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PubMed1997

Urinary adenosine excretion in patients receiving amphotericin B.

BACKGROUND: Intravenous amphotericin B (AMB) administration in animals causes renal vasoconstriction, ischemia, and oliguria that may result in irreversible renal injury; the mechanism of AMB nephrotoxicity may be similar in human beings. Adenosine is excreted in urine by the ischemic kidney. We hypothesized that adenosine excretion and oliguria would be a marker for patients who later would manifest AMB-associated renal insufficiency and that pre-AMB saline administration (which ameliorates AMB nephrotoxicity) would negate the change in adenosine excretion and urine output. METHODS: Twenty hospitalized patients being treated at the direction of their attending physician and who were receiving AMB (15 to 75 mg intravenously) had urine collected for 1 hour before and for 2 hours during AMB infusion. Eleven patients received normal saline solution (500 ml intravenously) before the AMB infusion; the other nine formed the comparator group. An aliquot of each urine collection was precipitated with perchloric acid to remove protein and cellular elements and centrifuged, and the supernatant was assayed for adenosine by using high-pressure liquid chromatography. RESULTS: Infusion of AMB was associated with a decrease in mean urine output both in patients who received saline solution (245 before versus 149 ml/hr during AMB infusion, p = 0.04) and in patients in comparator group (139 versus 89 ml/hr, p = 0.027). The mean urinary adenosine excretion was unchanged in the saline-loaded group (0.1354 before versus 0.1255 mmol/hr during drug infusion, p = 0.25) and was decreased in the comparator group (0.2276 versus 0.1127 mmol/hr, p = 0.01). Development of renal insufficiency did not correlate with the change in urine output or adenosine excretion. CONCLUSIONS: AMB infusion in human beings results in decreased urine output and decreased adenosine excretion. The latter effect is prevented by a pre-AMB saline load. The changes in urine output and adenosine excretion are not predictive of the development of renal insufficiency.

Adenosine↗
PubMed1984

Hydroxyproline excretion in urine of smokers and passive smokers.

Urinary hydroxyproline excretion was investigated in 125 male cigarette smokers, 194 male pipe and/or cigar smokers, and 24 male nonsmokers. Hydroxyproline excretion was calculated either as hydroxyproline/creatinine ratio or as body surface-standardized amounts of hydroxyproline excreted in urine sampled during day, during night, or over 24 hr. The association of hydroxyproline excretion with smoke uptake variables such as daily cigarette consumption, carboxyhemoglobin, serum cotinine, and nicotine in urine and with self-reported passive smoking exposure in nonsmokers was analyzed. The hydroxyproline/creatinine ratio was found to be unsuitable as a measure of hydroxyproline excretion since creatinine urine concentrations correlate inversely with smoke uptake in cigarette and pipe/cigar smokers. The amount of hydroxyproline excreted in 24-hr urine and standardized for body surface was not significantly associated with smoke uptake in pipe/cigar smokers or exposure to passive smoking in nonsmokers. In cigarette smokers the situation appeared similar, although the results were less clear-cut. The data do not favor the premise that measuring urinary hydroxyproline excretion is an accurate method of investigating a lung-damaging effect of smoking, passive smoking, or air pollution.

Adult↗
PubMed1991

Relation between renal and hepatic excretion of drugs. XIV. Elimination of ioglycamic acid after nephrectomy, bile duct ligation, and after treatment with hormones or xenobiotics in young and adult rats.

Ioglycamic acid (IGA) is effectively eliminated in young and adult rats via urine and bile. After administration of low doses hepatic excretion dominates whereas following high supply renal elimination surpasses biliary excretion. Hepatic transport of IGA is active, indicated by the occurrence of a transport maximum in vivo and by a distinct accumulation of this drug within liver slices in vitro. Renal removal of IGA is preferentially caused by glomerular filtration. A tubular reabsorption obviously does not occur because forced diuresis (mannitol, furosemide) does not increase renal excretion of this substance. As calculated from our clearance data and as a result of accumulation experiments in vitro on renal cortical slices the active tubular secretion of this organic anion can be excluded. In principle there are no qualitative changes in IGA elimination between the 20th and 55th day of life, but active hepatic transport of the drug is significantly lower in young, immature rats. After bile duct ligation, renal excretion of IGA increases distinctly in both age groups, whereas in adult rats bilateral nephrectomy (NX) is followed by a significant decrease in its hepatic excretion in dependence on time after kidney removal. In young rats NX is without consequences on hepatic excretion of IGA. It is possible to stimulate renal and/or hepatic excretion of IGA by repeated administration of T3, dexamethasone, or phenobarbital. The effect of stimulation is different in kidney and liver and depends on age, too.

Animals↗
PubMed1993

The association of non-insulin-dependent diabetes mellitus and hypertension with urinary excretion of albumin and transferrin.

Abnormal urinary excretion of albumin is a nonspecific sign of nephropathy, commonly occurring in persons with hypertension as well as diabetes. Transferrin, rather than albumin, is more readily excreted by the kidney in those with diabetes compared with those with hypertension alone. One hundred eighty non-insulin-dependent diabetic mellitus patients were age, race, and sex matched to 90 nondiabetic control subjects who had mild to moderate hypertension. Overnight urine collections were analyzed by immunoturbidity for albumin and transferrin. The average duration of hypertension was 11 years among controls. Mean blood pressures were 134/79 mm Hg for diabetic subjects and 145/87 mm Hg for controls (P < 0.001). Diabetic patients had higher mean excretion rates of albumin (128 micrograms/min v 49 micrograms/min; P = 0.04) and transferrin (7.3 micrograms/min v 0.9 microgram/min; P = 0.0001) and higher excretion ratios of albumin (0.179 g/g creatinine v 0.069 g/g creatinine; P = 0.02) and transferrin (0.0065 g/g creatinine v 0.0013 g/g creatinine; P < 0.001) than hypertensive controls. Ratios of transferrin to albumin excretion for those with diabetes and hypertension greatly exceeded expected ratios for those with hypertension or diabetes alone if the effects of these disorders were additive. While diabetic patients were twice as likely as controls to have abnormal albumin excretion ratios (P = 0.01), they were three times as likely to have elevated transferrin excretion ratios (P = 0.0001), even though the diabetic group was half as likely as the controls to have systolic blood pressure > or = 160 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1997

A new classification for renal defects in net acid excretion.

The traditional classification of the group of disorders called renal tubular acidosis (RTA) into proximal and distal subclasses is based on which nephron segment is thought to have an abnormal function. Nevertheless, such a distinction may not be correct and also does not characterize the pathophysiology of the renal acidosis in each patient. In this article, we propose an alternative classification, one that is based on the component of net acid excretion that is abnormal. We also suggest expanding the definition of net acid excretion to include a term that describes the renal handling of metabolizable organic anions because their loss in the urine represents the loss of "potential bicarbonate." Because a low rate of excretion of ammonium (NH4+) is present in patients with both distal and isolated proximal RTA, our initial clinical step in patients with hyperchloremic metabolic acidosis (HCMA) is to evaluate the rate of excretion of NH4+. The basis for a low rate of excretion of NH4+ is shown by examining the urine pH. If the urine pH is low, further studies are performed to determine why the availability of NH3 is low; if the urine pH is high, further investigations are initiated to examine if the defect in H+ secretion involves the proximal or the distal nephron. Conversely, if the rate of excretion of NH4+ is high in a patient with HCMA, a component of the degree of acidosis could be attributable to a high rate of excretion of metabolizable organic anions. Case examples are provided to illustrate the approach and its implications for future molecular studies.

Acidosis, Renal Tubular↗
PubMed1998

Effects of experimental salt depletion on urinary prostanoid excretions in normal women.

The effects of moderate salt depletion on urinary excretions of prostanoids (PG)E2, 6-keto-PGF1alpha (6KPGF) and thromboxane (TX)B2 have been investigated in healthy women (SD group, n = 14). Salt depletion was obtained by combining a low sodium chloride dietary intake (< 60 mmol per day) with natriuretic and potassium sparing treatment. At the end of the treatment, the cumulative sodium deficit was 438 +/- 42 mmol (mean +/- SEM). Plasma renin activity (PRA) and urinary aldosterone excretion were determined in basal conditions. Renal functional exploration was performed during hypotonic polyuria (by oral water load) and subsequent moderate antidiuresis (by low dose infusion of an antidiuretic hormone analogue). In both phases, renal function was estimated by the clearance (cl.) method and the urinary concentrations of PGE2, 6KPGF and TXB2 by RIA method. The control group was composed of 20 healthy women in normal sodium and potassium balance (N group). Salt depletion was effective in increasing the basal values of plasma renin activity (PRA) and urinary aldosterone excretion. Moreover, it was effective in inducing the following during polyuria: (a) a depression of the diuretic response to water load in presence of a reduction in plasma osmolality; (b) a reduction in creatinine cl. in the absence of significant changes in mean arterial pressure; (c) an increase in the fractional reabsorption of sodium and chloride, in particular at the level of the diluting segments. Both in polyuria and in antidiuresis, the excretions of 6KPGF and TXB2 were higher in the SD vs. N group, while the excretion of PGE2 was not significantly different. In SD and N pooled groups, significant positive correlations were shown between basal PRA and urinary excretions during polyuria of 6KGPF and TXB2, (but not of PGE2) as well as between the excretions of the two metabolites. In conclusion, functionally effective salt depletion induces in healthy women a stimulation of renal synthesis of both prostacyclin and thromboxane. The excretory data do not give evidence of a similar effect on PGE2 synthesis.

6-Ketoprostaglandin F1 alpha↗
PubMed1999

Increased urinary excretion of 8-oxo-2'-deoxyguanosine, a biomarker of oxidative DNA damage, in urban bus drivers.

Oxidative damage to DNA could be involved in the increased risk of cancer associated with exposure to polluted urban air, which contains a number of oxidants. CYP1A2 is induced by and metabolizes polyaromatic hydrocarbons (PAH) and aromatic amines and could modify effects of exposure to ambient air pollution. Similarly, DNA repair may be influenced by occupational and other exposures as well as modify the effect of DNA damaging agents. As part of a large investigation of the genotoxic burden to diesel exposed workers in transport sectors we studied oxidative DNA damage in 57 non-smoking bus drivers from the greater Copenhagen area. The drivers were studied on a workday and on a day off work. Comparisons were made between drivers from the central (n=30) and rural/suburban (n=27) areas of Copenhagen. The rate of oxidative DNA damage was estimated from 24 h urinary excretion of 8-oxo-2'-deoxyguanosine (8-oxodG), a repair product of the highly mutagenic oxidation of guanine in DNA or the cellular pool of GTP. CYP1A2 activity was estimated from the urinary excretion of metabolites of dietary caffeine. The DNA repair was estimated by unscheduled DNA synthesis (UDS) in mononuclear cells isolated on the workday. Repeated measures ANOVA and multifactorial ANCOVA with CYP1A2 activity, age and UDS as covariates were used for statistical evaluation. On the workday, the 8-oxodG excretion was 190+/-108 and 146+/-89 pmol/kg 24 h in the bus drivers from central and the suburban/rural areas Copenhagen, respectively (p<0.05). The 8-oxodG excretion was not significantly different between the workday and the day off. CYP1A2 activity was not affected by driving area but was correlated with the 8-oxodG excretion on the workday (r=0.53; p<0.05). UDS was not significantly affected by driving area or correlated with the 8-oxodG excretion. The increased excretion of 8-oxodG in bus drivers from central Copenhagen as compared with drivers from rural/suburban greater Copenhagen suggests that exposure to ambient air pollution causes oxidative damage to DNA. This effect may be modified by the activity of CYP1A2 or a coregulated enzyme.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1995

Urinary excretion of type I collagen crosslinked N-telopeptides in healthy Japanese adults: age- and sex-related changes and reference limits.

A new immunoassay for measuring urinary excretion of type I collagen crosslinked N-telopeptides (NTx) has been reported to be a specific and sensitive method for assessing bone resorption. We have studied factors affecting biological variations in urinary NTx excretion in a population of 452 healthy Japanese adults, comprising 238 men and 214 women, 20-79 years of age. Urinary NTx excretion increased significantly with age in women (> or = 25 years of age) (r = 0.55, p < 0.0001) and modestly correlated with lumbar bone mineral density (L-BMD) in both sexes (> or = 25 years of age) (r = 0.31, p < 0.0001 for men; r = 0.50, p < 0.0001 for women). Urinary NTx levels in women were significantly higher than in the corresponding male age groups after the fifth decade (p < 0.0001). None of the anthropometric variables (weight, height, and body mass index) showed a linear effect on the urinary NTx excretion independent of age and L-BMD. In women, menopause was reflected by a twofold increase in urinary NTx excretion, from a mean of 28-59 pmol bone collagen equivalents (BCE)/mumol creatinine, and this menopause-related increase persisted for the entire postmenopausal period. In postmenopausal women, the interindividual variations of urinary NTx excretion were much more marked than in men and in premenopausal women. Moreover, in the subgroups of pre- and postmenopausal women, urinary NTx excretion correlated with neither age nor L-BMD. These data show that the major biological factor that modifies urinary NTx level is menopause and suggest that the bone turnover rates in the elderly women are increased, on average, irrespective of bone mineral density.

Absorptiometry, Photon↗
PubMed1975

The effect of antibiotic therapy on the faecal excretion of Salmonella typhimurium by experimentally infected chickens.

Chickens in groups of 40 were infected orally with a nalidixic acid-resistant mutant of Salmonella typhimurium and then fed continuously on diets containing ampicillin, chloramphenicol, furazolidone, neomycin, oxytetracycline, polymixin, spectinomycin, streptomycin or a mixture of trimethoprim and sulphadiazine. The amount of S. typhimurium excreted in their faeces was estimated at intervals by culture on brilliant green agar containing sodium nalidixate, both direct and after enrichment in selenite broth; the amount of Escherichia coli excreted was estimated by culture on MacConkey agar. The feeding of diets containing 500 mg./kg. of ampicillin, furazolidone, neomycin, polymixin, spectinomycin or streptomycin or 100 mg./kg. of trimethoprim and 500 mg./kg. of sulphadiazine for 46 days reduced to a varying degree the amount of S. typhimurium and E. coli excreted, the greatest reduction in S. typhimurium being brought about by the last treatment. The effect was less obvious when the concentration of the antibiotics in the food was decreased fivefold. An important reason for the very limited effect of some of the antibiotics was the emergence of antibiotic-resistant populations of S. typhimurium and E. coli. High concentrations of antibiotic-resistant organisms also arose in the faeces of the chickens fed diets containing tetracyclines and chloramphenicol, treatments which had no apparent effect on the amount of S. typhimurium and E. coli excreted. Much of the antibiotic resistance encountered was determined by R factors, a particular R factor usually being found in the E. coli populations of individual chickens before it was found in their S. typhimurium populations. No S. typhimurium or E. coli were isolated that possessed R factors determining resistance to polymixin, furazolidone or trimethoprim. No S. typhimurium or E. coli were isolated that were polymixin-resistant and no S. typhimurium that were furazolidone-resistant. The few trimethoprim-resistant S. typhimurium isolated were thymine-dependent. The feeding of diets containing the higher concentrations of trimethoprim/sulphadiazine, neomycin, furazolidone or ampicillin for 9 days reduced the amount of S. typhimurium excreted. After the withdrawal of these diets, the amount of S. typhimurium excreted increased to the numbers found in chickens given ordinary diets throughout; the chickens that had been given trimethoprim/sulphadiazine or furazolidone did not remain faecal excreters of S. typhimurium longer than the chickens that had been given ordinary diets. Similar results were obtained with trimethoprim/sulphadiazine when the start of the 9-day treatment period was delayed for an extra 9 days or when it was extended to 18 days.

Animal Feed↗
PubMed1990

Reduction in faecal excretion of Salmonella typhimurium strain F98 in chickens vaccinated with live and killed S. typhimurium organisms.

Chickens given orally at 4 days of age a smooth spectinomycin resistant mutant (Spcr) of Salmonella typhimurium strain F98 excreted the organism in their faeces for approximately 4 weeks. Following oral administration of a nalidixic acid resistant (Nalr) mutant of the same strain 4 weeks later when the chickens had virtually cleared themselves of the first infection, these chickens excreted far fewer salmonella organisms and for a shorter time than did a previously uninfected control group of chickens which were infected at the same time with the Nalr mutant. Chickens inoculated intramuscularly at 4 days developed a similar immunity to challenge and also excreted the immunizing strain in their faeces. In contrast intramuscular inoculation or incorporation into the food of formalin-killed S. typhimurium organisms had little lasting effect on the faecal excretion of the challenge strain. Two attenuated mutants of strain F98 Nalr were produced: one was a rough strain produced by lytic bacteriophage and the other was an aro A auxotrophic mutant which had been cured of the 85 kilobase-pair virulence-associated plasmid. These mutants were avirulent for chickens, mice, calves and man and when ingested by human volunteers did not persist in the faeces. When inoculated intramuscularly into chickens they produced an early reduction in faecal excretion of the challenge strain (Spcr) which was not maintained. Oral administration of both strains produced reductions in faecal excretion of the challenge strain. This was much more noticeable with the rough strain which was itself excreted for a much longer period than the parent strain.

Agglutination Tests↗
PubMed1999

Excretion of (14)C-fumonisin B(1), (14)C-hydrolyzed fumonisin B(1), and (14)C-fumonisin B(1)-fructose in rats.

14C-Fumonisin B(1) (FB(1)) was produced by Fusarium proliferatum M-5991 in modified Myro liquid medium and purified to >95% purity with a specific activity of 1.7 mCi/mmol. Nine male and nine female F344/N rats were each dosed by gavage with 0.69 micromol of (14)C-FB(1), (14)C-hydrolyzed FB(1), or (14)C-FB(1)-fructose/kg body weight. Urinary excretion of (14)C-FB(1) and (14)C-FB(1)-fructose was 0.5% and 4.4% of the total dose, respectively, and was similar between male and female rats. Urinary excretion of (14)C-hydrolyzed HFB(1) was significantly greater (P > 0.05) in female rats as compared with male rats (17.3% vs 12.8% of the total dose, respectively). There were no significant (P > 0.05) differences in biliary excretion of the three fumonisin compounds with a mean of 1. 4% of the dose excreted at 4 h after dosing. Lesser amounts continued to be excreted up to 9.25 h after dosing. Although biliary excretion of the (14)C-FB(1), (14)C-hydrolyzed FB(1), and (14)C-FB(1)-fructose was similar, increased urinary excretion of the (14)C-hydrolyzed FB(1) as compared to (14)C-FB(1) and (14)C-FB(1)-fructose indicated a greater absorption of the hydrolyzed form.

Animals↗
PubMed1998

Effects of organic anions and bile acid conjugates on biliary excretion of pravastatin in the rat.

PURPOSE: Biliary organic anion excretion is mediated by an ATP-dependent primary active transporter, a so-called canalicular multispecific organic anion transporter (cMOAT). As there appear to be many canalicular organic anion transports, we examined the effects of various organic anions and bile acid conjugates on the biliary excretion of pravastatin in rats. METHODS: [14C]pravastatin was intravenously injected into rats with bile drainage in the presence and absence of the continuous infusion of organic anions and bile acids, and radioactivity of its biliary excretion was studied. RESULTS: Biliary excretion of [14C]pravastatin was markedly inhibited by sulfobromophthalein-glutathione, taurolithocholate-3-sulfate, ursodeoxycholate-3, 7-sulfate, and ursodeoxycholate-3-O-glucuronide. In contrast, dibromosulfophthalein only slightly inhibited biliary pravastatin excretion, and cefpiramide did not affect biliary pravastatin excretion. CONCLUSIONS: These findings further support the multiplicity of canalicular organic anion transport, and pravastatin is considered to be excreted through a canalicular transporter which is absent in EHBR in addition to through cMOAT.

Animals↗
PubMed1996

Biliary excretion of glycyrrhizin in rats: kinetic basis for multiplicity in bile canalicular transport of organic anions.

PURPOSE: To examine the presence of multiplicity for the biliary excretion of xenobiotic conjugates, we studied the disposition of glycyrrhizin (GR), which has glucuronide within its molecular structure and has the ability to inhibit the biliary excretion of liquiritigenin (LG) glucuronides. METHODS: GR was administered intravenously as a bolus to Sprague-Dawley (SD) rats which received an i.v. infusion of inhibitors (dibromosulfophthalein (DBSP) and indocyanine green (ICG)) at their transport maximum rates. Biliary excretion of GR was also examined in Eisai hyperbilirubinemic rats (EHBR), which have a hereditary defect in the canalicular transport system of several organic anions. RESULTS: Infusion of ICG did not affect the biliary excretion of GR, whereas infusion of DBSP reduced it significantly. The plasma concentration of GR was increased by DBSP but not by ICG. In EHBR, the biliary excretion of GR was severely impaired, resulting in an increase in the plasma concentration of GR. CONCLUSIONS: These findings suggest (1) that the biliary excretion of GR is mediated by the system which is shared by DBSP and LG glucuronides but not by ICG and (2) that this system is hereditarily defective in EHBR. Together with our previous findings, the multiplicity for the biliary excretion of organic anions is shown.

Animals↗
PubMed1975

Effects of dietary protein restriction and glucocorticoid administration on urea excretion in rats.

Rats were sampled for clearance studies under anesthesia after 0, 2, 4, 7 and 14 days of dietary protein restriction. Mean fractional urea excretion decreased between day 2 and day 7 of protein restriction after a two-day lag in response. Seven-day administration of dexamethasone in protein-restricted rats caused a significant increase in mean fractional urea excretion. Adrenalectomized rats fed a normal diet had fractional urea excretion values resembling those in protein-restricted rats. Chronic administration of dexamethasone in adrenalectomized rats caused a consistent increase in fractional urea excretion. Fractional urea excretion values were no lower in protein-restricted adrenalectomized rats fed a normal diet. The mean plasma corticosterone concentration (measured 6 to 8 PM) was decreased in rats fed a low protein diet relative to rats fed a high protein diet. The results suggest that glucocorticoids may play a role in the tubular regulation of urea excretion either by a direct effect on the renal tubule or through some intermediate factor. A mediating role of glomerular filtration rate in glucocorticoid-induced changes of fractional urea excretion could not be ruled out, however.

Adrenalectomy↗
PubMed1980

Adaptive change in ammonia excretion in renal insufficiency.

Experiments were performed to study the mechanism of the compensatory increase in the excretion of metabolic acid by residual nephrons after reduction in renal mass. Despite a decrease in nephron population to 20% of control, total excretion of acid remained similar to pair-fed controls due to an increase in nephron excretion from 5.4 +/- 0.5 in controls to 22.3 +/- 1.9 nEq/24 hr (P < 0.25), including a threefold rise in ammonia excretion and a ninefold increase in excretion of titratable acid. Further studies showed that the in vivo production of ammonia by residual nephrons paralleled, in general, the nephron excretion rate, and increased from the control value of 0.23 +/- 0.02 to 0.54 +/- 0.09 ng/min (P < 0.05). Because the production rate of ammonia per milligram of DNA was not increased in experimental animals above control and because changes were not found in enzymes and substrates associated with increased ammoniagenesis in the rat, these data suggest that formation of additional ammonia-producing cells, due to hyperplasia, plays a role in the compensatory increase in ammonia excretion by residual nephrons. During acute acidosis, cellular ammonia production rose in a parallel manner in control and experimental kidneys, indicating that the capacity to form ammonia is not impaired in chronic renal insufficiency.

Acidosis↗
PubMed1981

Renal net acid excretion in the adrenalectomized rat.

Although adrenalectomy is usually associated with an impairment of ammonium and/or titratable acid excretion by the kidney, it is uncertain whether rates of renal net acid excretion are also reduced. Further, it is unclear whether the absence of the adrenal gland itself or other factors of adrenal insufficiency mediate such changes in renal acidification parameters. For example, dramatic increases in ammonium excretion can accompany correction of the hyperkalemia seen in adrenal insufficiency. There is also evidence that reduced rates of acid excretion can result from changes in food intake, urine flow rate, urine pH or distal sodium delivery rates. With these considerations in mind, we undertook studies to isolate the chronic effects of adrenalectomy on renal net acid excretion rates in the unanaesthetized rat. To avoid supranormal potassium stores, we gave the adrenalectomized animals potassium-restricted diets. In balance studies, urine flow rates, urine pH, food intake, and distal sodium delivery rates were all successfully controlled for 13 days by pair feeding and by appropriately changing the sodium and potassium contents of diets. Adrenalectomized rats excreted less net acid than did control animals with or without ammonium chloride loading. Further, the severe metabolic acidosis associated with ammonium chloride loading was clearly mitigated by steroid replacement. Accordingly, we conclude that the adrenal gland is essential for normal renal net acid excretion.

Acid-Base Equilibrium↗
PubMed1991

Elevated urinary excretion of the C5b-9 complex in membranous nephropathy.

In experimental membranous nephropathy, antibody binding to glomerular epithelial cell membrane antigens results in complement activation and formation of complement C5b-9 membrane attack complexes in glomeruli. During active disease, the C5b-9 complexes are shed into the urine. To test the hypothesis that a similar mechanism might be operative in human membranous nephropathy, we measured urinary excretion of C5b-9 and C5 in 146 proteinuric patients with biopsy-proven glomerular diseases or diabetes mellitus. Urinary excretion of C5b-9 relative to C5 excretion was higher in 40 patients with membranous nephropathy than in 106 patients with proteinuria due to non-membranous glomerulonephritis when analyzed by covariance analysis (P less than 0.0002). Urinary C5b-9 excretion was higher in membranous nephropathy than in membranoproliferative glomerulonephritis (N = 13, P less than 0.05), minimal change-focal sclerosis (N = 33, P less than 0.001), mesangial proliferative glomerulonephritis (N = 9, P less than 0.02) and IgA nephropathy (N = 7, P less than 0.025). Urinary C5b-9 excretion was also higher in patients with lupus nephritis (N = 18, P less than 0.02) compared to those with non-membranous glomerulonephritis. The lupus patients with the highest excretion had clinical or pathological features of membranous nephropathy. Nine patients with membranous nephropathy and elevated urinary C5b-9 excretion had a shorter duration of disease (P less than 0.05), lower serum creatinine levels (P less than 0.05) and more proteinuria (P less than 0.02) than the 31 membranous nephropathy patients with normal values.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2002

Sirolimus/cyclosporine/tacrolimus interactions on bile flow and biliary excretion of immunosuppressants in a subchronic bile fistula rat model.

The new immunosuppressive agent sirolimus generally is combined in transplant patients with cyclosporine and tacrolimus which both exhibit cholestatic effects. Nothing is known about possible cholestatic effects of these combinations which might be important for biliary excretion of endogenous compounds as well as of immunosuppressants. Rats were daily treated with sirolimus (1 mg kg(-1) p.o.), cyclosporine (10 mg kg(-1) i.p.), tacrolimus (1 mg kg(-1) i.p.), or a combination of sirolimus with cyclosporine or tacrolimus. After 14 days a bile fistula was installed to investigate the effects of the immunosuppressants and their combinations on bile flow and on biliary excretion of bile salts, cholesterol, and immunosuppressants. Cyclosporine as well as tacrolimus reduced bile flow (-22%; -18%), biliary excretion of bile salts (-15%;-36%) and cholesterol (-15%; -47%). Sirolimus decreased bile flow by 10%, but had no effect on cholesterol or bile salt excretion. Combination of sirolimus/cyclosporine decreased bile flow and biliary bile salt excretion to the same extent as cyclosporine alone, but led to a 2 fold increase of biliary cholesterol excretion. Combination of sirolimus/tacrolimus reduced bile flow only by 7.5% and did not change biliary bile salt and cholesterol excretion. Sirolimus enhanced blood concentrations of cyclosporine (+40%) and tacrolimus (+57%). Sirolimus blood concentration was increased by cyclosporine (+400%), but was not affected by tacrolimus. We conclude that a combination of sirolimus/tacrolimus could be the better alternative to the cotreatment of sirolimus/cyclosporine in cholestatic patients and in those facing difficulties in reaching therapeutic ranges of sirolimus blood concentration.

Animals↗