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PubMedDate not supplied

Influence of water and sodium diuresis and furosemide on urinary excretion of vitamin B(6), oxalic acid and vitamin C in chronic renal failure.

Urinary excretion of vitamin B(6), oxalic acid and vitamin C was investigated in 15 healthy subjects during maximal water diuresis and in the group of 12 patients in polyuric stage of chronic renal failure without dialysis treatment receiving a diet containing high sodium chloride (15g/day). Urinary excretions of the same parameters were investigated in another group of 15 patients in polyuric stage of chronic renal failure without dialysis treatment after i.v. administration of 20 mg furosemide. Urinary excretion of vitamin B(6), oxalic acid and vitamin C significantly increased during maximal water diuresis while during high intake of sodium chloride the urinary excretions of these substances were not affected. The results suggest that urinary excretion of vitamin B(6), oxalic acid and vitamin C depends on the urinary excretion of water. Intravenous administration of 20 mg furosemide led to an increase of urinary excretion of vitamin B(6), oxalic acid and vitamin C in patients with chronic renal failure. The increased urinary excretion of vitamin B(6) and vitamin C is a new negative side effect of furosemide and increased urinary excretion of oxalic acid is a new positive side effect in patients with chronic renal failure.

Adult↗
PubMed1982

Effect of exogenous adenosine 3':5'-cyclic monophosphate, parathyroid hormone and acetazolamide on electrolyte hormone and acetazolamide on electrolyte excretion by the isolated perfused rat kidney.

The effects of exogenous adenosine 3':5'-cyclic monophosphate (cyclic AMP), parathyroid hormone (PTH) and acetazolamide (Az) on renal calcium and phosphate excretion of the isolated perfused rat kidney were compared. Both PTH and Az evoked an early increase in urinary cyclic AMP excretion followed by a later more prolonged increase in phosphate excretion. All of the increased urinary cyclic AMP was derived from renal cells. Calcium excretion decreased with PTH but was unchanged with Az. Sodium and potassium excretion increased with Az but not PTH. Transitory urinary cyclic AMP excretion rates following bolus additions of exogenous cyclic AMP to perfusate were up to twentyfold greater than those evoked by PTH or Az but unassociated with changes in calcium, phosphate, sodium or potassium excretion. Sustained perfusate levels (above 0.5 microM) and excretion rates of cyclic AMP induced phosphaturia proportional to the perfusate cyclic AMP concentrations achieved up to 2.0 microM. Clearances of exogenous cyclic AMP exceeded inulin clearance at perfusate concentrations greater than 1.0 microM. Aminophylline evoked a small phosphaturia which increased further on addition of cyclic AMP to 5 microM. Glomerular filtration was not affected by any of the agents except Az. Since increased phosphate excretion could be evoked only at perfusate concentrations exceeding either plasma or intracellular concentrations observed in vivo, it is concluded that circulating cyclic AMP at levels in vivo is unlikely to mediate a significant fraction of the renal effects of PTH.

Acetazolamide↗
PubMed1981

Urinary excretion of alpha 2 mu-globulin and albumin by adult male rats following treatment with nephrotoxic agents.

Nephrotoxic agents such as puromycin aminonucleoside (PAN) and sodium maleate (MAL) have been used to induce experimental glomerular proteinuria and tubular disease, respectively. Current studies show that PAN caused a massive loss of albumin in the urine while not affecting the excretion of the smaller, sex-dependent alpha 2 mu-globulin. On the other hand, MAL which inhibits the reabsorption of proteins, increased the loss of both alpha 2 mu and albumin. Both nephrotoxic agents increased the excretion of albumin when administered to female rats. MAL-induced proteinuria was used as a direct measure of the renal load for alpha 2 mu and albumin. Renal loads and excretion of alpha 2 mu and albumin were measured in male rats maintained on 0, 20, and 50% casein diets. On the protein-free diet, the excretion of both alpha 2 mu and albumin was reduced (less than 1 mg daily); their renal loads were almost totally reabsorbed. On a 50% casein diet the reabsorption of alpha 2 mu was reduced from a normal of 60% to 10% of the renal load. Thus the high protein diet increased the excretion of alpha 2 mu while having little effect on the excretion of albumin. We suggest that dietary protein exerts two levels of control on the excretion of protein in the urine of the adult male rat. Protein-deficient diets stimulate the general reabsorption of proteins thereby minimizing the excretion of alpha 2 mu and albumin. High protein diets appear to reduce selectively the reabsorption of alpha 2 mu-globulin, thereby increasing its excretion in the urine.

Albumins↗
PubMed1991

Urine calcium excretion, nephrogenous cyclic-adenosine monophosphate and serum parathyroid hormone levels in patients with essential hypertension.

To evaluate the role of calcium and the parathyroid gland in the pathophysiology of essential hypertension, creatinine clearance, urinary excretion of sodium, calcium and nephrogenous cyclic adenosine monophosphate (NcAMP) and serum parathyroid hormone (PTH) levels were measured in 25 newly diagnosed essentially hypertensive patients before institution of any treatment and in 25 age- and sex-matched normal volunteers. While no significant differences in creatinine clearance, serum total calcium levels or 24-hour sodium excretion existed between the two groups, hypertensives had a higher mean (+/- SD) 24-hour calcium excretion rate (199.0 +/- 44.7 vs. 152.8 +/- 33.6 mg, p less than 0.001), a higher mean NcAMP excretion rate (2.54 +/- 0.8 vs. 1.87 +/- 0.5 nmol/100 ml glomerular filtrate, p less than 0.001) and a higher mean serum PTH concentration (1.87 +/- 0.6 vs. 1.53 +/- 0.4 ng/ml, p less than 0.001) than the normotensives. A significant positive correlation existed between calcium and sodium excretion in both hypertensives (r = 0.66, p less than 0.001)) and normotensives (r = 0.67, p less than 0.001), but given the same levels of creatinine clearance and sodium excretion, hypertensives excreted more calcium than normotensives (p less than 0.001)). In both hypertensives and normotensives, serum PTH levels were positively correlated with NcAMP excretion (r = 0.42, p less than 0.05, and r = 0.41, p less than 0.05, respectively) and the ratio of urinary sodium to urinary calcium excretion (r = 0.59, p less than 0.001, and r = 0.75, p less than 0.001), respectively). The above results suggest that in essential hypertension, increased activity of parathyroid glands may occur as a consequence of increased urinary calcium losses which are presumably due to an intrinsic defect in renal calcium handling.

Adult↗
PubMed1992

Enhanced urinary excretion of eicosanoids in fawn-hooded rats.

Compared to Wistar (WAG) rats, rats of the fawn-hooded (FH) strain have a high level of glomerular filtration rate (GFR) and urinary protein excretion (UpV). To investigate the possible role of vasoactive eicosanoids in this spontaneous model of hyperfiltration and proteinuria, we compared the urinary excretion of thromboxane-B2 (TxB2), 6-keto-prostaglandin (Pg)F1 alpha and PgE2 in male FH and WAG rats during normal ageing. All measurements were performed sequentially in the same animals 12, 24, 36, 48 and 60 weeks after weaning. Throughout the study, GFR was higher in FH rats as were the filtration fraction and UpV. From week 24, UpV in FH rats increased progressively. No elevations in UpV were observed in WAG rats. At weeks 12 and 24, the urinary excretion of TxB2, 6-keto-PgF1 alpha and PgE2 was 2-4 times higher in FH rats compared to WAG rats. With time, a shift in the urinary excretion from vasodilator to vasoconstrictor eicosanoids was observed, i.e., the excretion of PgE2 declined and that of TxB2 increased. Proteinuria in FH rats was positively correlated with TxB2 excretion and negatively correlated with PgE2 excretion. We conclude that in FH rats, early hyperfiltration coincides with enhanced urinary excretion of all eicosanoids. Subsequent progressive proteinuria is associated with an increase in TxB2 and a decrease in PgE2 excretion.

Age Factors↗
PubMed1997

Urinary excretion of endogenous ouabain-like substance is reduced in NaCl supplemented premature infants.

Ouabain or an isomer has been identified as endogenous ouabain-like substance (EOLS). The role of EOLS in the adaptation of premature infants to alterations of sodium balance was investigated by measuring urinary ouabain excretion serially in 9 low birth weight premature infants with (group S, mean birth weight 1,578 g, mean gestational age 30.4 weeks) and without (group NS, mean birth weight 1,537 g, mean gestational age 30.8 weeks) NaCl supplementation. The study was performed on the 7th day and weekly thereafter until the 5th week of life. NaCl supplementation was given in a dose of 3-5 and 1.5-2.5 mmol/kg/day at the postnatal ages of 8-21 and 22-35 days, respectively. Prior to NaCl supplementation, urinary ouabain excretion was similar in the two groups (146.2 +/- 16.8 pg/kg/h in group S versus 180.0 +/- 9.6 pg/kg/h in group NS) and remained at about the same level throughout the study when supplemental NaCl was provided. In infants of group NS, urinary ouabain excretion increased significantly by the 3rd week (p < 0.01) and no consistent change occurred later on. As a result, the differences in urinary ouabain excretion between the two groups proved to be significant during weeks 2-5 (p < 0.001). Essentially the same pattern of ouabain excretion was seen when it was expressed in terms of pg/mg creatinine. In infants receiving high sodium diet there was a significant positive correlation between urinary sodium and ouabain excretion. It is concluded that premature infants receiving low sodium intake have elevated EOLS excretion by the 3rd week of life. Although the relationship between ouabain and sodium excretion in supplemented premature infants suggests some physiological significance for sodium excretion, ouabain does not appear to be regulated by extracellular volume.

Cohort Studies↗
PubMed1997

Urinary excretion of endogenous ouabain-like substance in furosemide-treated neonates: its relation to renal excretory pattern and endocrine factors.

The present study was undertaken to define the possible role of endogenous ouabain-like substance (EOLS) in controlling renal excretory pattern, in mediating the renal responses to furosemide and in inducing endocrine reactions in furosemide-treated neonates. Ten newborn infants with mean birthweight of 2,752 g and mean gestational age of 37.1 weeks were given furosemide in a dose of 1 mg/kg. Prior to and following furosemide therapy, urine was collected for a period of 12 h and analyzed for creatinine, osmolality, sodium and potassium, as well as for EOLS, arginine vasopressin (AVP), aldosterone and endothelin-1 (ET-1). In response to furosemide administration, urine flow rate and urinary osmolar, sodium and potassium excretion increased significantly, whereas creatinine excretion remained unchanged. Furthermore, following furosemide therapy, urinary excretion of EOLS (148.7 +/- 70.8 vs. 200.1 +/- 98.1 pg/kg/h) and AVP (19.5 +/- 5.4 vs. 27.8 +/- 7.8 pg/kg/h) tended to increase, whereas ET-1 (36.0 +/- 5.6 vs. 61.4 +/- 8.7 fmol/kg/h, p < 0.01) and aldosterone (507 +/- 120 vs. 751 +/- 203 ng/kg/h, p < 0.05) increased significantly. Prior to furosemide, urinary EOLS excretion was found to correlate positively with diuresis (r = 0.80, p < 0.01), sodium (r = 0.91, p < 0.001), creatinine (r = 0.75, p < 0.001), osmolar (r = 0.96, p < 0.001), ET-1 (r = 0.90, p < 0.001) and AVP (r = 0.92, p < 0.001) excretion. After furosemide, urinary EOLS excretion significantly correlated only with diuresis (r = 0.69, p < 0.05), ET-1 (r = 0.77, p < 0.01) and AVP (r = 0.92, p < 0.001). Urinary EOLS proved to be independent of aldosterone excretion irrespective of furosemide administration. It is concluded that urinary EOLS excretion is closely related to neonatal renal excretory pattern and it may have a role in controlling diuresis and natriuresis. The renal response to furosemide appears to be independent of EOLS, although interdependent endocrine reactions can be induced by furosemide which may modulate the production rate and urinary excretion of EOLS.

Aldosterone↗
PubMed1984

Urinary kallikrein excretion in patients with primary aldosteronism: differentiation of adrenal adenoma from idiopathic adrenal hyperplasia.

Following 7 days on a low sodium diet, a regular sodium diet or a high sodium diet each, urine samples were collected from 37 subjects in the final days of each sodium treatment. Urinary kallikrein excretion was determined in 9 patients with primary aldosteronism, 15 normal subjects and 13 patients with essential hypertension. Urinary aldosterone excretion, plasma renin activity (PRA), urinary sodium excretion, urinary potassium excretion and p-aminohippuric acid clearance were also determined on the same days. Levels of urinary kallikrein excretion in patients with primary aldosteronism due to aldosterone-producing adenoma (APA) were greater (p less than 0.05 to p less than 0.001) than those in patients with primary aldosteronism due to idiopathic adrenal hyperplasia (IHA) under any sodium diet. Other examined variables were of limited value in differentiating patients with APA from those with IHA. Urinary kallikrein excretion, urinary excretion of electrolyte, urinary aldosterone excretion, PRA and PAH clearance were similar in normal subjects and patients with essential hypertension. It appears reasonable to conclude from these data that urinary kallikrein does not play an important role in the pathogenesis of essential hypertension, and elevated urinary kallikrein excretion in patients with primary aldosteronism due to APA can be used for biochemical differentiation from those with IHA.

Adenoma↗
PubMed1978

Role of hemodynamic changes in the increased cation excretion after acute unilateral nephrectomy in the anesthetized dog.

Studies were carried out in anesthetized dogs to characterize the increase in cation excretion which occurs after acute unilateral nephrectomy (AUN). 60 min after AUN, cation excretion had increased from 31.5+/-2.7 to 66.3+/-12.0 mueq/min (P < 0.005) and fractional cation excretion had increased from 0.56+/-0.05 to 1.03+/-0.14% (P < 0.005), as the glomerular filtration rate was unchanged and renal blood flow fell. The increased cation excretion was accompanied by an increase in fractional phosphate excretion, no change in chloride excretion, and a fall in renin secretion. These alterations in renal function were associated with marked changes in systemic hemodynamics: cardiac output fell from 2.52+/-0.24 to 1.85+/-0.16 liters/min (P < 0.001), as diastolic pressure rose without an overall increase in mean arterial pressure, and heart rate fell. To assess the importance of these hemodynamic changes in the renal response, AUN in a separate group of dogs was accompanied by the simultaneous opening of a surgically created femoral artery-to-vein fistula at flow matching the blood flow to the removed kidney. When this was done, no alterations in systemic or renal hemodynamics were observed, and cation excretion did not differ from control. Subsequent closure of the fistula then caused a fall in cardiac output from 2.15+/-0.25 to 1.77+/-0.20 liters/min (P < 0.05), and an increase in cation excretion from 34.6+/-9.5 to 52.3+/-13.7 mueq/min (P < 0.01), thus mimicking the findings with AUN alone.These results demonstrate that AUN causes hemodynamic changes resembling those seen on closure of a chronic arteriovenous fistula. Prevention of these hemodynamic changes after AUN also prevents the functional adjustment of the remaining kidney, suggesting that they may be important in initiating the renal response. The increased electrolyte excretion after AUN may occur through mechanisms similar to that seen on closure of an arteriovenous fistula.

Animals↗
PubMed1986

Role of atrial natriuretic peptide in adaptation of sodium excretion with reduced renal mass.

The kidney maintains constancy of body fluid volume by regulating urinary sodium (Na) excretion. In chronic renal failure, the reduction in glomerular filtration rate (GFR) is accompanied by an increase in Na excretion per nephron if dietary Na intake is not changed. Reduction in Na intake in proportion to reduced GFR obviates this adaptive increase in tubule Na excretion. To examine the potential role of endogenous atrial natriuretic peptide (ANP) in modulating the enhanced Na excretion per nephron in chronic renal failure, we studied rats subjected to 5/6 nephrectomy or sham operation on low, normal, and high Na intakes. Urinary Na excretion increased with increasing dietary Na in all groups, and Na excretion per nephron was increased in 5/6 nephrectomized rats as compared with sham-operated rats on the higher Na intakes. Plasma ANP levels were unaffected by dietary Na manipulations in sham-operated rats, but rose progressively in 5/6 nephrectomized rats with increasing Na intake. Despite extensive nephron reduction, however, plasma ANP levels failed to rise in uremic rats on low Na diets and in this group Na excretion per nephron also failed to rise. We conclude that enhanced ANP secretion may play an important role in promoting the adaptive increase in Na excretion per nephron in chronic renal failure. Restriction of dietary Na in the setting of reduced GFR obviates the stimulation of ANP secretion as well as the adaptive increase in Na excretion rate per nephron.

Adaptation, Physiological↗
PubMedDate not supplied

Effects of age, feeding regimen, and glucocorticoids on catecholamine and cortisol excretion in preterm infants.

BACKGROUND: The sympathoadrenal system is important in maintaining normal physiologic functioning in infants and increased output also can reflect stress. We sought to determine the effects of age, feeding regimen, and glucocorticoids on catecholamine and cortisol excretion in preterm infants and to assess whether a particular strategy of feeding enhanced sympathoadrenal development or was stressful. METHODS: Preterm infants (26-30 wk gestation; n = 171) were assigned randomly to begin trophic feedings from day 4 through 14 (trophic group) or to start feedings at day 15 (standard group) with feedings administered either by bolus every 3 hours (bolus) or continuously over 24 hours (continuous). At 10, 28, 40, 50, and 60 days of age, urine was collected continuously for 6 hours for measurement of catecholamines (norepinephrine, epinephrine, dopamine), cortisol, and creatinine. Data were available for 98 infants. RESULTS: Norepinephrine excretion increased with postnatal age. The increase with age was significantly greater in the trophic group compared with that in the standard group. Epinephrine excretion did not change with age, and there were no differences between trophic and standard groups. Dopamine excretion increased with age but was similar between trophic and standard groups (borderline significantly greater in the trophic group). Cortisol excretion increased with age and also was similar between trophic and standard groups. There was no effect on catecholamine or cortisol excretion of bolus vs continuous feedings, antenatal or postnatal corticosteroids, gestational age at birth, age at which full feedings were attained, or use of human milk compared with preterm formula. CONCLUSIONS: The greatest determinant of catecholamine and cortisol excretion is postnatal age. Feeding method, type of feeding, and glucocorticoid administration in the amounts customarily used have little significant effect on catecholamine or cortisol excretion. The apparent link between early feeding and norepinephrine (and possibly dopamine) excretion warrants further investigation.

Age Factors↗
PubMedDate not supplied

Polyamine excretion in depleted patients with gastrointestinal malignancy: effect of perioperative nutrition and tumor removal.

Polyamines, synthesized by all mammalian cells, are involved in protein and energy metabolism. We measured urinary excretion of polyamines, putrescine, spermidine, spermine, and their metabolites N1-acetylspermidine and N8-acetylspermidine, resting energy expenditure, and nitrogen excretion in 12 depleted patients with gastrointestinal malignancy during preoperative and postoperative parenteral nutrition and in 7 patients with multiple trauma receiving similar parenteral nutrition. During preoperative nutrition support, the excretion of putrescine (p less than .05) and total polyamines (p less than .01) increased by 420% and 60%, respectively. Increases in energy balance and resting energy expenditure during nutrition could entirely explain the observed changes in polyamine excretion. Preoperatively, the excretion of N1-acetylspermidine (p less than .05), N8-acetylspermidine (p less than .001) and total polyamines (p less than .05) was higher in patients with a surgically noncurable tumor than in those with a surgically curable tumor. The energy balance and resting energy expenditure could also explain the differences in polyamine excretion between patients with surgically curable and noncurable disease, excluding the increased N8-acetylspermidine. Postoperatively, the excretion of N8-acetylspermidine in patients with multiple trauma without malignancy and in patients with palliative operation was similar, and was higher than in patients with a totally resected malignancy (p less than .01). Our results suggest that the excretion of polyamines reflects the activity of energy metabolism in general and that polyamine excretion is not specific for any particular disease.

Adult↗
PubMed1980

Parathyroid hormone does not increase nephrogenous cyclic AMP excretion by the dog.

The renal excretion of nephrogenous cyclic AMP (NcAMP) increases in response to parathyroid hormone (PTH) in man, and thereby serves as a test of parathyroid function. However, during studies of calcium-PTH (PTH) in man, and thereby serves as a test of parathyroid function. However, during studies of calcium-PTH interrelationships in dogs we observed no change in total urinary cAMP (UcAMP) excretion when endogenous plasma PTH levels were increased up to 10-fold. This study was designed to investigate the effects of physiologic and pharmacologic levels of PTH on NcAMP and UcAMP excretion in the dog. Maintaining plasma Ca 2 mg/dl below normal for 40 minutes caused an 8-fold increase in plasma PTH concentration, a 50% increase in the urinary fractional excretion of phosphate (FEP) but no changes in plasma cAMP levels or in UcAMP or NcAMP excretion. Infusion of a pharmacologic amount of parathyroid extract (15 U/min for 20 min) increased plasma cAMP 5-fold, UcAMP excretion 3-fold and FEP by 50% but was without effect on NcAMP excretion. We conclude that NcAMP excretion is not stimulated by PTH in the dog and thus cannot be used as an index of PTH action in vivo. The increase in UcAMP excretion by pharmacologic amounts of PTH results from glomerular filtration of increased plasma cAMP, which may be generated in bone.

Animals↗
PubMed1993

Chiroinositol deficiency and insulin resistance. I. Urinary excretion rate of chiroinositol is directly associated with insulin resistance in spontaneously diabetic rhesus monkeys.

Previously, we demonstrated that nondiabetic insulin-resistant monkeys had reduced covalent insulin activation of muscle glycogen synthase (GS) compared to normal monkeys and that covalent insulin activation of adipose tissue GS was absent in these monkeys. Covalent insulin activation of muscle and adipose tissue GS in monkeys with impaired glucose tolerance and noninsulin-dependent diabetes (NIDDM) was also absent. As in humans, monkeys with NIDDM have a lower urinary excretion rate of chiroinositol (CI), a component of a putative mediator of insulin action, compared to normal monkeys. To determine whether the urinary excretion rate of CI was related to insulin resistance, which develops naturally in many obese rhesus monkeys, we examined the relationships between 24-h urinary CI excretion rate and 1) whole body insulin-mediated glucose disposal rates (M) and insulin-mediated changes in 2) the skeletal muscle GS activity ratio (sm delta GSAR), 3) the skeletal muscle glycogen phosphorylase activity ratio, and 4) the adipose tissue GS activity ratio (at delta GSAR) in 27 monkeys ranging from normal (n = 12) to insulin resistant (n = 8) to overtly diabetic (n = 7). The urinary CI excretion rate was significantly correlated with M (r = 0.47; P < 0.02), sm delta GSAR (r = 0.38; P < 0.05), skeletal muscle glycogen phosphorylase activity ratio (r = -0.49; P < 0.01), and at delta GSAR (r = 0.46; P < 0.02). The urinary CI excretion rate was also correlated with glucose tolerance (r = 0.39; P < 0.05). There was a wide range of urinary CI excretion rates (0.42-5.17 mumol/day) in monkeys with normal fasting plasma glucose concentrations. However, of the 7 diabetic monkeys, 6 had a urinary CI excretion rate below 2.0 mumol/day, and in the subgroup of 16 monkeys with a urinary CI excretion rate less than 2.0 mumol/day, the associations of urinary CI with M rate (r = 0.65; P < 0.005), glucose tolerance (r = 0.63; P < 0.01), and sm delta GSAR (r = 0.73; P < 0.001) increased in strength and significance. We propose that the urinary CI excretion rate may be 1) a biochemical indicator of both in vivo and in vitro insulin resistance and 2) a noninvasive diagnostic tool with potential for the identification of those individuals at risk for NIDDM and other related diseases with insulin resistance.

Analysis of Variance↗
PubMed1983

Effects of alterations in sodium and water metabolism on urinary excretion of active and inactive kallikrein in man.

Renal kallikrein is present in human urine in both an active and an inactive form. Several previous studies have examined the response of active kallikrein excretion to alterations in sodium and water metabolism, but the response of inactive kallikrein has not been evaluated systematically. We have developed a method for determining inactive kallikrein in urine using two assays. Active kallikrein is measured using a kininogenase assay. Total (active plus inactive) kallikrein is measured using a direct RIA. Inactive kallikrein is calculated from the difference between active and total kallikrein excretion. We have used this technique to study the effect of alterations in sodium and water metabolism on kallikrein excretion. Acute volume expansion with saline and moderate acute or chronic increases in water intake did not alter the excretion of either active or inactive kallikrein. Dietary sodium restriction increased the excretion of total kallikrein by 30%; active kallikrein increased 82%, while inactive kallikrein excretion was found to be unchanged. Spironolactone reduced total kallikrein excretion in subjects on a low salt diet. Again, the change in excretion was entirely attributable to the active form of the enzyme. Total kallikrein excretion increased during the first 3 days of fludrocortisone administration in subjects on a high salt intake and then plateaued. Active kallikrein increased progressively throughout the 7-day study period. Inactive kallikrein increased during the first 4 days, then fell to control levels. Thus, mineralocorticoid initially stimulates the formation and/or release into urine of both active and inactive kallikrein. Later, reciprocal changes in active and inactive enzymes occur.

Body Water↗
PubMed1994

The impact of gender and puberty on reference values for urinary growth hormone excretion: a study of 3 morning urine samples in 517 healthy children and adults.

Some recent studies have indicated that measurement of urinary GH (U-GH) excretion may be a useful tool for the evaluation of GH insufficiency in children with growth disorders, although some investigators are skeptical about the diagnostic value of U-GH. Most current assays are only available for specific laboratories or require time-intensive pretreatments of the specimens. This limits the possibility for many centers to compare their patients' data with others or to establish their own reference ranges for U-GH excretion. Therefore, we investigated the performance of a commercially available kit, which allows direct measurement of U-GH in untreated urine specimens. We established a reference range for the geometric mean of 3 morning urine samples in 446 healthy children and 71 adults. U-GH could be determined in all but 9 of 1526 samples (99.4%). U-GH excretion was significantly dependent on pubertal maturation (P < 0.001) and sex (P < 0.001), whereas age had no significant influence in the prepubertal group (P > 0.3). Peak values occurred in Tanner stages 3 and 4 (369 and 391 pg/h in females; 503 and 882 pg/h in males), corresponding to an age interval of 11-18 yr in boys and 9-15 yr in girls. Short collection periods (< 6 h) were related to low values for U-GH excretion (nanograms per night; P < 0.02). This time effect disappeared if U-GH excretion was expressed as picograms per h. If U-GH was related to creatinine output, there was a decrease in U-GH excretion during prepuberty, a blunting of the pubertal peak, and lower values in adults than in prepubertal children (P < 0.0002). The intraindividual variation in U-GH excretion (picograms per h) ranged from 40-61%, constituting approximately two thirds of the interindividual variation. This variation was not lowered by relating U-GH to creatinine. We conclude that the assay was suitable for measurement of U-GH excretion in virtually all healthy volunteers. Sex and pubertal stage as well as urinary volume and clock times for collection periods should be registered when establishing a reference range for U-GH excretion and applying it for clinical purposes. Our reference values may be useful for further studies of patients with GH disorders.

Adolescent↗
PubMed1990

Biliary excretion of mitomycin C dextran conjugates in relation to physicochemical characteristics of carrier dextran.

Biliary excretion characteristics of polymeric prodrugs of mitomycin C (MMC), mitomycin C-dextran conjugates with cationic or anionic charge (MMC-Dcat, MMC-Dan) and with different molecular weights of dextran (10,000, 70,000, and 500,000) were studied in rat. Following intravenous injection, bile was periodically collected and concentrations of free and dextran-conjugated MMC in it were determined by bioassay. MMC administered as a free form was excreted rapidly into bile and 1.8% of the dose was recovered within 2 h. A small amount of MMC was gradually excreted into bile after administration of all MMC-Ds and total recovery at 8 h was less than 1% of dose. In this case, a major part of excreted MMC was recovered as a conjugated form. MMC-Dcat gave a larger total excretion of MMC than MMC-Dan and excretion was also affected by the molecular weight of carrier dextran. The biliary recovery of MMC-Dcat labeled with 14C at a spacer moiety was significantly higher than that of conjugated MMC determined by bioassay suggesting release and/or inactivation of MMC in MMC-D during the circulation in the body. These results were compared with biliary excretion of model macromolecules with the same molecular weight but different electric charge in order to clarify the effect of electric charge on the biliary excretion of macromolecules. Cationic macromolecules exhibited higher biliary excretion in relation to greater hepatic uptake.

Animals↗
PubMed1985

Urinary excretion characteristics of a polymeric prodrug of mitomycin C, mitomycin C-dextran conjugate.

Urinary excretion characteristics of a polymeric prodrug of mitomycin C (MMC), mitomycin C-dextran conjugate (MMC-D), following intravenous administration was studied in rats. Three types of MMC-D, conjugates with dextrans of molecular weights of 10000, 70000 and 500000, were tested and urine concentration of MMC, dextran and spacer were determined by three analytical methods, i.e., bioassay, anthrone method and radioactivity counting. MMC was assayed separately as a free form and conjugated form based on antimicrobiological activity. MMC administered as a free form was excreted rapidly into urine but only a small amount of MMC was excreted following the administration of MMC-D. The excreted amount of MMC in a conjugated form varied with the size of carrier dextran while similar sustained excretion was observed regardless of the carrier size. The excretion of carrier dextran determined by anthrone method was confined as the molecular weight was increased. The effect of molecular weight was also observed in the case of spacer-introduced dextran (dextran-C6 spacer) and original dextran. Compared with neutral dextran, cationic MMC-D and anionic dextran-C6 spacer exhibited diminished excretion, indicating the effect of charge on urinary excretion. The urinary recovery of radioactivity was almost in accordance with that of carrier dextran. However, the urinary recovery of MMC based on biological activity was considerably lower than that of carrier dextran. It was suggested that MMC-D underwent inactivation to a great extent before releasing active MMC in the body. The effect of physicochemical properties such as molecular weight and electric charge on the urinary excretion of the polymeric prodrug was thus elucidated.

Animals↗