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In male Wistar rats urinary kallikrein excretion was positively correlated with urinary flow and glomerular filtration rate and negatively with urinary osmolality and with TcH2O. The mechanism of urinary kallikrein excretion is interpreted as a wash-out effect of renal kallikrein. The renal kallikrein regulates the water excretion decreasing the reabsorption of water in the distal nephron.
The excretion of sulfated steroids was investigated in the urine and feces of six boys aged 9 months to 7 years and 10 months who had recessive X-linked ichthyosis. Profiles of urinary total steroids as well as sulfated steroids were normal. Cholesterol sulfate excretion in the urine was not elevated. In the feces 2-20% of total cholesterol was cholesterol sulfate, whereas in the feces of 28 healthy children no cholesterol sulfate was demonstrable. In the 6 patients total cholesterol excretion (500-2,500 mumol/kg feces) was also elevated in comparison with the 28 healthy controls (150-700 mumol/kg feces, mean 365 mumol/kg feces).
Glycation involves both circulating proteins, such as albumin, and structural proteins, such as the components of the glomerular basement membrane. A preferential excretion of glycated albumin (more anionic at physiological pH compared with unmodified plasma albumin) has been reported by some authors, but not by others. We therefore investigated the selectivity index (renal clearance of non-glycated albumin/clearance of glycated albumin) in 25 insulin-dependent diabetic patients with normal urinary albumin excretion and in 19 well-matched control subjects. The selectivity index was significantly higher in diabetic patients than in control subjects: 1.38 +/- 0.05 SEM vs 0.98 +/- 0.02, p less than 0.0001. This result is not consistent with a preferential urinary excretion of glycated albumin, at least in normoalbuminuric uncomplicated insulin-dependent diabetic patients.
The circadian rhythm of the excretion of the catecholamines and some main metabolites is investigated in five normal subjects and two patients with a high excretion. In the normal subjects there are remarkable differences in the amplitudes of the variables. At high catecholamine excretions these differences seem to disappear.
H-EXCRETION is a program written in BASIC language for microcomputers and designed to facilitate the calculation of excretion for acid or base from a tissue into the surrounding media. The program is designed in such a way to allow considerable variability in different experimental parameters. Five examples of calculation of H+ excretion in the urinary bladder of the toad Bufo marinus are presented.
Normal conscious female Sprague-Dawley rats were treated with chlorazanil (3 mg/kg i.p.), and urine was collected for 3 hours. Urine prostaglandin E2-excretion increased from 25 +/- 3 to 271 +/- 32 ng/kg/3 h. The enhancement of urine PGE2-excretion was inhibited by pretreatment with bumetanide (75 mg/kg p.o.). In separate experiments the papillary quantity of PGE2 was determined in freshly homogenized tissue. The basal level (14 +/- 2 ng PGE2/papilla) was increased by chlorazanil to 51 +/- 11 ng PGE2/papilla and 24 +/- 7 ng PGE2/papilla at one and two hours respectively after drug administration. The capacity of chlorazanil to increase medullary PGE2 accumulation was unaffected by bumetanide pretreatment. The results show that bumetanide dissociated the medullary PGE2 level from the excretion of PGE2 in urine, when the former was elevated by chlorazanil.
In calcium lithiasis, pathogenesis inhibitors have a significant role to play which permits raising of the upper metastability limit in the urine, thus reducing the crystallization processes. The aim of this work is to evaluate glycosaminoglycans excretion and concentration in a group of patients with idiopathic calcium lithiasis, and in a control group for detecting possible differences between the 2 groups. Analysis of our results shows that no significant differences exist between the 24-hour average excretion of glycosaminoglycans in normal and stone forming subjects, but there was a significant difference in the mean concentration values between the 2 groups, either as whole or when separately considered with respect to normal or increased uric acid excretion. Particularly interesting was the correlation study between glycosaminoglycans and uric acid which shows a linear relationship with a positive slope in all groups but in stone formers with hyperuricosuria.
BACKGROUND: To better understand the mechanisms of glomerular epithelial cell (GEC) injuries in various diseases, we compared GEC excreted during chemotherapy (antineoplastic drugs) and GEC excreted in renal diseases. METHODS: For 19 patients undergoing chemotherapy (85 courses), 69 patients with IgA nephropathy and 16 patients with Henoch-Schölein purpura nephritis, the number of excreted GEC and GEC casts were counted by an immunofluorescent study. The morphological features of GEC were also studied in an immunofluorescent study combined with Hoechst stain. RESULTS: Glomerular epithelial cells were detected in 78% of the chemotherapy courses and in 94% of the patients with renal diseases. The GEC casts were observed in 2% of chemotherapy courses, while in renal diseases GEC casts were observed in 60% of the patients. Proteinuria (>30 mg/dL) and hematuria were not identified in any of the chemotherapy courses. The morphology and size of GEC were more variable than that in patients with nephropathy. Furthermore, GEC in patients undergoing chemotherapy often showed small nuclei and fragmented nuclei, which were rarely observed in patients with nephropathy. CONCLUSIONS: These results showed that the detachment of podocytes was not directly associated with proteinuria or hematuria. The findings also suggest that GEC are damaged via an apoptotic process by chemotherapy. On the contrary, GEC may be detached through a non-apoptotic process in renal diseases.
The rate of elimination of administered N tau-[14CH3]methyl histidine was used to assess the validity of N tau-methyl histidine excretion as an index of muscle protein breakdown in poultry. Broiler chicks (2-3 and 4-5 weeks old), laying hens, adult quail (Coturnix coturnix japonica), adult cockerels and turkey poults (2-4 weeks old) were tested. All except the turkey poults showed quantitative recoveries of N tau-[14CH3]methyl histidine within 1 week. Turkeys showed a different pattern of N tau-[14CH3]methyl histidine output; the mean total recovery after 14 d was less than 50% of the injected dose. The majority of the label remaining after this time was found in breast muscle. All birds tested excreted N tau-methyl histidine unchanged, although a small amount sometimes appeared as another metabolite. No significant oxidation of N tau-[14CH3]methyl histidine by broiler chicks turkey poults or adult quail was found. The results show that excretion of N tau-methyl histidine is a useful measure of muscle protein breakdown in the domestic fowl and quail but not in turkeys.
The endogenous urinary excretion of the purine derivatives allantoin, uric acid and xanthine plus hypoxanthine were measured in twenty-nine lambs, ten cattle (six steers, one cow and three preruminant calves) and four pigs. The sheep and mature cattle were nourished by intragastric infusion and the calves were given a milk-substitute. The pigs were fed on a purine-free diet. The excretion of total purine derivatives was substantially greater by the cattle, being 514 (SE 20.6) mumol/kg live weight (W)0.75 per d compared with 168 (SE 5.0) mumol/kg W0.75 per d by the sheep and 166 (SE 2.6) mumol/kg W0.75 per d by the pigs. Plasma from normally fed sheep, cows and pigs was incubated with either xanthine or uric acid. Sheep and pig plasma had no xanthine oxidase (EC 1.2.3.2) activity whereas plasma from cattle did. Uricase (EC 1.7.3.3) was not present in plasma of cattle and pigs and appeared to be present in trace amounts only in sheep plasma. It is suggested that the species differences in endogenous purine derivative excretion were probably due to the different profiles of xanthine oxidase activity in tissues and particularly in the blood. This is because a high xanthine oxidase activity would reduce the chance to recycle purines, by increasing the probability of degradation to compounds which could not be salvaged.
In an experiment with 20 15N-labelled growing rats the excretion of amino acids and the excretion of metabolic faecal amino acids were investigated after the feeding of soybean oil meal as sole protein source. A low, yet statistically significant increase of the excretion of amino acids and metabolic faecal amino acids was ascertained in accordance with a growing quota of soybean oil meal in the ration. The true digestibility of amino acids ascertained according to conventional methods is above 90% and, under consideration of the increase of metabolic faecal amino acids, on average increases by 3.5 digestibility units (1.4 to 6.2).
The urinary excretion of dimethylnitrosamine (DMN) was studied in male Sprague-Dawley rats. Animals were given DMN (3, 5, 10, 20, 30 and 50 mg/kg body weight, i.p.) or [3H]DMN (0.1, 1 and 3 mg; 8.7, 1.5 and 0.28 mCi/kg body weight, respectively, i.p.) diluted with sterile 0.9% NaCl. Urine was collected for 24 h after dosing. DMN was quantitated by gas chromatography using a Thermal Energy Analyzer as detector and [3H]DMN by liquid scintillation counting after purification by high pressure liquid chromatography. Multiple regression analysis programs were used to evaluate the fit of the data to a variety of models relating excretion to dose. All models which gave an acceptable fit including a term for dose squared. The models are discussed in terms of the relationship between urinary excretion and blood clearance of DMN.
BACKGROUND: Albumin and alpha1-microglobulin (alpha1M) are absorbed by two specific receptors in tubular epithelial cells. Any cell injury will disturb the reabsorption of these proteins, The increased urinary excretions of albumin or alpha1M could thus serve as a marker of subclinical graft lesions and as an early indicator of chronic allograft dysfunction. METHODS: We measured 24-hour urinary excretions of albumin, alpha1M, and transforming growth factor (TGF)-beta1 at 6 months after transplantation in 79 renal-graft recipients and recorded the changes in 24-hour creatinine clearance an average 51 (range 14-72) posttransplant follow-up months. RESULTS: At 6 months from transplantation, 46 of 79 (58%) patients were normoalbuminuric, 25 (32%) microalbuminuric, and 8 (10%) macroalbuminuric. In normoalbuminuric patients, urinary alpha1M/creatinine ratio was 10 times, and TGF-beta1/creatinine ratio approximately 5 times, higher than in the healthy subjects but lower than in albuminuric patients. In all patients, urinary alpha1M correlated with urinary TGF-beta1 (r=0.508, P<0.001), with albumin (r=0.220, P<0.05), and with the annual changes in 24-hour creatinine clearance (r=-0.273, P<0.05). During follow-up, renal function deteriorated in 20 of 33 (60%) patients with alpha1M/creatinine ratio greater than 5 mg/mmol, but only in 1 of 46 (2%) patients whose ratio was less than 5 mg/mmol (P<0.01), giving the ratio 5 mg/mmol or greater a 95% sensitivity to detect patients with poor long-term outcome. CONCLUSIONS: We show proximal tubular injury, measured by increased urinary alpha1M, to be present even in normoalbuminuric patients and to be associated with increased excretion of TGF-beta1 and with the annual deterioration of glomerular filtration rate. These findings show increased alpha1M/creatinine ratio to be an early and sensitive indicator of poor long-term outcome in renal-transplant patients.
The effect of 5-fluorouracil (5-FU) concentration in the perfusate on the salivary excretion of 5-FU was investigated in the rat mandibular gland perfused with modified Ringer solution containing pilocarpine (10 microM). The saliva to venous-effluent concentration ratio (S/E ratio) of 5-FU increased gradually during the perfusion. The 5-FU concentration in the perfusate ranging from 10 to 200 micrograms/ml caused elevation in the mean value of S/E ratio. This non-linearity suggested that the present perfusion method would be useful to further investigation for the mechanism of salivary excretion of 5-FU, since the tendency of the non-linearity was similar to that in in vivo studies as reported previously. The salivary flow rate declined with time, and the greater mean value of the flow rate was obtained during perfusion with the perfusate containing the lower level of 5-FU. Statistically significant correlation was found between the S/E ratio of 5-FU and salivary flow rate (p less than 0.01). Therefore, in the perfused rat mandibular gland, it was concluded that 5-FU itself had an influence on the salivary excretion of 5-FU via decreasing salivary flow rate. On the other hand, the salivary clearance of 5-FU showed no distinct increase and/or decrease not only with time but also with the change of 5-FU concentration in the perfusate. It seems to result from the cancellation of the increased S/E ratio of 5-FU by the decreased salivary flow rate in perfused rat mandibular gland.
One hundred and one young-adult female Sprague-Dawley rats were acclimatized to metabolic cages for 2 days. After that time 24-hour urine was collected at a constant cooling temperature of 0-4 degrees C. After gel filtration the enzyme activities were determined, and the resulting values were used to calculate 24-hour excretions. The following reference ranges (2.5 and 97.5 percentiles) were determined (in mU/24 h): lactate dehydrogenase 43-181; phosphohexoseisomerase 45-1445; glutathione-S-transferase 1-299; alkaline phosphatase 27-1239; leucine arylamidase 72-377; gamma-glutamyltransferase 1334-9188; arylsulphatase A 59-309; beta-galactosidase 76-305; beta-glucuronidase 20-2756; beta-N-acetyl-D-glucosaminidase 66-491; glutamate dehydrogenase 7-711. There was a significant (though not very high) correlation with diuresis for the lysosomal enzymes beta-N-acetyl-D-glucosaminidase, arylsulphatase A and beta-galactosidase, and for glutamate dehydrogenase, lactate dehydrogenase, phosphohexoseisomerase and alkaline phosphatase. The relation to creatinine excretion was markedly close for the lysosomal enzymes beta-N-acetyl-D-glucosaminidase, arylsulphatase A and beta-galactosidase (r = 0.71-0.83), as well as for alkaline phosphatase, leucine arylamidase and gamma-glutamyltransferase. There was a relatively high correlation between the excretion of beta-N-acetyl-D-glucosaminidase, arylsulphatase A and beta-galactosidase among themselves (r = 0.63-0.81) as well as between leucine arylamidase and gamma-glutamyltransferase (r = 0.75).
Effects of physical loads on the excretion of urinary glycine conjugates, which are commonly used as an index of organic solvent intake, were examined. After physical exertion by Kendo exercise university students for about 2 hours, urinary protein excretion changed from the levels of (-) or (+) before the exercise to (+) to (formula: see text) after the exercise revealed by the test-tape semi-quantitative indication, and the levels of urinary creatinine increased to approximately 1.9 time and initial level. Under the present experimental conditions, the following results were obtained. 1) Statistically no significant change was observed in the levels of urinary hippuric acid, but an increasing trend was recognized. 2) The glycine levels in the urine decreased and the significance was stressed when the values were adjusted with reference to the specific gravity of urine or to the levels of urinary creatinine. 3) The ratio of hippuric acid to the glycine in the urine increased almost twice as high as the initial ratio and the physical load seemed to promote the glycine conjugation. 4) As to the adjusted levels of urinary metabolites, especially due to several organic solvents, values adjusted with reference to the specific gravity of urine and those to the levels of urinary creatinine correlated well in the samples collected before the exertion. But a poor correlation was observed in the samples collected after the exertion. Therefore, a notice should be given when the adjustment of the values with reference to the levels of urinary creatinine, which is widely used in the health administration practice for organic solvent workers to assess the levels of exposure, since the adjusted values were lowered unnecessarily by excess excretion of creatinine after the physical exertion and the tendency would be exaggerated especially under the low level exposure to organic solvent vapours in the work yard.
Most cephalosporin antibiotics are excreted into urine via glomerular filtration and active tubular secretion by renal organic anion transporters. In this study, we investigated the interaction of cephalosporins with rat organic anion transporter rOAT1, mainly expressed at the basolateral membrane of the renal proximal tubules, using Xenopus laevis oocytes, to assess the roles of rOAT1 in renal excretion of cephalosporin antibiotics. The expression of rOAT1 significantly stimulated the uptake of cefazolin, cefotiam and cephalexin into oocytes, but not of cefoperazone. The inhibition constants of these cephalosporins to rOAT1-mediated p-aminohippurate (PAH) uptake were 72 microM for cefazolin, 298 microM for cefoperazone, 718 microM for cefotiam and 6 mM for cephalexin. Eadie-Hofstee plot analysis revealed that cefoperazone as well as cefotiam inhibited rOAT1-mediated PAH uptake competitively. These results suggest that rOAT1 mediates basolateral uptake of cephalosporin antibiotics in the renal tubules. Furthermore, it is suggested that a minor contribution of the kidney to cefoperazone excretion could be related to the finding that cefoperazone is a poor substrate of rOAT1.
The absorption and endogenous excretion of iron in man was studied by monitoring the fecal excretion of a stable iron isotope (58Fe). The study was carried out for 12 healthy volunteers who were divided into two groups. Group I received 58Fe-labeled ferric ammonium citrate (III) (58FeAC) equivalent to 6 mg of iron as a control, and group II received a combination of 500 mg of vitamin C and 58FeAC. A new formula was used to calculate the 58Fe absorption ratio reflecting the pool of iron in the intestinal cells, and the ratio was compared with that obtained from Janghorbani's formula, which has been used as one of the common methods. As a result, the 58Fe absorption ratio in group II was statistically significantly higher than that of group I (34.4 +/- 6.1% vs. 15.0 +/- 5.5%, M +/- SD) using Janghorbani's formula. The similar absorption ratio (34.1 +/- 6.0% vs. 14.8 +/- 5.5%) was also obtained by our new formula. Our results confirmed the previous findings that the availability of iron is stimulated by the supplementation of vitamin C. Both formulae agreed in the absorption of iron, indicating that the endogenous excretion of iron (caused by the desquamated cells) in the intestine does not disguise the iron absorption.