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Fractional Excretion of Sodium

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101. Renal Sodium-Potassium-Activated Adenosine Triphosphatase and Sodium Reabsorption (PubMed)

in the infused kidney. Despite over 90% enzyme inhibition in many experiments, at least 80% of the filtered sodium continued to be reabsorbed. The per cent change in enzyme activity correlated with the rate of digoxin administration and the total dose administered but not with changes in sodium excretion. Changes in medullary Na(+),K(+)-ATPase activity, however, bore a direct relationship to alterations in fractional solute free water reabsorption (T(c) (H2O)). Inhibition of cortical enzyme activity alone (...) was not associated with natriuresis, suggesting that medullary enzyme activity must be depressed for increased sodium excretion to occur during digoxin infusion. In high-dose experiments, significant inhibition of cortical and medullary enzyme in the contralateral control kidney was also observed, but natriuresis did not occur. In these experiments the rate at which digoxin reached the control kidney rose progressively but never equaled the rates in the directly infused kidney with either dose. Nevertheless

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1972 Journal of Clinical Investigation

102. Urinary excretion of AQP2 and ENaC in autosomal dominant polycystic kidney disease during basal conditions and after a hypertonic saline infusion. (PubMed)

), and prostaglandin E(2) (u-PGE(2)); free water clearance (C(H2O)); fractional sodium excretion (FE(Na)); and plasma vasopressin (p-AVP), renin (p-Renin), angiotensin II (p-ANG II), aldosterone (p-Aldo), and atrial and brain natriuretic peptide (p-ANP, p-BNP) in patients with ADPKD and healthy controls during 24-h urine collection and after hypertonic saline infusion during high sodium intake (HS; 300 mmol sodium/day) and low sodium intake (LS; 30 mmol sodium/day). No difference in u-AQP2, u-ENaC(β), u-cAMP, u (...) Urinary excretion of AQP2 and ENaC in autosomal dominant polycystic kidney disease during basal conditions and after a hypertonic saline infusion. Renal handling of sodium and water is abnormal in chronic kidney diseases. To study the function and regulation of the aquaporin-2 water channel (AQP2) and the epithelial sodium channel (ENaC) in autosomal dominant polycystic kidney disease (ADPKD), we measured urinary excretion of AQP2 (u-AQP2), the β-subunit of ENaC (u-ENaC(β)), cAMP (u-cAMP

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2012 American journal of physiology. Renal physiology

103. Abnormal increase in urinary aquaporin-2 excretion in response to hypertonic saline in essential hypertension. (PubMed)

-ENaC(β-CR)), prostaglandin E2 (u-PGE2) and cyclic AMP (u-cAMP), fractional sodium excretion (FE(Na)), free water clearance (C(H2O)), as well as plasma concentrations of vasopressin (AVP), renin (PRC), angiotensin II (Ang II), aldosterone (Aldo), and atrial and brain natriuretic peptide (ANP, BNP) in 21 patients with essential hypertension and 20 normotensive controls during 24-h urine collection (baseline), and after hypertonic saline infusion on a 4-day high sodium (HS) diet (300 mmol sodium/day (...) Abnormal increase in urinary aquaporin-2 excretion in response to hypertonic saline in essential hypertension. Dysregulation of the expression/shuttling of the aquaporin-2 water channel (AQP2) and the epithelial sodium channel (ENaC) in renal collecting duct principal cells has been found in animal models of hypertension. We tested whether a similar dysregulation exists in essential hypertension.We measured urinary excretion of AQP2 and ENaC β-subunit corrected for creatinine (u-AQP2(CR), u

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2012 BMC nephrology

104. Effects of pioglitazone on renal calcium excretion. (PubMed)

for 6 wk) or placebo on renal calcium and phosphate excretion and PTH levels during different sodium intakes in 16 individuals (eight with type 2 diabetes and eight with essential hypertension).Pioglitazone had no effect on corrected plasma calcium and phosphate levels but decreased significantly the alkaline phosphatase and PTH levels. Pioglitazone induced on average a 45% increase in urinary calcium excretion. The fractional excretion of calcium rose to the same extent, suggesting a glomerular (...) Effects of pioglitazone on renal calcium excretion. Glitazones increase fracture risk in long-term users and in postmenopausal women. Studies have demonstrated deleterious effects of glitazones on bone metabolism. Glitazones also have direct renal tubular effects increasing sodium reabsorption. We hypothesized that glitazones may also regulate renal calcium excretion.In this double-blind, randomized, placebo-controlled, four-way, crossover study, we examined the effects of pioglitazone (45 mg/d

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2011 The Journal of clinical endocrinology and metabolism

105. Effect of volume expansion with hypertonic- and isotonic saline and isotonic glucose on sodium and water transport in the principal cells in the kidney. (PubMed)

of AQP2 (u-AQP2) and the γ-fraction of ENaC (u-ENaCγ). The effects of an acute intravenous volume load with isotonic saline, hypertonic saline and glucose on u-AQP2, u-ENaCγ and underlying mechanisms have never been studied in a randomized, placebo-controlled trial in healthy humans.We studied the effects of 0.9% saline (23 ml/kg), 3% saline (7 ml/kg) and 5% glucose (23 ml/kg) on u-AQP2 and u-ENaCγ, fractional sodium excretion (FENa), free water clearance (CH2O), and plasma concentrations (...) Effect of volume expansion with hypertonic- and isotonic saline and isotonic glucose on sodium and water transport in the principal cells in the kidney. The renal distal nephron plays an important role in the maintenance of sodium balance, extra cellular volume and blood pressure. The degree of water transport, via aquaporin2 water channels (AQP2), and sodium transport, via epithelial sodium channels (ENaC) in renal collecting duct principal cells are reflected by the level of urinary excretion

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2013 BMC Nephrology

106. Effect of volume expansion with hypertonic- and isotonic saline and isotonic glucose on sodium and water transport in the principal cells in the kidney. (PubMed)

of AQP2 (u-AQP2) and the γ-fraction of ENaC (u-ENaCγ). The effects of an acute intravenous volume load with isotonic saline, hypertonic saline and glucose on u-AQP2, u-ENaCγ and underlying mechanisms have never been studied in a randomized, placebo-controlled trial in healthy humans.We studied the effects of 0.9% saline (23 ml/kg), 3% saline (7 ml/kg) and 5% glucose (23 ml/kg) on u-AQP2 and u-ENaCγ, fractional sodium excretion (FENa), free water clearance (CH2O), and plasma concentrations (...) Effect of volume expansion with hypertonic- and isotonic saline and isotonic glucose on sodium and water transport in the principal cells in the kidney. The renal distal nephron plays an important role in the maintenance of sodium balance, extra cellular volume and blood pressure. The degree of water transport, via aquaporin2 water channels (AQP2), and sodium transport, via epithelial sodium channels (ENaC) in renal collecting duct principal cells are reflected by the level of urinary excretion

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2013 BMC nephrology

107. Blood Pressure in Relation to Interactions Between Sodium Dietary Intake and Renal Handling. (PubMed)

, respectively. We calculated fractional excretion of lithium and fractional distal reabsorption rate of sodium, as markers of proximal and distal sodium handling, respectively. The 766 subjects included 379 men and 478 ambulatory hypertensive patients. They were never treated (n=697) or did not take antihypertensive medication for ≥2 weeks (n=69). In adjusted analyses, none of the associations of urinary sodium excretion, fractional excretion of lithium, and fractional distal reabsorption rate of sodium (...) with clinic or ambulatory blood pressure were statistically significant (P≥0.09). However, there was significant (P=0.01) interaction between urinary sodium excretion and fractional excretion of lithium in relation to nighttime diastolic blood pressure. In tertile 3 but not tertiles 1 and 2 of fractional excretion of lithium, nighttime diastolic pressure was positively associated with urinary sodium excretion (P=0.03). However, nighttime diastolic pressure was higher in tertile 1 than tertile 3

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2013 Hypertension

108. The Effect of Sodium Nitrite on Renal Function and Blood Pressure in Healthy Humans. A Dose-response Study

: Placebo Continuous 2 hour infusion of sodium chloride, 25 ml/hour Drug: Placebo Continuous 2 hour infusion of sodium chloride, 25 ml/hour Other Name: Sodium chloride Outcome Measures Go to Primary Outcome Measures : Fractional urinary sodium excretion [ Time Frame: One day ] Secondary Outcome Measures : Nitrite clearance [ Time Frame: One day ] Nitrate clearance [ Time Frame: One day ] Glomerular filtration rate [ Time Frame: One day ] Measured by determent renal clearance of 51Cr-EDTA (51-chrome (...) will be evaluated. Hypothesis Sodium nitrite infusion increases urinary sodium excretion and renal filtration rate lowers blood pressure, central as well as peripheral affects vasoactive hormones it is possible to establish a dose that affects the renal function with only minor effect on the blood pressure. Condition or disease Intervention/treatment Phase Healthy Drug: Sodium nitrite, 40 micrograms/kg/hour Drug: Sodium nitrite, 120 micrograms/kg/hour Drug: Sodium nitrite, 240 micrograms/kg/hour Drug: Placebo

2013 Clinical Trials

109. Epithelial Sodium Channel (ENaC) as a Novel Mechanism for Hypertension and Volume Expansion in Type 2 Diabetes

Go to Primary Outcome Measures : Blood Pressure [ Time Frame: one month ] Change in clinic systolic BP. This BP measure will be the average of three serial BP measurements taken one minute apart after 5 minutes of sitting quietly. Secondary Outcome Measures : Hypertension [ Time Frame: one month ] To demonstrate effect size on relevant hypertension outcomes such as volume status and urinary sodium excretion. Also assess the fractional excretion of sodium (FENa) and chloride (FECI). Endpoint (...) Epithelial Sodium Channel (ENaC) as a Novel Mechanism for Hypertension and Volume Expansion in Type 2 Diabetes Epithelial Sodium Channel (ENaC) as a Novel Mechanism for Hypertension and Volume Expansion in Type 2 Diabetes - 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

2013 Clinical Trials

110. The Effects of Functional Adaptation of Residual Nephrons on the Urinary Excretion of Drugs (PubMed)

normal value of 50 percent as an exponential function of the decrease of GFR, and as a linear function of the fractional excretion of water or of sodium. Dietary sodium restriction had no influence on C(CHL) in the patients, while water diuresis, in normal subjects, enhanced the urinary excretion of chloramphenicol. The data suggest that chloramphenicol is reabsorbed by back-diffusion and that increases of the rate of flow of urine and tubular fluid prevent back-diffusion. (...) The Effects of Functional Adaptation of Residual Nephrons on the Urinary Excretion of Drugs In patients with chronic renal failure due to glomerulonephritis, pyelonephritis or polycystic kidneys the urinary clearance of free chloramphenicol (C(CHL)) was depressed proportionally to GFR (C(In)). The ordinate intercept of the regression line of C(CHL) on C(In), however, consistently was positive (+3 to +5 ml/min). The fractional excretion of chloramphenicol in renal failure increased from its

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1978 The Yale journal of biology and medicine

111. Mechanism of Impaired Water Excretion in the Hypothyroid Rat (PubMed)

Mechanism of Impaired Water Excretion in the Hypothyroid Rat The ability to excrete an oral water load and the renal diluting mechanism were studied in hypothyroid rats and in age-matched euthyroid controls. Hypothyroid animals excreted a significantly smaller fraction of a 50-ml/kg oral water load than controls, demonstrating the same limited ability to excrete free water as thyroid-deficient man. During hypotonic (0.45%) saline infusion, absolute sodium delivery to the diluting segment (...) in hypothyroid rats was further demonstrated in experiments in which distal delivery was increased by contralateral nephrectomy or by administration of carbonic anhydrase inhibitors which decrease proximal sodium reabsorption. In both studies, fractional free water clearance increased markedly reaching levels significantly greater than in euthyroid controls. These results demonstrate that the impaired ability of the hypothyroid rat to excrete a water load is not due to incomplete suppression of ADH

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1974 Journal of Clinical Investigation

112. Urinary excretion of C-20-reduction products of corticosterone (PubMed)

Urinary excretion of C-20-reduction products of corticosterone 1. A 200 mg. portion of corticosterone was ingested by a healthy man and the urine collected. Part of the urine was treated with the gastric juice of Helix pomatia and extracted with ethyl acetate, and the extract fractionated with Girard T. Paper-chromatographic separation of the non-ketonic fraction in the Bush (1952) system B(5) revealed the presence of two unknown polar components. 2. The unknown compounds did not possess (...) a reducing (blue tetrazolium) or a reducible (potassium borohydride) grouping. Both contained a terminal alpha-glycollic fragment as shown by the formation of formaldehyde, and of a non-volatile aldehyde on oxidation with sodium bismuthate. 3. Unknown compound (I) had paper-chromatographic mobilities identical with those of 5beta-pregnane-3alpha,11beta,20beta,21-tetraol. The oxidation product of compound (I) had a retention time (gas-liquid chromatography) on an SE30 column identical with that of 3alpha

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1965 Biochemical Journal

113. Heme oxygenase regulates renal arterial resistance and sodium excretion in cirrhotic rats. (PubMed)

Heme oxygenase regulates renal arterial resistance and sodium excretion in cirrhotic rats. Heme oxygenase (HO) catabolizes heme into biliverdin, carbon monoxide (CO), and free iron. CO generated in endothelial and smooth muscle layers of blood vessels modulates vascular tone by inducing relaxation of vascular smooth muscle cells. The aim of this study was to verify the role played by HO in regulating renal arterial resistance and Na(+) excretion in cirrhosis.Twenty control rats and 20 rats (...) showed higher urinary Na(+) concentration and fractional Na(+) excretion, compared to both untreated cirrhotic and control rats.In cirrhotic rats, an impaired HO-1 expression promotes vasoconstriction of renal interlobar arteries. Chronic HO induction normalizes the sensitivity to PE and promotes Na(+) excretion.Copyright © 2010 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.

2010 Journal of Hepatology

114. Effect of nitric oxide inhibition on blood pressure and renal sodium handling: a dose-response study in healthy man. (PubMed)

after 20 minutes of infusion. On the contrary, the fractional excretion of sodium was reduced equally in all three L-NMMA doses. This indicates that sodium excretion is highly sensitive to even small changes in renal NO bioavailability in healthy human. (...) Effect of nitric oxide inhibition on blood pressure and renal sodium handling: a dose-response study in healthy man. Nitric oxide (NO) is a ubiquitous vasodilator and an important regulator of renal sodium excretion. To further investigate the role of NO in renal sodium handling, we studied the effects of the NO synthase inhibitor, NG-monomethyl-L-arginine (L-NMMA), in a crossover dose-response study. During NO inhibition mean arterial pressure increased dose-dependently and reached a plateau

2012 Clinical and experimental hypertension (New York, N.Y. : 1993)

115. Failure to Downregulate the Epithelial Sodium Channel Causes Salt Sensitivity in Hsd11b2 Heterozygote Mice. (PubMed)

. In the present study, renal mechanisms underpinning salt sensitivity were investigated in Hsd11b2(+/-) mice fed low-, standard-, and high-sodium diets. In wild-type mice, there was a strong correlation between dietary sodium content and fractional sodium excretion but not blood pressure. High sodium feeding abolished amiloride-sensitive sodium reabsorption, consistent with downregulation of the epithelial sodium channel. In Hsd11b2(+/-) mice, the natriuretic response to increased dietary sodium content (...) Failure to Downregulate the Epithelial Sodium Channel Causes Salt Sensitivity in Hsd11b2 Heterozygote Mice. In vivo, the enzyme 11β-hydroxysteroid dehydrogenase type 2 influences ligand access to the mineralocorticoid receptor. Ablation of the encoding gene, HSD11B2, causes the hypertensive syndrome of apparent mineralocorticoid excess. Studies in humans and experimental animals have linked reduced 11β-hydroxysteroid dehydrogenase type 2 activity and salt sensitivity of blood pressure

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2012 Hypertension

116. High nutritional risk is associated with worse health-related quality of life in patients with heart failure beyond sodium intake. (PubMed)

HRQoL after controlling for daily sodium intake.A total of 134 consecutive patients with HF [age 63 ± 11 years, 35% female, 45% New York Heart Association (NYHA) class III/IV, ejection fraction (EF) 33 ± 13%] completed the Nutrition Screening Initiative (NSI) to assess nutritional risk and a 24-h urine sodium excretion assessment to estimate daily sodium intake at baseline. The Minnesota Living with HF Questionnaire was used to evaluate HRQoL at baseline and 6 months later. Hierarchical linear (...) High nutritional risk is associated with worse health-related quality of life in patients with heart failure beyond sodium intake. The most desirable outcome in heart failure (HF) management is to improve health-related quality of life (HRQoL) as a patient-centred health outcome. Nutrition is assumed to be important in HF management, whereas there is little evidence that nutritional risk affects HRQoL, except for sodium.We aimed to determine whether nutritional risk is associated with worse

2012 European Journal of Cardiovascular Nursing

117. Segmental sodium reabsorption by the renal tubule in prenatally programmed hypertension in the rat. (PubMed)

abundance of sodium:potassium:chloride (Na(+):K(+):2Cl(-)) co-transporter (NKCC2) leads to enhanced sodium uptake by the TAL. Pregnant Wistar rats were fed a control (18%) or LP (9%) diet. Amiloride (AM), bendroflumethiazide (BF), and furosemide (FUR) were administered acutely to male offspring at 4 weeks of age. Fractional excretion of sodium (FE(Na)) was significantly greater in vehicle-infused LP rats (3.0 ± 0.3%) compared with controls (1.7 ± 0.5, P < 0.01). FE(Na) by the LP proximal tubule did (...) Segmental sodium reabsorption by the renal tubule in prenatally programmed hypertension in the rat. Hypertension and renal dysfunction can be programmed in the rat by prenatal exposure to a low-protein (LP) diet. Expression of the renal thick ascending limb (TAL) sodium transporter NKCC2 is up-regulated, which has been predicted to result in greater sodium reabsorption. However, we have shown that LP rats excrete more not less sodium. The aim of this study was to determine whether the increased

2012 Pediatric Nephrology

118. Effect of Hypertonic Sodium Chloride on Urinary Biomarkers in Healthy Subjects and Patients With Chronic Kidney Disease

activity in the kidney and may be measured after an infusion with hypertonic saline in CKD patients and healthy subjects. Condition or disease Intervention/treatment Phase Nephropathy Other: hypertonic saline Not Applicable Detailed Description: The fractional sodium excretion is elevated as high as 10-20% In patients with chronic kidney disease (CKD) Changes in the sodium intake results in a slower expansion and/or reduction in extracellular fluid in CKD patients. Urinary biomarkers reflects (...) First Posted : June 20, 2012 Last Update Posted : March 4, 2014 Sponsor: Regional Hospital Holstebro Information provided by (Responsible Party): Erling Bjerregaard Pedersen, Regional Hospital Holstebro Study Details Study Description Go to Brief Summary: Patients with chronic kidney disease (CKD) have a defect in the tubular reabsorption of sodium, and therefore the ability to excrete a sodium load is diminished compared to healthy subjects. Urinary biomarkers reflects the water- and sodium-channel

2012 Clinical Trials

119. NADPH oxidase inhibition reduces tubular sodium transport and improves kidney oxygenation in diabetes (PubMed)

. The aim was to investigate the effects of acute NADPH oxidase inhibition on tubular Na(+) transport and kidney Po(2) in vivo. Glomerular filtration rate (GFR), renal blood flow (RBF), filtration fraction (FF), Na(+) excretion, fractional Li(+) excretion, and intrarenal Po(2) was measured in control and streptozotocin-diabetic rats during baseline and after acute NADPH oxidase inhibition using apocynin. The effects on tubular transporters were investigated using freshly isolated PTC. GFR was increased (...) Na(+) excretion (+112%) and decreased fractional lithium reabsorption (-10%) in diabetics, resulting in improved cortical (+14%) and medullary (+28%) Po(2). Qo(2) was higher in PTC isolated from diabetic rats compared with control. Apocynin, dimethylamiloride, and ouabain reduced Qo(2), but the effects of combining apocynin with either dimethylamiloride or ouabain were not additive. In conclusion, NADPH oxidase inhibition reduces tubular Na(+) transport and improves intrarenal Po(2) in diabetes.

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2012 American Journal of Physiology - Regulatory, Integrative and Comparative Physiology

120. Proximal tubular angiotensinogen in renal biopsy suggests nondipper BP rhythm accompanied by enhanced tubular sodium reabsorption. (PubMed)

Proximal tubular angiotensinogen in renal biopsy suggests nondipper BP rhythm accompanied by enhanced tubular sodium reabsorption. The renal capacity for sodium excretion is impaired by a reduction in the glomerular ultrafiltration coefficient and by enhancement of the fractional tubular sodium reabsorption (FRNa), leading to a nondipper circadian blood pressure (BP) rhythm. Angiotensin II in the systemic circulation can be easily filtered across the glomerular capillary walls and stimulates (...) directly with the FRNa (r = 0.39, P = 0.01) and the night/day ratio of BP (r = 0.38, P = 0.02), but not creatinine clearance (r = -0.008, P = 0.9). The night/day ratio of BP was determined by both creatinine clearance (r = -0.36, P = 0.03) and FRNa (r = 0.47, P = 0.006).Tubular sodium reabsorption is stimulated by intrarenal angiotensin II, as indicated by PT-AGT, and contributes to the genesis of the nondipper BP rhythm. Further studies are needed to evaluate whether or not treatment to prevent sodium

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2012 Journal of Hypertension

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