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PubMed1998

Urinary apolipoprotein (a) excretion in patients with proteinuria.

Increased plasma lipoprotein (a) (Lp(a)) levels are strongly associated with premature cardiovascular disease and stroke. Recently we, as well as other groups, found that apolipoprotein (a) (apo(a)) fragments appear in the urine of healthy individuals, and that renal transplant patients with impaired renal function excrete fewer apo(a) fragments into their urine compared with controls. As the excretion mode of apo(a) is presently unknown, we determined plasma Lp(a) levels and urinary apo(a) excretion in relation to kidney function in 58 proteinuric patients and 58 healthy controls. For the first time, urinary apo(a) excretion was related to apo(a) isoforms. Plasma Lp(a) values were higher in the proteinuric patients compared with the controls, independent of their renal function. The patients with low-molecular-weight apo(a) isoforms had higher Lp(a) plasma levels, whereas the patients with high-molecular-weight apo(a) isoforms had lower Lp(a) plasma levels. Urinary apo(a) showed a very similar pattern to that of plasma Lp(a), being significantly higher in patients with low-molecular-weight isoforms as compared with patients with high-molecular-weight isoforms. Urinary apo(a) excretion was significantly decreased in the patient group when compared with healthy controls. There was a close correlation (P < 0.001) between the plasma Lp(a) and urinary apo(a) excretion in both the patient group and the control group. Urinary apo(a) excretion did not correlate with protein excretion, creatinine clearance or plasma creatinine levels. We conclude that urinary apo(a) excretion correlates with plasma Lp(a) and Lp(a) isoforms, and that proteinuric patients excrete significantly less apo(a) into their urine than healthy controls, a factor that might contribute to increased plasma Lp(a) levels in these patients.

Adult↗
PubMed1999

Acute effects of acetaminophen on renal function and urinary excretion of some proteins and enzymes in patients with kidney disease.

The acute effects of acetaminophen, a commonly used as analgesic drug, upon the urinary excretion of some proteins and enzymes as markers of kidney damage, was investigated. Patients with chronic glomerulonephritis (GN) and Balkan endemic nephropathy (BEN), having kidney vulnerable to toxic drugs, were enrolled in the study. Timed urine specimens were collected: before drug administration, and in 3-hour periods for 24 hours after an oral dose of 2 g of acetaminophen. Urinary excretion of albumin before acetaminophen treatment was significantly higher in patients with GN and BEN than in healthy adults, however, beta 2-microglobulin excretion was increased in BEN patients only. Urinary excretion of creatinine markedly increased immediately after acetaminophen ingestion. Urinary excretion of total protein and albumin was not changed after acetaminophen administration. However, acetaminophen treatment produced a significant increase in beta 2-microglobulin excretion in patient with BEN and GN, and in clinically healthy members of nephropathic families. Excretion of aminopeptidase N (APN) activity before acetaminophen treatment was significantly higher in patients with GN, however, NAGA excretion was higher in both GN and BEN patients than in healthy controls. After acetaminophen administration urinary excretion of APN, dipeptidylpeptidase IV (DPP IV), gamma-glutamyltranspeptidase (GGT) and N-acetyl-beta-D-glucosaminidase (NAGA) did not increase significantly in any group studied. This study has shown that urinary excretion of APN, DPP IV, NAGA and GGT, as markers of kidney brush border and lysosomal damage, did not change after 2 g of acetaminophen taken orally. beta 2-microglobulin was a marker of acute acetaminophen nephrotoxicity in kidney disease patients and in clinically healthy adults from nephropathic families.

Acetaminophen↗
PubMed1980

Circadian rhythmicity of the urinary excretion of mercury, potassium and catecholamines in unconventional shift-work systems.

The round the clock urinary excretion rates of mercury were assessed for two series of unconventional patterns of activity and sleep in subjects who were not exposed to occupational, medical, or other obvious sources of mercury. In the first series the urine was collected in 3-h periods from six subjects during the first and last 2 d of a four-week, continuous 6-h shift (car ferry, watches either 0800--1400 and 2000--0200 or 1400--2000 and 0200--0800). In the second series the urine was collected in 4-h periods from five subjects working an 8-h experimental rotation shift compressed into 5 d (work two mornings--8-h interval--work two nights--8-h interval--work two afternoons). The mean daily excretion rate of the 11 subjects (48 investigation days, 334 urine samples) was 14.5 pmol of mercury/min (range 5.5--24.4 pmol of mercury/min). The mercury excretion oscillated regularly during 24 h by +/- 20--25% of the individual's daily mean excretion rates. The peak excretion rates were found at 0652 in the first and 0642 in the second series (cosinor treatment). Due to the circadian rhythm the mean 24-h excretion rates were best represented (correlation coefficient 0.92) by analyses of urine produced around noon (spot samples, collection periods 1100--1400 and 1000-1400, respectively). The circadian oscillations of mercury excretion were not influenced by the widely different and varying activity-sleep patterns of the two series. The rhythmicity of potassium excretion (peaks at around 1400) was more irregular. The stable oscillations of mercury excretion contrasted most with the excretion of adrenaline and noradrenaline, which, without losing the basic 24-h rhythmicity, closely followed the unconventional patterns of activity and sleep.

Adult↗
PubMed2003

Renal function in proteinuric glomerular diseases correlates to the changes in urine IgM excretion but not to the changes in the degree of albuminuria.

UNLABELLED: Renal function in proteinuric glomerular diseases correlates to the changes in urine IgM but not to the changes in the degree of albuminuria. BACKGROUND: Albuminuria is believed to correlate to the progression of renal failure in glomerular diseases. Nevertheless, many patients with glomerular disorders maintain their renal function despite persistent albuminuria. In previous studies, we found that the baseline urine excretion of IgM, rather than the degree of albuminuria, predicts the renal outcome in glomerulopathies. In the present study, we examine correlations between changes in the content and in the amount of urine proteins and renal survival during a follow-up time of 3.5 years. METHODS: An observational study of a mean of 44 (+/- 3.6) months was conducted in 37 proteinuric patients (21 males and 16 females) with biopsy-verified primary glomerular disease. The patients were subdivided, according to the findings at the end of the study, into 3 groups, 1 group with decreasing albuminuria (by more than 50%), 1 group with persisting albuminuria and low (< 0.04 mg/mmol creatinine) urinary IgM excretion and 1 group with persisting albuminuria and with high (> or = 0.04 mg/mmol) urinary IgM excretion. RESULTS: All patients that showed remission of albuminuria had also low IgM excretion at the end of the study. All these patients, except 1, maintained their renal function. Patients with persistent albuminuria and high urinary IgM excretion showed a decrease in the glomerular filtration rate (GFR) of a mean of 9.6 ml/min/year compared to a mean GFR increase by 1.5 ml/min/year in patients with low IgM excretion and the same degree of albuminuria (p < 0.01). Seven out of the 9 patients in the former group fall in GFR by more than 5 ml/min/year compared to only 1 of the 10 patients in the latter group. Furthermore, the GFR alterations that occurred during follow-up time correlated in a higher degree to the changes in urinary IgM excretion (r = 0.6, p < 0.01) than to the changes in the degree of albuminuria, (r = 0.4, p < 0.05). A stepwise regression analysis indicated that increased urine IgM excretion is a strong predictor of the GFR decline (r = 0.73, p < 0.001). CONCLUSION: High urinary IgM excretion correlates to decreased GFR in primary glomerular diseases regardless of the degree of albuminuria. In parallel, low urinary IgM excretion indicates beneficial prognosis in these diseases. Since IgM passes the glomerular barrier entirely through large shunts or defects in the glomerular capillary wall, decreased urine content of IgM might be considered as a sign of recovery in the glomerular damage.

Albuminuria↗
PubMed1999

Influence of centrifugation and hindlimb suspension on testosterone and corticosterone excretion in rats.

BACKGROUND: Alterations in mass loading have been shown to stimulate the pituitary-gonadal and pituitary-adrenal axes resulting in changes in testosterone (T) and corticosterone (B) production which may account for the previously reported variations in muscle mass under these conditions. HYPOTHESIS: Centrifugation and hindlimb suspension will induce opposing effects on testosterone and corticosterone excretion. METHODS: Effects of mass loading (centrifugation at -2Gx) and unloading (hindlimb suspension, HLS) on excreted T and B levels, and testicular mass were examined in Sprague-Dawley rats. For 12 d, 16 (8 controls and 8 centrifuged) rats and 20 (10 unsuspended controls and 10 suspended) rats were studied during the centrifugation and suspension portions of the study, respectively. Following the completion of each study, testicular mass was measured. RESULTS: Absolute testicular mass was not different, following 12 d of centrifugation. Excreted T was elevated between days 1 and 6 of centrifugation. Excreted B levels were elevated for the first 4 d of centrifugation. Suspension reduced absolute and relative testicular mass. Excreted T levels were reduced from days 3-12 of suspension, while excreted B levels were only elevated on the first day of suspension. CONCLUSIONS: Centrifugation stimulated an increase in T excretion despite a lack of a change in absolute testicular mass. Conversely, suspension resulted in a reduction in T excretion which may have been associated with a decrease in absolute testicular mass. The centrifugation-induced increase in T excretion is consistent with previously reported increases in lean body mass following centrifugation, while the HLS-induced reduction in T excretion correlates with previously reported decreases in lean body mass following suspension.

Adrenal Glands↗
PubMed1975

Metabolism of lethocholate in healthy man. I. Biotransformation and biliary excretion of intravenously administered lithocholate, lithocholylglycine, and their sulfates.

The metabolism of intravenously injected radiolabeled lithocholate, lithocholylglycine, and their 3alpha-sulfate esters was characterized in healthy subjects. Lithocholate radioactivity was excreted rapidly and predominantly in bile; the excreted radioactivity had the chromatographic properties of glycine and taurine conjugates of lithocholate, of which 60% were sulfated. Lithocholylglycine also was excreted rapidly and predominantly in bile, and 60% of excreted radioacitvity was sulfated. Sulfolithocholate radioactivity was only partially conjugated (about 60%) in association with biliary excretion. Sulfolithocholylglycine was excreted unchanged in bile. Neither sulfated derivative showed appreciable excretion in urine, although both were excreted more slowly in bile than unsulfated free or conjugated lithocholate. The data suggest that unconjugated lithocholate which is absorbed is completely conjugated and partially sulfated before excretion which occurs exclusively in bile. Since sulfation is not complete, some unsulfated lithocholate is always present in bile. This conjugated but unsulfated lithocholate, if reabsorbed, would be again partially sulfated during its next enterohepatic circulation. Thus, the end result of these biotransformations would be for absorbed lithocholate to be excreted in bile mostly, but not entirely as the sulfated conjugates.

Bile↗
PubMed2001

Angiotensin-converting enzyme inhibitors and probucol suppress the time-dependent increase in urinary Type IV collagen excretion of Type II diabetes mellitus patients with early diabetic nephropathy.

BACKGROUND: A multicenter prospective clinical trial was carried out in 9 National Hospitals in Japan to elucidate the time-dependent change in urinary Type IV collagen excretion rate of Type II diabetes mellitus (DM) patients, and to investigate whether an angiotensin-converting enzyme inhibitor (ACE-I) or probucol is effective in preventing progression of renal involvement of diabetics by evaluating urinary Type IV collagen excretion. METHODS: Normo- and microalbuminuric patients with Type II DM were recruited. Patients were assigned to either the control (n = 88), ACE-I (n = 43) or probucol (n = 37) group and treated for 24 months. Besides albumin excretion rate (AER), urinary Type IV collagen excretion rate was also measured. RESULTS: Although, AER, urinary N-acetyl-beta-D-glucosaminidase and beta2-microglobulin excretion rates in the control group did not vary over 24 months, urinary Type IV collagen excretion rate in the control group increased time-dependently (p < 0.01 vs baseline at 18 months and p < 0.005 vs baseline at 24 months). In the ACE-I and probucol groups, time-dependent increases in urinary Type IV collagen excretion rates were not observed. In the ACE-I group, the urinary Type IV collagen excretion rate was significantly lower than that in the control group at 24 months (p < 0.05). In the probucol group, the urinary Type IV collagen excretion rate was significantly lower than that in the control group at 6 months (p < 0.05). In the ACE-I group, AER decreased significantly compared with baseline at 18 months (p < 0.05) and at 24 months (p < 0.005). CONCLUSIONS: ACE-I has a beneficial effect and probucol may have a beneficial effect in preventing the progression of early diabetic nephropathy. Measurement of the urinary Type IV collagen excretion rate in combination with AER would be useful for the management of early renal involvement in Type II DM.

Acetylglucosaminidase↗
PubMed1991

Renal potassium excretion is reduced in children with idiopathic hypercalciuria.

Increased luminal calcium decreases potassium secretion in microperfused rat distal tubule. To determine if such an effect is also present in vivo, we evaluated renal potassium excretion in 49 children with idiopathic hypercalciuria (urinary excretion of Ca = 5.5 +/- 1.3 mg/kg/day) and in 214 age-matched control children (urinary excretion of Ca = 1.9 +/- 0.3 mg/kg/day). In comparison to controls, hypercalciuric children had significantly increased levels of sodium excretion (fractional excretion of Na = 0.7 +/- 0.3 vs. 0.6 +/- 0.3%, respectively; p less than 0.001) and decreased levels of fractional potassium excretion (7.2 +/- 2.9 vs. 9.2 +/- 3.4%, respectively; p less than 0.001) and of the transtubular potassium concentration gradient (4.2 +/- 1.5 vs. 5.9 +/- 1.5, respectively; p less than 0.001). All indices of potassium excretion correlated significantly and inversely with urinary calcium excretion (p less than 0.001). After an oral calcium load, performed in 30 hypercalciuric children, the increased rates of urinary calcium excretion were accompanied by increased rates of urinary sodium excretion and by a significant decrease in the transtubular potassium concentration gradient. These results support the hypothesis that increased luminal calcium concentration also inhibits renal potassium secretion in man.

Administration, Oral↗
PubMed1990

Renal net acid and electrolyte excretion in an experimental model of hypochloremic metabolic alkalosis in sheep.

Renal electrolyte and net acid excretion were characterized during generation and maintenance of hypochloremic metabolic alkalosis in a ruminant model. Two phases of renal response with regard to sodium and net acid excretion were documented. An initial decrease in net acid excretion was attributable to increase in bicarbonate excretion with associated increase in sodium excretion. As the metabolic disturbance became more advanced, a second phase of renal excretion was observed in which sodium and bicarbonate excretion were markedly decreased, leading to increase in net acid excretion and development of aciduria. Throughout the metabolic disturbance, chloride excretion was markedly decreased; potassium excretion also decreased. These changes were accompanied by increase in plasma renin and aldosterone concentrations. There was apparent failure to concentrate the urine optimally during the course of the metabolic disturbance, despite increasing plasma concentration of antidiuretic hormone.

Aldosterone↗
PubMed1988

Increased urinary excretion of digoxin-like immunoreactive substance by insulin-dependent diabetic patients: a linkage with hypertension?

Excretion of digoxin-like immunoreactivity (DLIS) was measured by RIA in timed overnight urine collections from 91 normotensive nondiabetic subjects and 104 normotensive insulin-dependent diabetic (IDDM) patients. The mean +/- SD DLIS excretion rate for the diabetic patients significantly exceeded that for the controls (73 +/- 41 vs 63 +/- 36 pg/min, P = 0.024). In both groups, the mean DLIS excretion rates for men were significantly higher (P = 0.0014, P = 0.006) than for women. In the controls, the DLIS excretion rate significantly correlated with the urinary excretion rate of creatinine (P less than 0.01), Na+ (P less than 0.05), and K+(P less than 0.05), and with the subjects' body weight (P less than 0.01), body mass index (P less than 0.05), and systolic blood pressure (P less than 0.05). In the diabetics, the DLIS excretion rate was significantly correlated with body weight (P less than 0.05) and with urinary excretion rates for albumin (P less than 0.01), creatinine (P less than 0.01), Na+ (P less than 0.05), and K+(P less than 0.05). Our data indicate that: (a) increased amounts of a cardiac glycoside-like substance (or a group of substances) are excreted in the urine of IDDM patients; (b) the urinary excretion of DLIS seems to depend on glomerular filtration rate and physiocochemical properties of glomerular membrane, as well as on subjects' body mass; and (c) because cardiac glycoside-like substances may increase peripheral vascular resistance, increased urinary excretion of DLIS by IDDM patients may indicate a tendency to develop hypertension.

Adult↗
PubMed1987

[Clinical studies on the recurrence of urolithiasis: (1). Influence of diet on urinary excretion of the stone forming constituents].

Twenty-four hour urinary excretion of the stone forming constituents, calcium, oxalate, uric acid, phosphate and magnesium were assayed either under the restricted diet (190 stone formers and 52 non-stone formers) or under the ambulatory free diet (93 stone formers and 14 non-stone formers). Under the ambulatory free diet, urinary excretion of calcium, uric acid and magnesium in the male stone formers, and urinary excretion of calcium and magnesium in the female stone formers was significantly higher than that under the restricted diet. Under the restricted diet, no difference in urinary excretion of calcium, oxalate, uric acid or phosphate was noted between the stone formers and non-stone formers. However, urinary magnesium excretion of the stone formers under the restricted diet was significantly lower than that of the non-stone formers. Under the free diet, no difference in urinary excretion of calcium, oxalate, uric acid, phosphate or magnesium was observed between the stone formers and non-stone formers. Also, there was no significant difference in urinary excretion of calcium, oxalate, uric acid, phosphate or magnesium between the unilateral urolithiasis patients without previous stone history and that of the bilateral or recurrent stone formers. We conclude that urinary excretion of calcium, oxalate, uric acid, phosphate and magnesium have no major role in the stone producing mechanism. However, reduction of urinary excretion of calcium, oxalate, uric acid and phosphate and augmentation of urinary excretion of magnesium are mandatory in preventing stone recurrence until a better understanding of the cause of urolithiasis is obtained.

Calcium↗
PubMed1979

Effect of sodium taurocholate on hepatic uptake and biliary excretion of organic anions in rats.

Hepatic uptake and biliary excretion of some exogenous organic anions administered simultaneously with sodium taurocholate (TC) have been investigated in anaesthetized (1.2 g/kg urethane i.p.) rats. TC (100 or 200 mumol/kg i.v.) significantly increased the biliary excretion of indocyanine green (ICG), bromcresol green (BCG), rose bengal (RB) and bromsulphthalein (BSP). The biliary excretion rates of eosine (EO) and bromsulphthalein-glutathione conjugate (BSP-GSH) were not affected by TC. However, simultaneously given TC significantly reduced the biliary excretion of amaranth (AM). The effect of TC on the biliary excretion rates of organic anions seems to depend on the properties of the anions investigated. ICG, BCG, RB and BSP depress bile production, inhibit mitochondrial respiration and are excreted at low rates. Biliary excretion of these anions was enhanced by TC. EO, BSP-GSH and AM had no depressing effect on the function of liver cells and showed higher excretory rates than the above-mentioned substances. The changes in biliary flow measured during excretion of drugs did not parallel the changes in biliary excretion rate. The hepatic uptake of all organic anions studied was depressed by TC. This finding indicates that no correlation exists between the effects of TC on hepatic uptake and biliary excretion of organic anions.

Animals↗
PubMed1983

Renal kallikrein and PGE in the exaggerated fractional Na excretion in patients with chronic renal failure.

The present study was performed to investigate the roles of renal kallikrein and prostaglandin (PG) E in the mechanism of the exaggerated fractional Na excretion in hypertensive patients with advanced renal disease by means of the determination of urinary excretion of kallikrein and PGE, and fractional Na excretion in 20 healthy volunteers and 41 patients with chronic glomerulonephritis (14 normotensive patients; 9 borderline hypertensive patients; 18 sustained hypertensive patients). Urinary excretion of kallikrein and PGE was significantly decreased in patients with sustained hypertension as compared with healthy volunteers, while not decreased in those with normotensive or borderline hypertensive patients. Four times higher values for the fractional Na excretion and four or five times higher values for the urinary excretion of PGE corrected for creatinine clearance, were found in patients with borderline or sustained hypertension. There was a significant positive correlation (r = 0.6777) between the two. These results suggest that PGE in the renal tubular compartment may be involved in the mechanism of the exaggerated fractional Na excretion in patients with advanced renal disease. The urinary excretion rate of kallikrein corrected by creatinine clearance was three times greater in patients with borderline hypertension, but no significantly increase in those with sustained hypertension compared with that in healthy volunteers. There was no significant correlation between the fractional Na excretion and urinary kallikrein excretion corrected for creatinine clearance.

Adult↗
PubMed1983

Paradoxical effects associated with supranormal urinary testosterone excretion in premenopausal women with breast cancer: increased risk of postmastectomy recurrence and higher remission rate after ovariectomy.

Urinary testosterone excretion was measured in 18 normal premenopausal women, 80 women studied shortly after mastectomy for primary operable breast cancer, and 93 women with either metastatic breast cancer (77) or primary inoperable breast cancer (16) who were to be ovariectomized. Forty-two of the 93 were restudied after the ovariectomy. The control women showed a normal distribution of testosterone excretion, up to 12 micrograms daily; the postmastectomy patients showed a bimodal distribution, with 14 patients (17.5%) having values above 12 micrograms (up to 39 micrograms) daily. In the metastatic group, 24 of 77 patients (31.1%) had urinary testosterone excretion greater than 12 micrograms daily (up to 77 micrograms). The difference in percentage of high excretors was significant (p less than 0.02). Of the patients treated by ovariectomy, 27 had supranormal testosterone excretion preoperatively, and 16 of these (59.2%) had remissions; 66 had normal excretion preoperatively, and 21 of these (31.8%) had remissions. The difference was significant (p less than 0.02). Urinary testosterone excretion was restudied postoperatively in 42 of the 93 ovariectomized patients. Values were normal preoperatively in 31, and these were unchanged postoperatively. Values were supranormal preoperatively in 11; all of these fell significantly after ovariectomy, to normal in 8 cases. These findings appear to confirm the ovarian source of the excessive urinary testosterone. The following conclusions were drawn. There is a subgroup of premenopausal women with primary operable breast cancer who have supranormal urinary testosterone excretion; the incidence of this abnormality in women with recurrent metastatic disease after mastectomy is nearly twice as high. It can be calculated that the finding of supranormal urinary testosterone shortly after mastectomy represents virtually a 100% risk of recurrence, in contrast to a recurrence rate of about 38% in women with normal testosterone excretion. Patients with supranormal testosterone excretion prior to therapeutic ovariectomy have nearly twice as high a remission rate as do those with normal testosterone excretion.

Adult↗
PubMed1980

Effect of dehydrocholic, chenodeoxycholic, and taurocholic acids on the excretion of bilirubin.

The effects of IV bile acid infusion (at approx 20% of normal excretion rate) on the biliary excretion of 3-alpha-hydroxy bile acids and bilirubin were investigated in ponies prepared surgically with chronic external biliary fistulas. Endogenous bile acid excretion (approx 45 mumol/min) decreased to the hepatic synthesis rate (approx 1.5 mumol/min) during the initial 4 to 5 hours of bile drainage. In type 1 studies, both chenodeoxycholic and taurocholic acid infusion (8 to 9 mumol/min) increased bilirubin excretion by 58% to 82% following 5 hours of biliary diversion. During type 2 studies, 3-hour IV infusions (10.5 mumol/mon) of dehydrocholic acid, 4 hours following biliary diversion, increased bile flow by 45% to 62% and excretion of 3-alpha-hydroxy bile acid by 34% to 36% above preinfusion (hepatic synthesis) levels. Bilirubin excretion was not significantly changed during those increases in bile flow and bile acid excretion. Immediately after dehydrocholic acid infusion, taurocholic acid infusion (8.1 mumol/min) greatly increased bilirubin excretion for 1 hour (a reversal of hepatic storage identical to that found during type 1 studies), prolonged excretion (mg/2 hours) being two to three times that caused by dehydrocholic acid infusion. Bilirubin excretion appeared to correlate with the micelle-forming capacity of endogenous bile acids as opposed to the nonmicelle-forming characteristic of synthestic dehydrocholic acid.

Animals↗
PubMed1994

Elevated urinary excretion of endothelin-like immunoreactivity in children with renal disease is related to urine flow rate.

Endothelin 1-21 belongs to a family of locally produced regulatory peptides with potent vasoconstrictor activity and profound renal effects. To study the biological significance of endothelin in children with renal diseases, we measured urinary endothelin-like immunoreactivity (ETir) excretion in children and adolescents (60 normal controls and 57 patients with renal disease). ETir excretion was constant during childhood and adolescence (4-18 years). Compared to these normal controls elevated urinary excretions of ETir were found in children with chronic renal failure, following renal transplantation and with idiopathic hypercalciuria (all groups p < 0.001). However, ETir excretion was unchanged in children with idiopathic steroid sensitive nephrotic syndrome, with stable chronic glomerulonephritis and in 4 patients with hemolytic uremic syndrome. Urinary ETir concentrations were similar in controls and in various patient groups. ETir excretion correlated positively with urine flow rate in normal controls (r = 0.71) and in all patients studied (r = 0.91). Fractional excretion of ETir correlated negatively with glomerular filtration rate. Eight healthy volunteers (23-27 years old, 4 female, 4 male) were studied before and after oral water load (20 ml/kg) to investigated the effect of ETir excretion on urine flow rate. Urine flow rose tenfold in response to water load and urine concentration of ETir fell only by factor 3 and urinary ETir excretion rose fivefold. These results indicate that urinary ETir excretion is related to and depends at least in part on urine flow rate. ETir excretion may so reflect a role of ETir in renal disease, especially in the diuretic state.

Adolescent↗
PubMed1996

Effect of acetylsalicylic acid, paracetamol, caffeine and a combination of these substances on the renal prostaglandin E2, 6-keto-prostaglandin F1 alpha, water, creatinine and electrolyte excretion of the rat.

The aim of the study was to investigate the effect of acetylsalicylic acid (CAS 50-78-2, ASA), paracetamol (CAS 103-90-2) and caffeine (CAS 58-08-2) and a combination of these substances on the renal prostaglandin excretion of rats loaded with water. In addition to the effects on the renal excretion of prostaglandin E2 (PGE2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), the effect on the electrolyte, creatinine and water excretion was measured. Even in low doses ASA led to a dose-dependent reduction in the renal PGE2 and 6-keto-PGF1 alpha excretion. In oral doses up to 200 mg/kg paracetamol did not have any effect on the renal prostanoid excretion. In the combination it did not change the effect of ASA on the prostaglandin excretion. Caffeine caused a marked dose-dependent increase in the PGE2 excretion. The effect of caffeine on the renal 6-keto-PGF1 alpha excretion was less marked. In combination with ASA, with and without the addition of paracetamol, caffeine reduced the inhibitory effect of ASA on the excretion of arachidonic acid metabolites. The values for the renal prostaglandin excretion did not show any clear correlation with the other parameters of diuresis.

6-Ketoprostaglandin F1 alpha↗
PubMed1976

Effects of desipramine treatment on the biliary, fecal and urinary excretion of methadone in the rat.

The effects of desipramine (DMI) given i.p. 1 hour before administration of 14C-methadone (5 mg/kg s.c.) on the excretion of methadone in bile, feces and urine were studied. Rats with cannulated bile ducts excreted 52% of administered 14C into bile within 4 hours, 60% of the excretion as 2-ethylidine-1,5-dimethyl-3,3-diphenylpyrrolidine (EDDP) and 30% as water-soluble metabolite (WSM). The percentages of 14C excreted within 48 hours into the feces and urine of rats without biliary fistula were 60.6 and 17.4%, respectively. The excretion of 14C in feces consisted mostly of EDDP. Urinary excretion consisted of unchanged methadone, EDDP and WSM in the first 12 hours and consisted mostly of WSM thereafter. DMI treatment increased biliary flow but decreased the biliary excretion of 14C, mainly by a decrease in WSM. The fecal output was greatly decreased by DMI, thus decreasing fecal excretion of 14C in the first 12 hours. DMI treatment markedly decreased urinary volume but did not change the urine pH. The decreased urinary excretion of WSM in DMI-treated rats during the first 12-hour urine sample accounted for most of the decreased elimination of 14C. It is suggested that DMI-induced inhibition of methadone metabolism in the liver is a major factor responsible for the observed decreases in the biliary and urinary excretion of WSM...

Animals↗