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PubMed1995

Urinary organic anion excretion in response to dietary acid and base loading.

Animals eating a base-loaded or base-forming diet excrete urine containing large amounts of organic anions (OA). Although citrate is the only OA previously identified as being excreted in appreciable amounts during base loading, citrate excretion accounts for only part of total OA excretion. The objectives of this study were to identify other OA excreted by rats and to see how their excretion changed in response to moderate (8 micro Eq/g per day) and heavy (30 micro Eq/g per day) loads of NaHCO3 and NH4Cl. Urinary OA were identified by high-performance liquid chromatography and were measured by enzymatic techniques as well. It was found that, in addition to citrate, significant quantities of alpha-ketoglutarate (alpha-KG) were excreted by base-loaded rats and that the excretion of citrate, alpha-KG, and succinate increased with base loading and decreased with acid loading. Citrate plus alpha-KG excretion rates were, respectively, two-thirds and one-third the rate of HCO3- excretion in rats given moderate and heavy base loads. The excretion of creatinine, glutamine, and hippurate showed no clear pattern in response to acid or base loading. It was concluded that, especially in animals experiencing moderate base loads, increases in the excretion of citrate and alpha-KG represent a much more significant component of base excretion than has been recognized previously.

Acid-Base Equilibrium↗
PubMed1990

Renal excretion of zinc in patients with chronic uremia.

Though uremic patients have been reported to have subnormal zinc levels in plasma and an abnormal zinc metabolism, data on their renal excretion of zinc are still unavailable. In our study, 55 nondialyzed uremic patients had a markedly lower concentration of zinc in plasma and a lower urinary zinc excretion. They had a higher excretory fraction of zinc in the renal tubules and a higher ratio of zinc to creatinine excretion than normal subjects. We found that the total daily excretion of zinc, calcium, phosphate and ammonia was reduced, and that the ratio of calcium or ammonia to creatinine excretion decreased in uremic patients. Urinary zinc excretion was correlated with renal creatinine clearance (r = 0.50, p less than 0.001) in both normal subjects and uremic patients, but ammonia excretion was correlated with zinc excretion in normal subjects only. In uremia, urinary zinc excretion was correlated with urinary calcium (r = 0.55, p less than 0.001) and urinary phosphate excretion (r = 0.30, p less than 0.05). We conclude that the increased ratio of zinc to creatinine excretion and the excretory fraction of zinc in the renal tubules of uremic patients may increase the urinary zinc excretion, but a severe diminution of the glomerular filtered load of zinc may be the major factor in decreasing the urinary zinc excretion in uremia.

Adult↗
PubMed1988

Role of the hepatocyte microtubular system in the excretion of bile salts and biliary lipid: implications for intracellular vesicular transport.

The role of the hepatocyte microtubular system in the transport and excretion of bile salts and biliary lipid has not been defined. In this study the effects of microtubule inhibition on biliary excretion of micelle- and non-micelle-forming bile salts and associated lipid were examined in rats. Low-dose colchicine pretreatment had no effect on the baseline excretion of biliary bile salts and phospholipid in animals studied 1 hr after surgery (basal animals), but slightly retarded the excretion of tracer [14C]taurocholate relative to that of lumicolchicine-pretreated (control) rats. However, colchicine pretreatment resulted in a marked reduction in the excretion of 2 mumol/100 g doses of a series of four micelle-forming bile salts of differing hydrophilicity, but had no significant effect on the excretion of the non-micelle-forming bile salt, taurodehydrocholate. Continuous infusion of 0.2 mumol of taurocholate/(100 g.min) following 24 hr of biliary drainage (depleted/reinfused animals) resulted in physiologic bile flow with biliary excretion rates of bile salts, phospholipid, and cholesterol that were markedly inhibited (mean 33, 39, and 42%, respectively) by colchicine or vinblastine pretreatment. Excretion of tracer [14C]taurocholate also was markedly delayed by colchicine in these bile salt-depleted/reinfused animals. In contrast, colchicine did not inhibit bile salt excretion in response to reinfusion of taurodehydrocholate. Thus, under basal conditions, the microtubular system appears to play a minor role in hepatic transport and excretion of bile salts and biliary lipid. However, biliary excretion of micelle-forming bile salts and associated phospholipid and cholesterol becomes increasingly dependent on microtubular integrity as the transcellular flux and biliary excretion of bile salts increases, in both bile salt-depleted and basal animals. We postulate that cotransport of micelle-forming bile salts and lipids destined for biliary excretion, via an intracellular vesicular pathway, forms the basis for this microtubule dependence.

Animals↗
PubMedDate not supplied

Effect of arsenicals on biliary excretion of endogenous glutathione and xenobiotics with glutathione-dependent hepatobiliary transport.

Sodium arsenite (25-100 mumol/kg, i.v.) and arsenate (75-300 mumol/kg, i.v.) injected into anaesthetized rats increased the biliary excretion of endogenous non-protein thiols (NPSH) in a dose-dependent fashion up to 24- and 31-fold, respectively. Simultaneously with NPSH, glutathione (GS) excretion was increased to a similar extent suggesting that the increment in biliary thiol output originated from enhanced hepatobiliary transport of GS. After administration of labelled arsenicals, biliary excretion of 74As and NPSH followed similar time-courses. Biliary excretion of 74As was more efficient after arsenite than arsenate administration corresponding to the greater potency of arsenite compared to arsenate to increase biliary output of NPSH. Coadministered sulfobromophthalein (BSP) inhibited the biliary excretion of 74As and prevented the arsenical-induced increase in biliary NPSH. Thus, hepatobiliary transport of arsenic apparently proceeds coordinately with that of GS. However, excretion of each molecule of arsenic compound generates transport of several molecules of GS. Though mercuric, methylmercuric, cadmium and zinc ions are thought to be excreted into bile as complexes with GS, the marked arsenical-induced increase in GS excretion only doubled the biliary excretion of inorganic mercury and hardly influenced the transport of other metals into bile. This finding suggests that arsenicals markedly enhance biliary excretion of GS with a free thiol group but barely or not at all that of GS with a thiol group blocked by a firmly bound metal ion. Both arsenicals diminished the biliary excretion of BSP-glutathione conjugate after BSP administration presumably because they impaired conjugation of BSP with GSH due to decreased GS availability. It is assumed that arsenite, and arsenate after reduction to arsenite, forms an unstable complex with GS that is efficiently transported into bile resulting in increased biliary output of GS. It is demonstrated that arsenite-induced perturbation of hepatobiliary disposition of endogenous GS differentially affects biliary excretion of xenobiotics with GS-dependent hepatobiliary transport.

Animals↗
PubMed1980

Effects of indomethacin on furosemide-stimulated urinary PGE2 excretion in man.

We studied the effects of furosemide on urinary excretion of PGE2 and sodium and the effects of inhibition of prostaglandin (PG) synthesis with indomethacin or furosemide-induced PGE2 excretion and natriuresis in normal man. Furosemide (20 mg i.v.) increased the urinary excretion of PGE2 from 71.2 +/- 17.2 to 255.9 +/- 41.0 ng/4 h. Sodium excretion increased in parallel. Indomethacin, in a dose sufficient to decrease basal urinary PGE2 excretion by > 90%, significantly decreased both urinary PGE2 and sodium excretion under furosemide without affecting delivery of furosemide into the urine. The urinary excretion of furosemide was 9.4 +/- 0.4 and 9.3 +/- 1.4 mg/24 h with and without indomethacin, respectively. However, the furosemide-induced increment in PGE2 excretion correlated significantly with sodium excretion rate with and without indomethacin. Indomethacin changed the relationship between absolute amounts of furosemide in urine and PGE2 excretion but did not affect the increment in excretion over baseline or the significant correlation of urinary PGE2 with sodium excretion.

Drug Interactions↗
PubMed1987

Hepatobiliary excretion of organic anions in double-mutant rats with a combination of defective canalicular transport and uridine 5'-diphosphate-glucuronyltransferase deficiency.

Mutant rats with a selective defect for the hepatobiliary excretion of organic anions (GT+TR- rats) are valuable models to study hepatic transport processes. However, retained conjugates in the livers of these rats may secondarily affect hepatic uptake, metabolism, and excretion of other compounds and this may confound the interpretation of test results. We have developed double mutants (GT-TR-) rats with both a conjugation and an excretion defect by cross-breeding uridine 5'-diphosphate-glucuronyl-transferase-deficient GT-TR+ Gunn rats with transport-deficient GT+TR- rats. Phenotypically, GT-TR- rats and Gunn rats are alike in that both have unconjugated hyperbilirubinemia. Intravenous administration of tetrabromosulphthalein, bilirubin diglucuronide, and bilirubin monoglucuronide revealed a significant difference in that the clearance of these compounds was reduced to 10%, 10%, and 20%, respectively, in GT-TR- rats when compared with Gunn rats. The hepatic elimination of tetrabromosulphthalein in GT-TR- rats and in GT+TR- rats is impaired to the same extent. Thus, both have a similar hepatic excretion defect. However, bile flow and bile acid excretion in GT+TR- rats are more depressed than in GT-TR- rats: bile flow, 88 +/- 3 vs. 36 +/- 1 microliters/min.kg and bile acid excretion, 3.4 +/- 0.2 vs. 1.5 +/- 0.1 mumol/min.kg in GT-TR- and GT+TR- rats, respectively. This suggests that accumulated glucuronides in the liver inhibit bile flow and bile acid excretion. To test whether conjugated bilirubin and the photoisomers of unconjugated bilirubin are excreted via the same transport pathways, the effect of phototherapy was studied in GT-TR- rats and in Gunn rats. Photoexposure caused a 120% increase in biliary excretion of bilirubin isomers in Gunn rats and only 40% in GT-TR- rats. This shows that the biliary excretion of bilirubin photoisomers is indeed affected by the hepatic excretion defect of GT-TR- rats and suggests that hepatic excretion of bilirubin photoisomers proceeds via the same route as other organic anions such as conjugated bilirubin and tetrabromosulphthalein.

Animals↗
PubMed1986

Disposition of metals in rats: a comparative study of fecal, urinary, and biliary excretion and tissue distribution of eighteen metals.

Fecal (0-4 days), urinary (0-4 days), and biliary (0-2 hr) excretion and tissue distribution of 18 metals were examined in rats after iv administration. Total (fecal + urinary) excretion was relatively rapid (over 50% of dose in 4 days) for cobalt, silver, and manganese; was between 50 and 20% for copper, thallium, bismuth, lead, cesium, gold, zinc, mercury, selenium, and chromium; and was below 20% for arsenic, cadmium, iron methyl mercury, and tin. Feces was the predominant route of excretion for silver, manganese, copper, thallium, lead, zinc, cadmium, iron, and methyl mercury whereas urine was the predominant route of excretion for cobalt, cesium, gold, selenium, and chromium; while both excretion routes were equally important for bismuth, mercury, arsenic, and tin. Biliary excretion seems to be an important determinant for the fecal excretion of silver, arsenic, manganese, copper, selenium, cadmium, lead, bismuth, cobalt, and methyl mercury. Between 45 (silver) and 0.8% (methyl mercury) of the dosages administered of these metals was excreted into bile in 2 hr, and they exhibited high bile/plasma concentration ratios. The biliary excretion of copper, selenium, lead, and chromium did not increase proportionally with dosage, suggesting that the hepatobiliary transport of these metals is saturable. The fraction of dosage excreted into bile was independent of the dosage for silver, arsenic, manganese, bismuth, methyl mercury, mercury, gold, cesium, thallium, and tin, but markedly increased with increase in dosage of cadmium, cobalt, zinc, and iron. The latter phenomenon is probably due to saturation of hepatic (cadmium, zinc) or extrahepatic (iron) metal-binding sites. Comparison of biliary and fecal excretion rates indicates that arsenic and selenium undergo intestinal reabsorption, whereas thallium and zinc enter the feces also by non-biliary routes. Most of the metals reached the highest concentration in liver and kidney. However, there was no direct relationship between the distribution of metals to these excretory organs and their primary route of excretion.

Animals↗
PubMed2006

Plasma concentrations and urinary excretion of purine bases (uric acid, hypoxanthine, and xanthine) and oxypurinol after rigorous exercise.

To investigate the effects of exercise on the plasma concentrations and urinary excretion of purine bases and oxypurinol, we performed 3 experiments with 6 healthy male subjects. The first was a combination of allopurinol intake (300 mg) and exercise (VO2max, 70%) (combination experiment), the second was exercise alone (exercise-alone experiment), and the third was allopurinol intake alone (allopurinol-alone experiment). In the combination experiment, exercise increased the concentrations of purine bases and noradrenaline in plasma, as well as lactic acid in blood and the urinary excretion of oxypurines, whereas it decreased the urinary excretion of uric acid and oxypurinol as well as the fractional excretion of hypoxanthine, xanthine, uric acid, and oxypurinol. In the exercise-alone experiment, exercise increased the concentrations of purine bases and noradrenaline in plasma, lactic acid in blood, and the urinary excretion of oxypurines, whereas it decreased the urinary excretion of uric acid and fractional excretion of purine bases. In contrast, in the allopurinol-alone experiment, the plasma concentration, urinary excretion, and fractional excretion of purine bases and oxypurinol remained unchanged. These results suggest that increases in adenine nucleotide degradation and lactic acid production, as well as a release of noradrenaline caused by exercise, contribute to increases in plasma concentration and urinary excretion of oxypurines and plasma concentration of urate, as well as decreases in urinary excretion of uric acid and oxypurinol, along with fractional excretion of uric acid, oxypurinol, and xanthine. In addition, they suggest that oxypurinol does not significantly inhibit the exercise-induced increase in plasma concentration of urate.

Adult↗
PubMedDate not supplied

Urinary excretion of amino acids in normal and cystinuric dogs.

The 24-h urine excretion of 20 amino acids was investigated in 24 cystinuric and 15 normal dogs. The diagnosis of cystinuria was based on infrared spectroscopy of removed uroliths, which in all cases were composed of pure cystine. Seven of 24 cystinuric dogs showed normal cystine excretion compared to normal dogs, and four of 24 dogs showed normal total amino acid excretion. In contrast to earlier investigations, almost half of the cystinuric dogs (46%) showed elevated excretion of five or more amino acids. Isolated cystinuria, or isolated dibasic amino aciduria was not found. Compared to normal dogs, the cystinuric dogs showed a significantly (P < 0.05) increased excretion of cystine, arginine, lysine, cystathionine, glutamic acid, threonine and glutamine. There was a significant correlation (P < 0.05) between the urinary excretion of cystine and 10 other amino acids, with the highest correlation found (P < 0.001) for arginine, lysine, cystathionine, ornithine and 1-methyl-histidine. Three patterns of amino acid excretion could be identified: (1) increased excretion and a significant correlation with cystine for the three dibasic amino acids (lysine, arginine and ornithine), compatible with a common reabsorption mechanism as shown in man. This pattern was also found for cystathionine and glutamic acid, which might indicate a relation in metabolism or transport; (2) increased excretion but no correlation with cystine for glutamine, threonine and citrulline; (3) good correlation with cystine, but no increased excretion for 1-methyl-histidine, phenylalanine, 3-methyl-histidine, leucine and alanine. The great variation in urinary cystine excretion suggests that factors other than the excretion of cystine must be considered as causes of cystine urolith formation. For example, cystinuric dogs were found to have lower diuresis than normal dogs and produced urine with higher cystine concentration thereby increasing the risk of cystine urolith formation.

Amino Acids↗
PubMed1995

Diurnal variation of urinary leukotriene E4 and histamine excretion rates in normal subjects and patients with mild-to-moderate asthma.

BACKGROUND: Leukotriene E4 (LTE4) and histamine excreted into the urine reflect the in vivo synthesis and release of cysteinyl leukotrienes and histamine, respectively. We examined the diurnal variation of the excretion rate of these mediators over 4 consecutive days in normal subjects (n = 5) and patients with stable mild-to-moderate asthma (n = 8). METHODS: Sixteen consecutive 6-hour urine samples were collected over 4 days. Urinary LTE4 concentrations were determined by reverse-phase high-pressure liquid chromatography, followed by ELISA. Urinary histamine concentrations were measured by ELISA. The excretion rates of these compounds were normalized relative to urinary creatinine content. RESULTS: The mean urinary LTE4 excretion rate was 83.8 +/- 38.2 pg/mg creatinine (mean +/- SD) in normal subjects; in patients with asthma, the urinary LTE4 excretion rate (110.0 +/- 59.2 pg/mg creatinine) was significantly higher than that in normal subjects (p < 0.05). The urinary histamine excretion rate was not different between normal subjects (24.0 +/- 12.5 ng/mg creatinine) and patients with asthma (31.5 +/- 25.8 ng/mg creatinine). A robust and systematic within-day variation (p < 0.01), but no day-to-day variation, was observed in histamine excretion rate. Although the magnitude of variation in LTE4 excretion within a day was significantly greater in patients with asthma than in normal subjects (p < 0.05), we could not identify any specific diurnal variation pattern in either the normal or the asthma group. No significant correlation was observed between urinary LTE4 and histamine excretion rate within any subject. CONCLUSIONS: Patients with asthma excrete LTE4 in the urine at a greater rate than normal subjects. Although no systematic variation in urinary LTE4 excretion rates over the course of a day was observed in either normal subjects or patients with stable asthma, the presence of a systematic diurnal variation of urinary histamine excretion exists in both groups.

Adult↗
PubMed2001

The time-course change of nitrogenous excretion in the Kuruma shrimp Penaeus japonicus following nitrite exposure.

Penaeus japonicus (12.83 +/- 1.24 g) which were exposed individually to 0.002 (control), 0.076, 0.362, 0.719 and 1.433 mM nitrite at 30 ppt of salinity were examined for hemolymph ammonia, urea and nitrite, and nitrogenous excretion after 3, 6, 12, 24 and 48 h, respectively. Hemolymph nitrite and hemolymph urea increased directly with ambient nitrite and exposure time, whereas hemolymph ammonia was inversely related to ambient nitrite and exposure time. Specific excretions of total-N (total nitrogen), ammonia-N, urea-N and organic-N (organic nitrogen) increased directly with ambient nitrite and exposure time. The contribution of ammonia-N excretion and urea-N excretion in the total-N excreted by the control shrimp was 41.7-90.8 and 2.8-10.5%, respectively. The contribution of ammonia-N in the total-N excreted by P. japonicus decreased to 10.0 and 3.8%, when they were exposed for 24 h to 0.076 and 1.433 mM nitrite, respectively. The contribution of urea-N excretion increased to 58.7 and 21.4%, and the organic-N excretion increased to 31.3 and 74.8% in the total-N excreted by the shrimp following 24 h exposure to 0.076 and 1.433 mM nitrite, respectively. It was concluded that P. japonicus following 24 h exposure to nitrite as low as 0.076 mM increased its ammonia-N excretion by a factor of 1.9, its urea-N excretion by 200, and its organic-N excretion by 37, as compared to those in the control solution.

Ammonia↗
PubMed1990

Urinary excretion of kappa light chains in patients with diabetes mellitus.

The urinary excretion of kappa light chains, beta 2-microglobulin and albumin was examined in patients with newly diagnosed and long-standing insulin-dependent (IDDM) and non-insulin-dependent (NIDDM) diabetes mellitus, and compared to age-matched control subjects. Patients with IDDM diagnosed within two months, presented with normal albumin excretion, whereas the concentrations of beta 2-microglobulin and kappa light chain in urine were higher than in control subjects. The initiation of insulin therapy reduced, but did not completely normalize, the elevated rate of kappa light chain excretion. Patients with IDDM of long duration showed increased urine excretion of kappa light chains and albumin. In keeping with the findings in IDDM, patients with newly diagnosed NIDDM (within one year) showed increased urinary excretion of kappa light chains compared with control subjects. There was, however, no further increase in light chain excretion with longer duration of NIDDM. To study the effect of short-term hyperglycemia on urinary protein excretion, 12 normal subjects participated in a three-step hyperglycemic clamp study, during which their plasma glucose concentration was raised by +50, +125 and +300 mg/dl. The urine excretion of albumin and beta 2-microglobulin rose progressively with each hyperglycemic clamp step, whereas that of kappa light chain excretion was unaffected by hyperglycemia. We conclude that increased urinary excretion of kappa light chain is a consistent finding in all types of diabetes mellitus, and can be observed even when the albumin excretion is normal. Since the serum concentration of kappa light chain is normal in diabetes, the increased urinary excretion of kappa light chains must be of renal origin.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Cell volume and bile acid excretion.

The interaction between cell volume and taurocholate excretion into bile was studied in isolated perfused rat liver. Cell swelling due to hypo-osmotic exposure, addition of amino acids or insulin stimulated taurocholate excretion into bile and bile flow, whereas hyperosmotic cell shrinkage inhibited these. These effects were explained by changes in Vmax of taurocholate excretion into bile: Vmax. increased from about 300 to 700 nmol/min per g after cell swelling by 12-15% caused by either hypo-osmotic exposure or addition of amino acids under normo-osmotic conditions. Steady-state taurocholate excretion into bile was not affected when the influent K+ concentration was increased from 6 to 46 mM or decreased to 1 mM with iso-osmoticity being maintained by corresponding changes in the influent Na+ concentration. Replacement of 40 mM-NaCl by 80 mM-sucrose decreased taurocholate excretion into bile by about 70%; subsequent hypo-osmotic exposure by omission of sucrose increased taurocholate excretion to 160%. Only minor, statistically insignificant, effects of aniso-osmotic cell volume changes on the appearance of bolus-injected horseradish peroxidase in bile were observed. Taurocholate (400 microM) exhibited a cholestatic effect during hyperosmotic cell shrinkage, but not during hypo-osmotic cell swelling. Both taurocholate and tauroursodeoxycholate increased liver cell volume. Tauroursodeoxycholate stimulated taurocholate (100 microM) excretion into bile. This stimulatory effect was strongly dependent on the extent of tauroursodeoxycholate-induced cell swelling. During continuous infusion of taurocholate (100 microM) further addition of tauroursodeoxycholate at concentrations of 20, 50 and 100 microM increased cell volume by 10, 8 and 2% respectively, in parallel with a stimulation of taurocholate excretion into bile by 29, 27 and 9% respectively. There was a close relationship between the extent of cell volume changes and taurocholate excretion into bile, regardless of whether cell volume was modified by tauroursodeoxycholate, amino acids or aniso-osmotic exposure. The data suggest that: (i) liver cell volume is one important factor determining bile flow and biliary taurocholate excretion; (ii) swelling-induced stimulation of taurocholate excretion into bile is probably not explained by alterations of the membrane potential; (iii) bile acids modulate liver cell volume; (iv) taurocholate-induced cholestasis may depend on cell volume; (v) stimulation of taurocholate excretion into bile by tauroursodeoxycholate can largely be explained by tauroursodeoxycholate-induced cell swelling.

Amino Acids↗
PubMed1998

Dietary protein intake and urinary excretion of calcium: a cross-sectional study in a healthy Japanese population.

To evaluate whether habitual excess protein intake is a significant risk factor for calcium loss, we studied the relation between urinary excretion of calcium and protein intakes, in 349 male and 406 female Japanese aged 20-79 y. The subjects were apparently healthy, free-living, and consuming diets of their own choosing. We divided the subjects into two groups: those aged 20-49 y and those aged 50-79 y. In each group, we observed a significant positive correlation between daily urinary excretion of calcium and protein intake. Calcium excretion also correlated positively with daily urinary excretion of urea. Multivariate analyses revealed that in each age group the relation between calcium excretion and urea excretion remained significant even after sex, age, body weight, urinary sodium excretion, and calcium intake were adjusted for. The correlation of calcium excretion with animal protein intake was significantly positive in both sexes and in each age group whereas that with plant protein was not. We observed a significant positive correlation between daily calcium excretion and daily urinary excretion of sulfate. The correlation in 50-79-y old subjects remained significant even after sex, age, body weight, sodium excretion, and calcium intake were adjusted for. Our findings suggest that excess protein, especially that rich in sulfur-containing amino acids, in habitual diets may augment calcium excretion in the urine, at least in the elderly.

Adult↗
PubMed1996

Reduced renal allograft survival is related to low urinary N-acetyl-beta-D-glucosaminidase excretion during the first posttransplant month.

The excretion of urinary N-acetyl-beta-D-glucosaminidase (NAG) was measured daily between day 7 and day 28 in 33 renal allograft recipients enjoying an entirely uncomplicated first postoperative month. Graft status was evaluated after 4 and 6 years and related to NAG excretion. After 4 years, 6 patients had experienced graft loss due to chronic rejection. Posttransplant urinary NAG excretion in the group of patients with failing grafts was significantly lower (9.4 +/- 6.3 vs. 17.2 +/- 8.5 U/g urinary creatinine, P = 0.036). Univariant analysis of recipient and donor characteristics revealed urinary NAG excretion to be the only parameter significantly differing between the groups. After 6 years, a total of 8 patients had lost their grafts. The posttransplant urinary NAG excretion in this group was 10.8 +/- 6.2 U/g; in the 25 patients with functioning grafts NAG excretion was 17.4 +/- 8.8 U/g (P = 0.064). A very low urinary NAG excretion ( < 7 U/g) was seen in 5 patients and associated with poor graft survival after 4 and 6 years (odds ratios 12.5 (1.9-82.1) and 6.9 (1.1-44.8), respectively. Kaplan-Meier analysis showed a reduced graft survival in this subgroup (P = 0.031). Receiver operating characteristics (ROC) analysis demonstrated an association between low NAG excretion and graft survival rates both at 4 and 6 years (area under the ROC curve 0.799 +/- 0.115, P, 0.05, and 0.747 +/- 0.104, P < 0.05, respectively). Cox proportional hazards analysis identified a low urinary NAG excretion as an independent prognostic risk factor. Urinary NAG excretion was expressed as unit per gram of urinary creatinine; as the amount of NAG excreted depends on the graft mass, and the amount of urinary creatinine depends on the recipient body mass, a low NAG excretion (in terms of U/g urinary creatinine) could be a surrogate marker of an unfavorable low graft to body weight ratio, which, in turn, might be associated with a reduced graft survival.

Acetylglucosaminidase↗
PubMed2003

Urinary excretion of monocyte chemoattractant protein-1 in autosomal dominant polycystic kidney disease.

Autosomal dominant polycystic kidney disease (ADPKD) progresses to renal insufficiency in >50% of patients and is characterized by interstitial inflammation and fibrosis in the end stage. In a rat model of ADPKD, monocytes accumulate within the renal interstitium in association with increased levels of monocyte chemoattractant protein-1 (MCP-1) in cyst mural cells and increased excretion of this chemokine into the urine. For determining the extent to which this chemokine is abnormally expressed in patients with ADPKD, a cross-section study was performed of MCP-1 in urine, serum, and cyst fluid and MCP-1 production by mural epithelial cells cultured from the cysts of human patients with ADPKD. Upper boundaries for urinary MCP-1 excretion (>263 pg/mg creatinine) and serum creatinine concentration (>1.5 mg/dl) determined in 19 normal individuals were used to sort 55 ADPKD patients into three groups. In group 1 (n = 13), urine MCP-1 excretion (136 +/- 14 pg/mg creatinine) was not different from normal volunteers (152 +/- 16 pg/mg); serum creatinine levels and urine total protein excretion were normal as well. In group 2 (n = 27), urine MCP-1 excretion was increased (525 +/- 39 pg/mg creatinine), but serum creatinine levels and urine protein excretion were not different from normal. In group 3 (n = 15), urine MCP-1 excretion increased further (1221 +/- 171 pg/mg), serum creatinine levels increased to 4.3 +/- 0.8 mg/dl, and urine protein excretion rose to 0.64 +/- 0.28 mg/mg creatinine. Serum MCP-1 levels of ADPKD patients (84 +/- 9.9 pg/ml; n = 15) did not differ from normal. Levels of MCP-1 much higher than in serum or urine were found in cyst fluids obtained from nephrectomy specimens (range, 767 to 40,860 pg/ml; mean, 6434 +/- 841 pg/ml; n = 73). Polarized, confluent cultures of ADPKD cyst epithelial cells secreted MCP-1 into the apical fluid to levels eightfold greater than in the basolateral medium. Similar results were obtained with tubule epithelial cells cultured from normal human renal cortex. On the basis of these results, it is concluded that urinary excretion of MCP-1 is increased in the majority of adult patients with ADPKD and that the source of some of this chemokine may be the mural epithelium of cysts. Furthermore, it seemed that urinary MCP-1 excretion may have increased in these ADPKD patients before appreciable increases in serum creatinine concentration or urine protein excretion were detected. It is reasonable to include urine MCP-1 excretion among candidate surrogate markers in controlled, longitudinal studies of ADPKD.

Adult↗
PubMed1992

Short-term indomethacin administration does not impair excretion of acute potassium load in humans.

Maintenance treatment with prostaglandin synthesis inhibitors often causes some degree of hyperkalemia, indicating impaired potassium (K) excretion. Hypoaldosteronism probably is a mediating factor, but it is unknown whether these drugs also impair renal K excretion directly. Indomethacin, for example, stimulates NaCl reabsorption in Henle's loop, and thus may impair K excretion by decreasing distal NaCl delivery. We therefore studied the effect of 1 day administration of indomethacin (50 mg tid) on the excretion of a single oral KCl (1 mmol kg-1 body weight) in six healthy volunteers taking a 40 mmol sodium diet. To allow analysis of renal sodium handling, clearance studies were performed during water loading. In this acute setting, indomethacin had no effect on plasma K, and did not decrease plasma aldosterone. However, indomethacin clearly reduced NaCl excretion. Nonetheless, the excretion of the K load was entirely normal. Excretion of the K load was accompanied by increased clearance of phosphate and uric acid, and natriuresis. Data derived from the maximal free water clearance were compatible with increased delivery to and decreased reabsorption from the diluting segment. Occurrence of these effects was not prevented by indomethacin, although overall NaCl excretion remained less than observed without indomethacin. Indomethacin reduced prostaglandin E2 excretion substantially. Apparently, in normal man indomethacin does not impair K excretion directly, even though it greatly reduces NaCl excretion. Moreover, the effects of K on renal NaCl handling, probably contributing to the excretion of a K load, are not dependent on renal prostaglandins.

Administration, Oral↗
PubMed1981

Effect of repeated doses of hydroflumethiazide on renal excretion of electrolytes and uric acid in healthy subjects.

Urinary excretion of electrolytes and uric acid was investigated in six healthy subjects during repeated oral administration of 100 mg hydroflumethiazide (HFT) daily for seven days, and related to urinary thiazide excretion. Mean 24 hr-urinary excretion of sodium and chloride increased 100% (P less than 0.02) after the first HFT-dose, whereas 24 hr-excretion values were at control level after the fourth and seventh doses. Mean 24 hr-urinary excretion of potassium was increased by 31% after the first HFT-dose (P less than 0.05) and by 47% after the fourth dose (P less than 0.05). After HFT was discontinued, mean urinary excretion rates of sodium and chloride dropped to 30% and that of potassium to 70% of control. In the state of fluid deficiency and elevated aldosterone concentration, there was a significant positive correlation between log excretion rate of HFT and excretion rate of sodium (r=0.68, P less than 0.002) calculated from excretion data 0-67, 6-12, and 12-14 hrs after the seventh dose. After the first dose of HFT, sodium excretion was also significantly correlated to log excretion rate of HFT (r=0.86, P less than 0.001) but was probably influenced by other factors as well. Mean serum concentration of uric acid increased significantly, but mean 24 hr-urinary excretion of uric acid was constant during HFT-treatment.

Adult↗