA study (n = 563), aged 23-35 years, was studied. The sample was approximately balanced for sex and race (black/white). METHODS: Twenty-four-hour urinary cGMP levels were measured using an enzyme immunoassay; levels were adjusted for creatinine excretion. The blood pressure, smoking status, and risk factors for hypertension [including a family history of hypertension (FHH), the body mass index, education, alcohol intake, and sodium excretion] were also measured. RESULTS: Women excreted more cGMP than did men, and blacks excreted more cGMP than did whites (both P < 0.0001). Excretion of cGMP was also greater among smokers (P < 0.001) and those with an FHH (P = 0.05), and was related directly and independently to sodium excretion (P < 0.02). The diastolic blood pressure (DBP) was related inversely to the excretion of cGMP among individuals without an FHH (r = -0.36, P < 0.001), but not among individuals with an FHH. In multiple regression analysis, the excretion of cGMP remained related significantly to the DBP and accounted for more variance in DBP than did any other variable among those without an FHH (delta R2 = 0.08, P < 0.001). CONCLUSIONS: Urinary cGMP excretion is related inversely and independently to the DBP among those without an FHH but not among those with an FHH, suggesting that cGMP-related vasodilatation is impaired in those with an FHH. Sex differences in urinary excretion of cGMP are consistent with results from studies showing that estrogen increases the endothelial production of nitric oxide.

Adult↗
PubMed1992

The variability of urinary protein and creatinine excretion in patients with gestational proteinuric hypertension.

OBJECTIVE: To determine the variability of protein excretion in patients with proteinuric hypertension and the accuracy of either a urinary protein/creatinine ratio or a Multistix examination for the estimation of a 24 h protein excretion. DESIGN: An indwelling urinary catheter was placed for 24 h and successive 8 h specimens examined. SETTING: A tertiary referral hospital in Cape Town, South Africa. SUBJECTS: 22 women with significant proteinuria in pregnancy were studied. MAIN OUTCOME MEASURES: The urine volume, protein excretion and creatinine excretion in eight hourly periods were measured. Multistix examination of each specimen was recorded. RESULTS: A large coefficient of variation in urine volume (41%), amount of protein excreted (44%) and the amount of creatinine excreted (22%) in the eight hourly specimens were noted. The protein creatinine ratio did not accurately predict the 24 h protein excretion. The Multistix examination was less accurate with increasing amounts of proteinuria. The amount of creatinine excreted correlated with the volume of urine passed (r = 0.43). CONCLUSION: The analysis of a 24 h specimen or urine for protein excretion remains the best method of monitoring proteinuria in pregnancy. The amount of creatinine excreted in 24 h cannot be used as an index of completeness of collection of the 24 h specimen.

Circadian Rhythm↗
PubMed2004

Mutations in the uromodulin gene decrease urinary excretion of Tamm-Horsfall protein.

BACKGROUND: Mutations in the uromodulin (UMOD) gene that encodes Tamm-Horsfall protein (THP) cause an autosomal-dominant form of chronic renal failure. We have now investigated effects of UMOD gene mutations on protein expression by quantitatively measuring THP excretion. METHODS: THP excretion was determined by enzyme-linked immunosorbent assay (ELISA) of urine collections obtained from 16 related individuals with a 27 bp deletion in the UMOD gene and seven individuals with other UMOD mutations. THP excretion of 22 control subjects (18 genetically related individuals and four spouses in the UMOD deletion family) was also determined. RESULTS: The 16 individuals carrying the deletion mutation excreted 5.8 +/- 6.3 mg THP/g creatinine into their urine. The 18 unaffected relatives from the same family excreted 40.8 +/- 9.7 mg THP/g creatinine (P < 0.0001) and the four spouses excreted 43.9 +/- 25.1 mg THP/g creatinine (P < 0.0001 vs. individuals with the deletion mutation). THP excretion of seven individuals with other UMOD gene mutations was also extremely low (range of 0.14 to 5.9 mg THP/g creatinine). All individuals with UMOD mutations had low THP excretion, irrespective of gender, glomerular filtration rate (GFR), or age. CONCLUSION: These studies quantitatively show that the autosomal-dominant gene mutations responsible for UMOD-associated kidney disease cause a profound reduction of THP excretion. We speculate that this suppression of normal THP excretion reflects deleterious effects of mutated THP within the kidney. Such effects may also play an important role in the pathogenesis of the progressive renal failure observed in patients with UMOD gene mutations.

Adolescent↗
PubMed2002

Urinary excretion of N-methylhistamine as a marker of disease activity in inflammatory bowel disease.

OBJECTIVE: Mast cells are thought to participate in the pathogenesis of inflammatory bowel disease (IBD). In this study, urinary excretion of N-methylhistamine (UMH), a stable metabolite of the mast cell mediator histamine, was evaluated as an indicator of disease activity in patients with IBD. METHODS: Urinary excretion of UMH (microg/mmol creatinine x m2 body surface area) was measured by radioimmunoassay in 55 controls, 56 patients with Crohn's disease, and in 36 patients with ulcerative colitis. Excretion rates were correlated with clinical, serological, and endoscopic disease activity, disease extent, and location. RESULTS: Urinary excretion of UMH was found to be significantly elevated in IBD. Patients with active Crohn's disease (7.1 +/- 4.2, p = 0.002 vs controls) and active ulcerative colitis (8.1 +/- 4.8, p = 0.02 vs controls) had higher rates of UMH excretion than patients in remission (6.3 +/- 3.8 and 5.2 +/- 2.3, respectively) or controls (4.6 +/- 1.9). In Crohn's disease and ulcerative colitis, a significant correlation of UMH excretion with clinical disease activity was obtained (Crohn's Disease Activity Index r2 = 0.58, Clinical Activity Index r2 = 0.57, p < 0.0001). Serologically, orosomucoid showed the best positive correlation with disease activity (Crohn's Disease Activity Index r2 0.80, Clinical Activity Index r2 = 0.86, p < 0.0001), but UMH excretion was found to reflect disease activity more accurately than C-reactive protein (Crohn's Disease Activity Index r2 = 0.46, Clinical Activity Index r2 = 0.42, p < 0.0001). No association between UMH excretion and disease type or localization could be found in Crohn's disease. However, UMH excretion correlated strongly with endoscopic severity of inflammation in Crohn's disease (Crohn's Disease Endoscopic Index of Severity r2 = 0.70, p < 0.0001) or disease extent in ulcerative colitis. CONCLUSIONS: Urinary excretion of the histamine metabolite UMH is enhanced in IBD. It appears to represent an integrative parameter to monitor clinical and endoscopic disease activity in IBD, which appears to be influenced most likely by mediators released from histamine-containing cells, such as intestinal mast cell subtypes.

Adolescent↗
PubMed1998

Increased 24-hour urinary cortisol excretion in patients with post-traumatic stress disorder and patients with major depression, but not in patients with fibromyalgia.

There is now firm evidence that major depression is accompanied by increased baseline activity of the hypothalamic-pituitary-adrenal (HPA) axis, as assessed by means of 24-h urinary cortisol (UC) excretion. Recently, there were some reports that fibromyalgia and post-traumatic stress disorder (PTSD), two disorders which show a significant amplitude of depressive symptoms, are associated with changes in the baseline activity of the HPA axis, such as low 24-h UC excretion. The aim of the present study was to examine 24-h UC excretion in fibromyalgia and PTSD patients compared to normal controls and patients with major depression. In the three patient groups, severity of depressive symptoms was measured by means of the Hamilton Depression Rating Scale (HDRS) score. Severity of fibromyalgia was measured using a dolorimetrically obtained myalgic score, and severity of PTSD was assessed by means of factor analytical scores computed on the items of the Composite International Diagnostic Interview (CIDI), PTSD Module. Patients with PTSD and major depression had significantly higher 24-h UC excretion than normal controls and fibromyalgia patients. At a threshold value of > or = 240 micrograms/24 h, 80% of PTSD patients and 80% of depressed patients had increased 24 h UC excretion with a specificity of 100%. There were no significant differences in 24-h UC excretion either between fibromyalgia patients and normal controls, or between patients with major depression and PTSD patients. In the three patient groups, no significant correlations were found between 24-h UC excretion and the HDRS score. In fibromyalgia, no significant correlations were found between 24-h UC excretion and the myalgic score. In PTSD, no significant correlations were found between 24-h UC excretion and severity of either depression-avoidance or anxiety-arousal symptoms. In conclusion, this study found increased 24-h UC excretion in patients with PTSD comparable to that in patients with major depression, whereas in fibromyalgia no significant changes in 24-h UC were found.

Adult↗
PubMed1986

Renal electrolyte excretion and renin release during calcium and parathormone infusions in conscious rabbits.

Following a random block experimental design in each case, three repeated measurement studies were carried out in three different groups of conscious rabbits, to investigate the renal effects of increasing doses of intravenous calcium chloride (CaCl2) and bovine parathyroid hormone (PTH). In the first study, each rabbit received either CaCl2 (0.15, 0.3, 0.5 or 1.0 mg kg-1 min-1) or vehicle alone (control) for 160 min. In the second study, rabbits were given either PTH (0.15 microgram kg-1 min-1), CaCl2 (1.0 mg kg-1 min-1), PTH plus CaCl2 (0.15 microgram kg-1 min-1 and 1.0 mg kg-1 min-1, respectively) or vehicle alone; PTH was infused for just over 60 min. In the third study, a much smaller dose (0.05 mg kg-1 min-1) of CaCl2 was infused for 100 min. CaCl2 infusion produced a striking fall in fractional excretion of sodium of at least 50% (P less than 0.01), but this was not dose related, being almost maximal at the smaller doses infused. Although this effect was evident in the absence of any changes in total plasma calcium concentration at the lower doses of CaCl2, renal calcium excretion was increased between 2- and 20-fold (P less than 0.01) at all doses infused. Fractional excretion of chloride doubled at the two higher doses of CaCl2 (P less than 0.01), but potassium excretion was unchanged. There were no consistent alterations in mean arterial blood pressure, effective renal plasma flow, glomerular filtration rate or plasma renin activity (PRA); total plasma calcium concentration was consistently elevated only during infusion of the high dose by just under 1 mmol l-1. PTH infusion had no measured effect on fractional excretion of sodium or renal calcium excretion, but doubled fractional potassium excretion (P less than 0.05). Heart rate and PRA increased (P less than 0.01 and less than 0.05, respectively), the latter by 50%, but systemic pressure and renal haemodynamics were not significantly affected. By contrast, PTH infused with CaCl2 produced a 4-fold rise in fractional sodium excretion and although renal calcium excretion remained increased, it was reduced by ca. 80% when compared with renal calcium excretion during infusion of CaCl2 alone. Infusion of PTH alone increased PRA, but when PTH and CaCl2 were infused together, PRA did not change.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1970

Urinary crystalloid excretion in patients with inflammatory bowel disease.

Because of the potential relationship of increased urinary crystalloid excretion and concentration to stone formation, urinary calcium and uric acid excretion patterns were studied prospectively in 65 patients with inflammatory bowel disease and compared with excretion patterns in patients with functional bowel disease (controls) receiving similar dietary prescriptions. Mean 24-hr urinary calcium excretion was higher in both ulcerative colitis (212 mg, p <0.02) and granulomatous bowel disease (168 mg, p = n.s.) than in controls (118 mg). Urinary calcium excretion exceeded 250 mg/24 hr in 11 of 34 patients with inflammatory bowel disease but in none of the controls. Eight of these 34 patients compared with one of 10 controls excreted urine with calcium concentrations greater than 20 mg/100 ml. Mean 24-hr uric acid excretion was slightly higher in granulomatous bowel disease (520 mg) than in ulcerative colitis (450 mg) or functional bowel disease (451 mg). Eight patients with inflammatory bowel disease but no control subject excreted > 700 mg. The mean urinary uric acid concentration was significantly higher in ulcerative colitis (538 mug/ml, p <0.05) and granulomatous bowel disease (558 mug/ml, p <0.02) than in controls (338 mug/ml). The mean morning urine pH was lower (5.5, p <0.01) in ulcerative colitis than in the other groups.These results indicate increased excretion and higher concentration of calcium and uric acid in some patients with inflammatory bowel disease on the usual treatment programmes. Only very long-term prospective studies of such patients can help to document the true contribution of increased crystalloid concentration and excretion to kidney stone formation in inflammatory bowel disease patients.

Adult↗
PubMed2003

Urinary excretion of salicyluric and salicylic acids by non-vegetarians, vegetarians, and patients taking low dose aspirin.

AIM: To compare amounts of salicyluric acid (SU) and salicylic acid (SA) excreted daily in the urine of non-vegetarians and vegetarians not taking salicylate drugs, and patients taking 75 or 150 mg aspirin/day. METHODS: Urine excreted over 24 hours was collected from volunteers in the four groups. The volumes were recorded and the concentrations of SU and SA were determined electrochemically after separation by high performance liquid chromatography. RESULTS: Significantly more SU was excreted daily by vegetarians (median, 11.01; range, 4.98-26.60 micro mol/24 hours) than by non-vegetarians (median, 3.91; range, 0.87-12.23 micro mol/24 hours), although amounts were significantly lower than those excreted by patients taking aspirin. Median amounts of SU excreted by patients taking 75 and 150 mg/day of low dose aspirin were 170.69 (range, 13.15-377.18) micro mol/24 hours and 165.17 (range, 5.61-429.12) micro mol/24 hours, respectively. The amount of SU excreted by patients taking either 75 or 150 mg of aspirin/day was not significantly different. Significantly more SA was excreted by vegetarians (median, 1.19; range, 0.02-3.55 micro mol/24 hours) than by non-vegetarians (median, 0.31; range, 0.01-2.01 micro mol/24 hours). The median amounts of SA excreted by vegetarians and the patients taking aspirin were not significantly different. CONCLUSIONS: More SU and SA is excreted in the urine of vegetarians than in non-vegetarians, consistent with the observation that fruits and vegetables are important sources of dietary salicylates. However, significantly less SU was excreted by vegetarians than patients taking aspirin, indicating that the daily intake of bioavailable salicylates by vegetarians is considerably lower than that supplied by a single 75 or 150 mg dose of aspirin.

Adolescent↗
PubMed1983

Urinary hippuric acid and orthocresol excretion in man during experimental exposure to toluene.

It is not known whether urinary excretion of hippuric acid (HA) or orthocresol (O-Cr) is to be preferred for the biological monitoring of workers with occupational exposure to toluene. To study this, 42 printing trade workers with more than 10 years' exposure to a mixture of organic solvents including toluene (0-20 ppm) and 43 control subjects matched by age, smoking habits, and living accommodation were investigated. Each matched pair was randomised to an experimental exposure of either 100 ppm or 0 ppm toluene for 6.5 hours under controlled conditions in an exposure chamber. Urinary excretion of HA and O-Cr was determined by high pressure liquid chromatography from samples obtained before exposure, during the first three hours, and during the last 3.5 hours of exposure. No difference in HA and O-Cr excretion was found between printing trade workers and controls. The median O-Cr excretion increased 29 times during exposure, whereas the HA excretion increased only five times. Thus only 3% of the O-Cr excretion originated from other sources than toluene whereas the corresponding value for HA was 19%. Standardisation of the concentrations of HA and O-Cr in relation to urinary creatinine reduced the relative variation by 29% and 56% respectively. This was not reduced further by expressing the excretions as average excretion rates based on total volume of urine collected. Background urinary O-Cr excretion was three to four times higher among smokers than non-smokers, probably due to the content of O-Cr in cigarettes. The O-Cr excretion in unexposed smokers was, however, 10 times lower that that of the non-smokers during the end of the experimental exposure to 100 ppm toluene.

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