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Fractional Excretion of Sodium

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1721. A Study to Evaluate the Effects of SB-751689 or rhPTH(1-34) on Excretion of Calcium and Phosphate in Women

100 mg Outcome Measures Go to Primary Outcome Measures : renal fractional clearance of calcium and phosphate [ Time Frame: over 1 month ] Secondary Outcome Measures : renal fraction clearance of electrolytes, cAMP, safety measures, and serum biomarkers [ Time Frame: over 1 month ] urinary excretion of sodium, magnesium, potassium, bicarbonate, and chloride Albumin-adjusted serum calcium levels Vitamin D and P1NP levels Plasma levels of SB-751689 and rhPTH(1-34) Plasma PTH Adverse event reports, 12 (...) of SB-751689 (400 mg or 100 mg) or rhPTH(1-34) on the Fractional Renal Excretion of Calcium and Phosphate in Healthy Postmenopausal Females. Study Start Date : August 2007 Actual Primary Completion Date : January 2008 Actual Study Completion Date : January 2008 Resource links provided by the National Library of Medicine related topics: available for: Arms and Interventions Go to Intervention Details: Drug: rhPTH(1-34) Drug: SB-751689 100 mg Drug: SB-751689 400 mg Other Names: rhPTH(1-34) SB-751689

2007 Clinical Trials

1722. Study Evaluating The Effect Of Ramipril On Urinary Protein Excretion In Renal Transplant Patients Converted To Sirolimus

Study Evaluating The Effect Of Ramipril On Urinary Protein Excretion In Renal Transplant Patients Converted To Sirolimus Study Evaluating The Effect Of Ramipril On Urinary Protein Excretion In Renal Transplant Patients Converted To Sirolimus - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save this study Warning You have reached the maximum (...) number of saved studies (100). Please remove one or more studies before adding more. Study Evaluating The Effect Of Ramipril On Urinary Protein Excretion In Renal Transplant Patients Converted To Sirolimus The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our for details. ClinicalTrials.gov Identifier: NCT00502242 Recruitment Status : Completed First

2007 Clinical Trials

1723. Effects of ibuprofen and indomethacin on urinary antidiuretic hormone excretion in preterm infants treated for patent ductus arteriosus. (Abstract)

of 5 mg/kg each after 24 and 48 h or three doses at 12-hour intervals of indomethacin (n = 24), 0.2 mg/kg, both infused continuously over a period of 15 min. Urinary ADH excretion, diuresis, serum creatinine, urinary sodium, fractional excretion of sodium, and urinary osmolality were measured before and after treatment.Indomethacin treatment caused a significant decrease in urinary ADH excretion (21.8 +/- 20.8 vs. 13.8 +/- 12.9 pg/ml; p < 0.05), along with a significant reduction in urinary sodium (...) (92.1 +/- 36.1 vs. 64.8 +/- 35.6; p < 0.05), fractional excretion of sodium (68.5 +/- 37.1 vs. 45.6 +/- 37.1; p < 0.05), and urinary osmolality (276.2 +/- 103.9 vs. 226.4 +/- 60.3; p < 0.05). Ibuprofen treatment did not modify urinary ADH excretion and caused a statistically insignificant decrease in urinary sodium and in fractional excretion of sodium.Compared with ibuprofen, indomethacin caused a significant reduction in urinary ADH excretion and a significant decrease in urinary sodium

2005 Fetal diagnosis and therapy Controlled trial quality: uncertain

1724. Urinary excretion of aquaporin-2 after furosemide and felodipine in healthy humans. (Abstract)

has not been studied in humans. We sought to test the hypotheses that urinary excretion of aquaporin-2 (U-AQP2) increases after a single intravenous dose of furosemide, and that U-AQP2 decreases after a single oral dose of felodipine.In two randomized, single-blind, placebo-controlled, cross-over studies, we measured the effect of furosemide and felodipine on U-AQP2, urine volume, free water clearance (CH2O), and fractional excretion of sodium (FENa) in 13 healthy subjects in each study. Plasma (...) Urinary excretion of aquaporin-2 after furosemide and felodipine in healthy humans. Furosemide inhibits renal sodium and chloride reabsorption in the loop of Henle. A compensatory increased reabsorption of sodium and water takes place in the collecting duct. It is not known whether aquaporin-2 (AQP2) renal water channels are involved in this compensatory reabsorption. In animals, dihydropyridine derivatives of calcium channel blockers down-regulate AQP2 in the collecting duct, but the effect

2005 Scandinavian journal of clinical and laboratory investigation Controlled trial quality: uncertain

1725. Increased urinary aquaporin-2 excretion in response to furosemide in patients with chronic heart failure. (Abstract)

tested the hypothesis that U-AQP2 increases after a single intravenous dose of furosemide in CHF patients.In a randomized, single-blind, placebo-controlled, crossover study, we measured the effect of furosemide (80 mg) on U-AQP2, urine volume, free water clearance (C(H2O)) and fractional excretion of sodium (FE(Na)) in 12 CHF patients. Plasma concentrations of vasopressin (AVP), renin (PRC), angiotensin II (Ang II), aldosterone (Aldo), atrial (ANP) and brain natriuretic peptides (BNP) were measured (...) Increased urinary aquaporin-2 excretion in response to furosemide in patients with chronic heart failure. Patients with chronic heart failure (CHF) have decreased ability to excrete water and increased urinary excretion of aquaporin-2 (U-AQP2). The natriuretic and diuretic effects of furosemide are antagonized by an increased reabsorption of sodium and water in the collecting ducts. It is unknown whether aquaporin-2 (AQP2) renal water channels are involved in this compensatory reabsorption. We

2006 Scandinavian journal of clinical and laboratory investigation Controlled trial quality: uncertain

1726. Maxi-K channels contribute to urinary potassium excretion in the ROMK-deficient mouse model of Type II Bartter's syndrome and in adaptation to a high-K diet. Full Text available with Trip Pro

Maxi-K channels contribute to urinary potassium excretion in the ROMK-deficient mouse model of Type II Bartter's syndrome and in adaptation to a high-K diet. Type II Bartter's syndrome is a hereditary hypokalemic renal salt-wasting disorder caused by mutations in the ROMK channel (Kir1.1; Kcnj1), mediating potassium recycling in the thick ascending limb of Henle's loop (TAL) and potassium secretion in the distal tubule and cortical collecting duct (CCT). Newborns with Type II Bartter (...) are transiently hyperkalemic, consistent with loss of ROMK channel function in potassium secretion in distal convoluted tubule and CCT. Yet, these infants rapidly develop persistent hypokalemia owing to increased renal potassium excretion mediated by unknown mechanisms. Here, we used free-flow micropuncture and stationary microperfusion of the late distal tubule to explore the mechanism of renal potassium wasting in the Romk-deficient, Type II Bartter's mouse. We show that potassium absorption in the loop

2006 Kidney International

1727. Reduced urinary excretion of thiazide-sensitive Na-Cl cotransporter in Gitelman syndrome: preliminary data. (Abstract)

Reduced urinary excretion of thiazide-sensitive Na-Cl cotransporter in Gitelman syndrome: preliminary data. The relationship between SLC12A3 mutations and actual sodium-chloride (Na-Cl) cotransporter (NCC) expression in patients with Gitelman syndrome (GS) was rarely evaluated. Detection of urinary thiazide-sensitive NCC was not tried in patients with GS.Case series.6 patients with GS and 1 patient with surreptitious vomiting.Renal clearance study, mutation analysis using reverse-transcription (...) polymerase chain reaction and direct sequencing for the SLC12A3 gene, and immunohistochemical staining for NCC, Na-K-2Cl-cotransporter, alpha1-subunit of Na(+),K(+)-ATPase, and calbindin-D(28K) of the renal biopsy specimens were performed. Membrane fractions of urine were obtained by using differential centrifugation and probed with antibodies against human NCC and aquaporin 2.Results of clearance studies were consistent with GS, showing decreased distal fractional chloride reabsorption with only

2007 American Journal of Kidney Diseases

1728. Angiotensin II blockade does not prevent renal effects of L-NAME in sodium-repleted humans. (Abstract)

placebo or 50 mg losartan to block Ang II receptors. With placebo, L-NAME produced no change in MAP from 0 to 45 minutes (period 1) and only a 5% increase at 45 to 90 minutes (period 2) of infusion. Effective renal plasma flow (ERPF, PAH clearance) and glomerular filtration rate (GFR, inulin clearance) declined by 11.7% and 8.0%, respectively in period 1 and by 14.6% and 11.6%, respectively, in period 2. Calculated renal vascular resistance (RVR) increased by 13.0% to 20.6%. Fractional excretion of Na (...) Angiotensin II blockade does not prevent renal effects of L-NAME in sodium-repleted humans. In seven healthy, young subjects on a 240 mmol sodium diet, mean arterial pressure (MAP), renal hemodynamics, and renal handling of Na and exogenous Li were measured at baseline and during short-term nitric oxide (NO) blockade with a 90-minute infusion of 3.0 microg x kg(-1) x min(-1) of N(G)-L-arginine methyl ester (L-NAME). The infusion was performed twice: after a 3-day pretreatment with either

1997 Hypertension

1729. Circulating angiotensin II and renal sodium handling in man: a dose-response study. (Abstract)

Circulating angiotensin II and renal sodium handling in man: a dose-response study. 1. Animal studies have shown that angiotensin II has a biphasic effect on urinary sodium excretion. To examine whether this is also true in man, we studied seven salt-replete male subjects in a single-blind placebo-controlled manner. 2. While undergoing maximum diuresis, subjects were infused with 0, 1, 2, 5 or 10 ng of angiotensin II min-1 kg-1 over 80 min. Subjects were studied while seated, and stood every 20 (...) min for urine collection. 3. Angiotensin II produced a dose-dependent antidiuretic effect. The urine flow rate, in ml/min expressed as the change from baseline with increasing dose of angiotensin, was: +3.4 +/- 1.77, -1.26 +/- 0.49 (P < 0.05), -2.75 +/- 1.23 (P < 0.05), -4.21 +/- 0.82 (P < 0.05) and -6.51 +/- 1.07 (P < 0.01). 4. In contrast, the effect of angiotensin II on sodium excretion showed a flat dose-response curve beyond 5 ng min-1 kg-1. The urinary sodium excretion, in mumol/min

1993 Clinical science (London, England : 1979)

1730. Sodium restriction versus daily maintenance replacement in very low birth weight premature neonates: a randomized, blind therapeutic trial. (Abstract)

sodium or salt restriction with physician-prescribed parenteral fluid intake. Maintenance-group infants received 3 to 4 mEq of sodium per kilogram per day; restricted infants received no sodium supplement other than with such treatments as transfusion. Sodium balance studies conducted for 5 days demonstrated that maintenance salt intake resulted in a daily sodium balance near zero, whereas sodium-restricted infants continued to excrete urinary sodium at a high rate, which promoted a more negative (...) sodium-restricted infants (less than 130 mEq/L); however, the restricted infants were more likely to have normal serum osmolality (p less than 0.05). Both groups of infants produced urine that was neither concentrated nor dilute, with a high fractional excretion of sodium; renal failure was not observed. The mortality rate was not affected, but the incidence of bronchopulmonary dysplasia was significantly less in the sodium-restricted babies (p less than 0.02). We conclude that in tiny premature

1992 The Journal of pediatrics Controlled trial quality: uncertain

1731. Atrial natriuretic peptide-cyclic GMP relationships in normal humans: effects of dietary sodium intake. (Abstract)

normotensive subjects on their normal sodium intake and (ii) 12 subjects on the 5th day of a low and on the 5th day of a high sodium intake. 3. Plasma cyclic GMP, urinary cyclic GMP and fractional excretion of cyclic GMP in 30 normotensive subjects on their normal sodium intake were (means +/- SEM) 5.4 +/- 0.5 pmol/ml, 434.5 +/- 31.8 pmol/min and 86.9 +/- 8.6%, respectively. There were significant correlations between urinary cyclic GMP and its corresponding filtered load (r = 0.55) and between the renal (...) clearance of cyclic GMP and that of creatinine (r = 0.44), but there were no significant associations between circulating atrial natriuretic peptide and plasma cyclic GMP or the fractional excretion of cyclic GMP or between urinary sodium and the fractional excretion of cyclic GMP. 5. Plasma atrial natriuretic peptide was significantly raised on the 5th day of the high sodium intake compared with the low sodium intake (10.6 +/- 1.6 versus 4.2 +/- 0.9 pg/ml; P < 0.05). Similarly, there were increases

1993 Clinical science (London, England : 1979) Controlled trial quality: uncertain

1732. Role of insulin resistance in the genesis of sodium sensitivity in essential hypertension. (Abstract)

sensitivity index, while was negatively correlated with fractional excretion of sodium (FE(Na)) obtained during a high sodium diet. In addition, the insulin resistance index had a positive relationship with overall creatinine clearance. Sodium sensitivity index was also negatively correlated with FE(Na) obtained during a high sodium diet. These results showed that insulin resistance might participate in the genesis of sodium sensitivity in essential hypertension by enhancing tubular sodium reabsorption (...) Role of insulin resistance in the genesis of sodium sensitivity in essential hypertension. We recently showed that cardiovascular morbidity was higher in sodium sensitive type of essential hypertension than in the non-sodium sensitive type. It was examined whether sodium sensitivity was associated with insulin resistance, an important atherosclerotic cardiovascular risk factor in essential hypertension. Fifty-three patients with essential hypertension, who had normal (n = 12) and impaired (n

1999 Journal of human hypertension Controlled trial quality: uncertain

1733. Effect of noradrenaline on renal sodium and water handling in euhydrated and overhydrated man. (Abstract)

fall in urinary sodium excretion and an increase in urinary flow rate. During overhydration similar doses of noradrenaline caused a fall in urinary sodium excretion but a decrease in urinary flow rate. 3. Although there was no detectable change in glomerular filtration rate, a dose-dependent fall in effective renal plasma flow was observed in both hydration states during noradrenaline infusion. 4. Noradrenaline infusion was associated with a dose-dependent increase in proximal tubular sodium (...) reabsorption as assessed by the lithium clearance method. Fractional reabsorption of sodium by the distal nephron was, however, unchanged by noradrenaline in both hydration states. 5. Plasma vasopressin concentration was unchanged by noradrenaline in euhydrated subjects. The renin-angiotensin-aldosterone axis was stimulated by noradrenaline in both euhydrated and overhydrated subjects. 6. Thus we conclude that plasma circulating noradrenaline has a dose-dependent antinatriuretic effect in man

1993 Clinical science (London, England : 1979) Controlled trial quality: uncertain

1734. Salt-dependent renal effects of an angiotensin II antagonist in healthy subjects. (Abstract)

washout period. On day 6, the subjects were water loaded, and blood pressure, renal hemodynamics, and urinary electrolyte excretion were measured for 6 hours after a single 100-mg oral dose of losartan (n = 16) or placebo (n = 7). Losartan induced no significant changes in blood pressure, glomerular filtration rate, or renal blood flow in these water-loaded subjects, whatever the sodium diet. In subjects on a low-salt diet, losartan markedly increased urinary sodium excretion from 115 +/- 9 to 207 (...) +/- 21 mumol/min (P < .05). The fractional excretion of endogenous lithium was unchanged, suggesting no effect of losartan on the early proximal tubule in our experimental conditions. Losartan also increased urine flow rate (from 10.5 +/- 0.4 to 13.1 +/- 0.6 mL/min, P < .05); urinary potassium excretion (from 117 +/- 6.9 to 155 +/- 11 mumol/min); and the excretion of chloride, magnesium, calcium, and phosphate. In subjects on a high-salt diet, similar effects of losartan were observed

1993 Hypertension Controlled trial quality: uncertain

1735. Stimulatory effect of insulin on tubular sodium reabsorption in normotensive subjects with a positive family history of hypertension. (Abstract)

estimated distal fractional sodium reabsorption increased, P < 0.01. At the end of the clamp a low-dose infusion of angiotensin II (0.1 ng/kg per min) was superimposed. GFR and RPF then decreased significantly concomitant with urinary excretion of sodium. In control subjects hyperinsulinaemia caused an unchanged GFR in both groups, increased RPF in the lean control group and 15-25% reduction in sodium excretion. No alteration was seen in estimated proximal tubular sodium reabsorption, but estimated (...) distal tubular sodium reabsorption increased (P < 0.05) in the lean control group. Angiotensin II elicited a further increase in distal fractional tubular sodium reabsorption in both groups (P < 0.05).In normotensive subjects with a positive family history of hypertension, in contrast to control subjects without such history, hyperinsulinaemia caused a marked decrease in urinary sodium excretion in presence of unchanged RPF and GFR indicating a renal tubular effect of insulin located at distal site

1996 Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association Controlled trial quality: uncertain

1736. Sodium intake and post-exercise rehydration in man. (Abstract)

, 3.5 and 5.5 h after the end of the rehydration period. Data were analysed by parametric or non-parametric statistical tests are appropriate. The volume of fluid consumed was the same on all trials [2045(45) ml]. From the 1.5-h sample onwards, a significant treatment effect on cumulative urine output was apparent, with the volume excreted being inversely related to the sodium content of the drink consumed. By the end of the trial, subjects were in net negative fluid balance on trials A [by 689(124 (...) of the rehydration period. At 1.5 h after the end of the rehydration period, the increase in plasma volume was greater on trials C and D than on trial A. These results suggest that the fraction of the ingested fluid that was retained was directly related to the sodium concentration.

1995 European journal of applied physiology and occupational physiology Controlled trial quality: uncertain

1737. [Reduction of the antihypertensive effects of enalapril by indomethacin. Its independence from renal sodium retention]. (Abstract)

). Enalapril dose increased up to 40 mg/d if inadequate response to 20 mg.Twenty-four patients with mild-moderated hypertension, showing an adequate response to enalapril (20-40 mg/d).Blood pressure evaluated by "casual" methods and by 24-hour ambulatory blood pressure monitoring, measurement of 24-hour urinary sodium excretion and fractional excretion of sodium: at the end of placebo, enalapril and enalapril + indomethacin treatments. Determination of the correlations between the changes induced (...) by indomethacin (when added to enalapril) on the blood pressure and on sodium excretion effects of enalapril.Enalapril significantly reduced casual blood pressure (systolic/diastolic) by 33/18 mmHg and 24-hour blood pressure by 20/9 mmHg. When added to enalapril, indomethacin attenuated (by 50%) the antihypertensive effects of enalapril and significantly decreased the 24-hour (from 120 +/- 11 mmol to 106 +/- 10 mmol) and fractional excretion of sodium (from 1.11 +/- 0.09% to 0.75 +/- 0.06%). However

1996 Revista portuguesa de cardiologia : orgão oficial da Sociedade Portuguesa de Cardiologia = Portuguese journal of cardiology : an official journal of the Portuguese Society of Cardiology Controlled trial quality: uncertain

1738. Oedema formation with the vasodilators nifedipine and diazoxide: direct local effect or sodium retention? (Abstract)

+/- 2% with placebo). Foot volume increased acutely after administration of nifedipine (by 2.6 +/- 0.4%), whereas it remained stable with placebo and the other drugs. Administration of captopril and nifedipine induced increases of fractional sodium excretion (by 20 +/- 9% and 40 +/- 20%, respectively) in contrast to the decreases with placebo and diazoxide (by 13 +/- 11% and 24 +/- 10%, respectively). Only administration of nifedipine induced significant, albeit small, increases in haemoglobin (...) Oedema formation with the vasodilators nifedipine and diazoxide: direct local effect or sodium retention? To determine whether the common side effect of ankle oedema with arteriolar vasodilators such as the calcium entry blocker (CEB) nifedipine and the potassium channel opener (PCO) diazoxide is the direct result of peripheral vasodilation or merely a consequence of renal sodium retention.In 12 healthy sitting volunteers we studied for 3 h the effects of 20 mg nifedipine, 150 mg diazoxide

1996 Journal of hypertension Controlled trial quality: uncertain

1739. Dopamine natriuresis in salt-repleted, water-loaded humans: a dose-response study. Full Text available with Trip Pro

), 107 (24-190), 121 (60-181), 253 (65-441), 284 (74-494), and 212 (111-312) %, respectively. There were only small, inconsistent decreases in absolute proximal reabsorption rate (APR = GFR-CL(Li)). Fractional distal reabsorption of sodium (FDR(Na) = (CL(Li)-CL(Na))/CL(Li)) decreased with all doses, reaching its nadir with 7.5 microg kg(-1) min(-1) [from 95.9 (94.6-97.2) % with placebo to 91.5 (90.0-93.0) % (P<0.01)] whereafter a flat dose-response curve was observed.In conclusion, the renal (...) an increase in proximal tubular outflow. Pressor doses further increased sodium excretion, indicating the presence of pressure natriuresis at these high doses.

1997 British journal of clinical pharmacology Controlled trial quality: uncertain

1740. Effects of the calcium antagonist felodipine on renal haemodynamics, tubular sodium handling, and blood pressure in cyclosporin-treated dermatological patients. (Abstract)

(RPF) were significantly higher compared to placebo (89.4 +/- 17.5 (mean +/- SD) vs 79.0 +/- 15.9 ml/min and 412.0 +/- 107.6 vs 326.1 +/- 78.0 ml/min respectively, P < 0.001 for both), and filtration fraction (FF) was lower (0.22 +/- 0.03 vs 0.25 +/- 0.03, P < 0.001). Both systolic and diastolic blood pressure were lower after felodipine compared to placebo (116 +/- 11/71 +/- 7 vs 133 +/- 18/83 +/- 10 mmHg, P < 0.001 for both). Furthermore, proximal output of sodium, i.e. fractional excretion (...) of lithium, was higher after felodipine (26.9 +/- 7.3% vs 20.4 +/- 5.5%, P < 0.001) as well as total sodium excretion (0.33 +/- 0.19 vs 0.19 +/- 0.08 mmol/min, P < 0.001).It is concluded, that felodipine 5 mg once daily for 4 weeks increased GFR, RPF, and sodium excretion in cyclosporin-treated dermatological patients with no primary renal disease. Furthermore, felodipine lowers blood pressure in these patients. The effects of felodipine may be due to an antagonizing effect against CsA-induced

1997 Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association Controlled trial quality: uncertain

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