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Fractional Excretion of Sodium

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161. Effect of Extracellular Volume Expansion upon Sodium Reabsorption in the Distal Nephron of Dogs Full Text available with Trip Pro

Effect of Extracellular Volume Expansion upon Sodium Reabsorption in the Distal Nephron of Dogs Micropuncture studies have disclosed that extracellular fluid (ECF) volume expansion inhibits sodium reabsorption in the proximal tubule. The diuresis that ensues represents only a portion of the increment in sodium and water escaping proximal reabsorption, since a large and variable fraction of the increment is reabsorbed distally. In certain experimental models proximal reabsorption may (...) /2 isotonic saline infusion. C(H2O) at high distal sodium loads was depressed by expansion of the ECF volume with hypotonic saline. The difference in free water formation between dogs which did and did not receive hypotonic saline was accounted for by the difference in sodium excretion. In one dog hypotonic saline expansion failed to depress free water formation; likewise the level of natriuresis in this dog was severely attenuated. The results of these experiments provide strong evidence

1973 Journal of Clinical Investigation

162. Failure to demonstrate a hormonal inhibitor of proximal sodium reabsorption Full Text available with Trip Pro

Failure to demonstrate a hormonal inhibitor of proximal sodium reabsorption Recently, it has been reported that a humoral inhibitor of proximal sodium reabsorption could be detected in plasma, and dialysates of plasma, of rats and dogs undergoing saline diuresis. We have repeated these studies using similar techniques and protocols. Fractional sodium reabsorption by the proximal tubule (as estimated in free-flow micropuncture studies from tubule fluid-to-plasma inulin ratios) was found (...) not to be lower during infusion of "natriuretic" plasma than during subsequent infusion of "hydropenic" plasma. Similarly, infusion of natriuretic plasma failed to prolong reabsorptive half-time of the shrinking drop beyond that seen during hydropenic plasma infusion. No increase in urine volume or rate of sodium excretion was observed during the period of natriuretic plasma infusion, nor did natriuretic plasma result in an increase in these measures in rats undergoing water diuresis. It also has been

1969 Journal of Clinical Investigation

163. Effects of salt loading and haemodilution on the responses of perfused cat kidneys to angiotensin Full Text available with Trip Pro

Effects of salt loading and haemodilution on the responses of perfused cat kidneys to angiotensin 1. Effects of single intra-arterial injections (0.1-1.0 mug) of angiotensin II have been observed on cat kidneys perfused with heparinized blood from heart-lung circuits.2. Angiotensin II always caused an abrupt decrease in renal plasma flow (R.P.F.) which reached maximum in 1-2 min and lasted over-all for only 3.5-4.0 min. Glomerular filtration rate (G.F.R.) usually and filtration fraction (F.F (...) .) always increased.3. Angiotensin II caused antidiuresis provided that the kidney had not been subjected either to salt loading or to haemodilution within the preceding 3 hr. These pretreatments converted the antidiuretic action of angiotensin into a diuresis.4. Angiotensin II raised the rate of Na excretion, the urinary concentration of Na and the urinary Na/K whether anti-diuretic or diuretic.

1967 The Journal of physiology

164. Effects of Hypotonic Saline Loading in Hydrated Dog: Evidence for a Saline-induced Limit on Distal Tubular Sodium Transport Full Text available with Trip Pro

during mannitol loading. In contrast, during hypotonic (0.45%) saline loading C(H2O) rose initially, but as urine flow (V) exceeded 25% of the filtered load C(H2O) attained maximal levels (up to 20% of the filtered load) and remained stable as V increased to 50% of the filtered load. It was concluded that saline loading progressively inhibits proximal sodium reabsorption. Initially, the distal tubule absorbes a large fraction of the proximal rejectate and sodium excretion rises slightly. Eventually (...) , an alteration in distal sodium transport appears which culminates in a maximal rate or transport limit. This distal transport limit provoked by saline loading could not be characterized by a classical Tm as seen with glucose and does not seem to be consequent to high rates of flow through the distal tubule. Regardless of the precise nature of this limit, the major increment in sodium excretion develops during saline loading only after saline alters the capacity of the distal tubule to transport sodium.

1967 Journal of Clinical Investigation

165. The Effects of Infusion of Water on Renal Hemodynamics and the Tubular Reabsorption of Sodium Full Text available with Trip Pro

. The extent to which fractional sodium reabsorption decreased and the excretion of sodium increased was inversely related to the degree to which the filtered load of sodium was depressed as a result of the decreased plasma sodium concentration. We conclude that, in the presence of the diuretic blockade of distal tubular sodium reabsorption, infusion of water depresses proximal tubular reabsorption of sodium and that these changes are qualitatively similar to those previously observed during infusions (...) of saline. Similar depression of tubular reabsorption of sodium and increased excretion of sodium occurred during water loading in the absence of diuretics in dogs undergoing saline diuresis, which presumably provided a high rate of distal sodium reabsorption before water loading. We suggest that volume expansion with water depresses proximal tubular reabsorption of sodium in a manner qualitatively similar to infusions of saline and that the extent to which sodium excretion is increased during water

1967 Journal of Clinical Investigation

166. The phosphaturic effect of sodium bicarbonate and acetazolamide in dogs Full Text available with Trip Pro

The phosphaturic effect of sodium bicarbonate and acetazolamide in dogs Urinary inorganic phosphate excretion was studied before and during the administration of sodium bicarbonate and acetazolamide in dogs that were not given infusions of phosphate. The excretion fraction of filtered phosphate increased after sodium bicarbonate or acetazolamide was given. This phosphaturia was attributed to decreased tubular reabsorption of phosphate consequent to alkalinization of either tubular urine

1968 Journal of Clinical Investigation

167. Fractional Excretion

Fractional Excretion Renal Fellow Network: Fractional Excretion | | | | | Thursday, September 8, 2011 Fractional Excretion The fractional excretion of sodium (FeNa) is a test that is often used in the setting of acute renal failure to help distinguish between pre-renal and intra-renal causes that has been mentioned in . In general, a FeNa of <1% suggests pre-renal disease, between 1-2% is indeterminate and >2% suggests ATN. There are some exceptions to this but overall, the specificity (...) of this test is more than 80% and this increases if it is used in combination with the fractional excretion of urea. By definition, the FeNa is the ratio between the quantity of Na excreted in the urine relative to the amount filtered at the glomerulus. So how can we make this calculation with a spot sample without reference to volume of filtrate or urine? Given that Na is freely filtered at the glomerulus, this means that: Filtered Na = Plasma Na x GFR And: Excreted Na = Urine Na x urine flow rate Thus

2011 Renal Fellow Network

168. Fractional excretion of sodium predicts worsening renal function in acute decompensated heart failure Full Text available with Trip Pro

Fractional excretion of sodium predicts worsening renal function in acute decompensated heart failure Renal impairment (RI), defined as an increase in creatinine level of greater than 26.5 mmol/L, develops in more than 30% of acute decompensated heart failure (ADHF) patients. Fractional excretion of sodium (FeNa) reflects sodium handling by the kidneys during diuresis.To study the relationship between FeNa and RI in patients admitted with ADHF.The hospital course and renal function of all ADHF (...) patients admitted to the hospital were prospectively observed. Patients were included if their admission creatinine level was 176 mmol/L or lower, they had been on a low-salt diet since admission, had urine sodium and creatinine samples collected more than 6 h after a furosemide dose in the first few days of admission, and they were on daily intravenous furosemide doses of 20 mg or more.Over six months, 51 patients met the inclusion criteria; the average daily dose of intravenous furosemide was 58.8 mg

2010 Experimental & Clinical Cardiology

169. The association of bile acid excretion and atherosclerotic coronary artery disease Full Text available with Trip Pro

The association of bile acid excretion and atherosclerotic coronary artery disease Excess cholesterol is usually eliminated from the body by conversion to bile acids excreted in feces as bile salts. The excretion of large amounts of bile protects against atherosclerosis, while diminished excretion may lead to coronary artery disease (CAD).To investigate a relationship between CAD and bile acid excretion.Bile acid excretion was compared between 36 patients with proven CAD and 37 CAD-free (...) versus 197.27 ± 126.87 mg; p < 0.01). Advanced age, male gender, left ventricular ejection fraction and total bile acid levels were significant independent factors that predicted CAD (p < 0.05). Mortality, CAD and cerebrovascular accident development rates were significantly lower for the controls at the 13-year follow up.CAD patients have significantly decreased bile acid excretion levels than non-CAD patients. An impaired ability to excrete cholesterol may be an additional risk factor for CAD

2011 Therapeutic advances in gastroenterology

170. Effects of pioglitazone on renal calcium excretion. Full Text available with Trip Pro

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

2011 The Journal of clinical endocrinology and metabolism Controlled trial quality: uncertain

171. Ca2+ entry mode of Na+/Ca2+ exchanger as a new therapeutic target for heart failure with preserved ejection fraction. Full Text available with Trip Pro

(2+) entry mode of Na(+)/Ca(2+) exchanger (NCX). Digitalis-like factors are known to promote collagen production in fibroblasts. The aim of this study was to explore whether the pharmacological inhibition of the NCX entry mode is effective in the prevention of LV fibrosis and in the development of HFPEF.(i) Dahl salt-sensitive rats fed 8% NaCl diet from age 6 weeks served as hypertensive HFPEF model. In this model, 24 h urine excretion of DLFs was greater than that in the age-matched control (...) Ca2+ entry mode of Na+/Ca2+ exchanger as a new therapeutic target for heart failure with preserved ejection fraction. Left ventricular (LV) fibrosis and stiffening play crucial roles in the development of heart failure with preserved ejection fraction (HFPEF). Plasma level of digitalis-like factors (DLFs) is increased in patients with hypertension, a principal underlying cardiovascular disease of HFPEF. Digitalis-like factors inhibit ion-pumping function of Na(+)/K(+)-ATPase and activate the Ca

2011 European Heart Journal

172. Phase I Study of Colistin Methanesulfonate Sodium

), Clearance (CL), Fraction of urinary excretion (fe), Accumulation ratio (Ro and Rs). Profile of safety (single) [ Time Frame: Vital: -24h, pre-dose, 2,4,8,12,24,36,48h after the start of infusion. ECGs: -24h, pre-dose, 12, 24, 36 and 48h after the start of infusion. Clinical lab: pre-dose, 24 and 48h after the start of infusion. Adverse event: All study period. ] Vital signs, ECGs, clinical laboratory test and adverse events. Profile of renal function [ Time Frame: Single and repeat dose day 3: Pre-dose (...) Phase I Study of Colistin Methanesulfonate Sodium Phase I Study of Colistin Methanesulfonate Sodium - 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. Phase I Study of Colistin Methanesulfonate Sodium

2011 Clinical Trials

173. Intrarenal Ghrelin Infusion Stimulates Distal Nephron-Dependent Sodium Reabsorption in Normal Rats. Full Text available with Trip Pro

PCR product. To test intrarenal ghrelin action, uninephrectomized rats received 3 cumulative 1-hour renal interstitial (RI) infusions of 5% dextrose in water (vehicle, n=21), ghrelin (n=10), ghrelin plus specific ghrelin receptor antagonist [D-Lys-3]-GHRP-6 (n=24), or [D-Lys-3]-GHRP-6 alone (n=32). Mean arterial pressure (MAP), urine sodium excretion rate (U(Na)V), glomerular filtration rate (GFR), fractional excretion of sodium (FE(Na)), and fractional excretion of lithium (FE(Li)) were (...) Intrarenal Ghrelin Infusion Stimulates Distal Nephron-Dependent Sodium Reabsorption in Normal Rats. Ghrelin is a 28-amino acid peptide hormone that exerts powerful orexigenic effects. Ghrelin receptor expression has been reported in the kidney, but the role of ghrelin in the kidney is unknown. The present studies confirmed ghrelin receptor mRNA expression in the kidneys of normal Sprague Dawley rats (n=6) using reverse transcription polymerase chain reaction (PCR) and sequencing of the 588-bp

2011 Hypertension

174. THE EPITHELIAL SODIUM-PROTON EXCHANGER, NHE3, IS NECESSARY FOR RENAL AND INTESTINAL CALCIUM (RE)ABSORPTION. Full Text available with Trip Pro

these epithelia by comparing Ca(2+) handling between wild-type and NHE3(-/-) mice. Serum Ca(2+) and plasma parathyroid hormone levels were not different between groups. However, NHE3(-/-) mice had increased serum 1,25-dihydroxyvitamin D(3). The fractional excretion of Ca(2+) was also elevated in NHE3(-/-) mice. Paracellular Ca(2+) flux across confluent monolayers of a PT cell culture model was increased by an osmotic gradient equivalent to that generated by NHE3 across the PT in vivo and by overexpression (...) THE EPITHELIAL SODIUM-PROTON EXCHANGER, NHE3, IS NECESSARY FOR RENAL AND INTESTINAL CALCIUM (RE)ABSORPTION. Passive paracellular proximal tubular (PT) and intestinal calcium (Ca(2+)) fluxes have been linked to active sodium (re)absorption. Although the epithelial sodium/proton exchanger, NHE3, mediates apical sodium entry at both these sites, its role in Ca(2+) homeostasis remains unclear. We, therefore, set out to determine whether NHE3 is necessary for Ca(2+) (re)absorption from

2011 American Journal of Physiology. Renal physiology

175. The effect of eprosartan on reflex sympathetic activation in sodium restricted patients with essential hypertension. (Abstract)

and vasoactive hormones with radioimmunoassays. Eprosartan had no effect on the increases in heart rate and plasma levels of noradrenaline during reflex activation of the sympathetic nervous system. However, eprosartan significantly decreased in fractional excretions of sodium (mean ± SD) (0.23 ± 0.22%) and lithium (3.1 ± 1.7%) during the sodium nitroprusside infusion, compared to placebo. Very short-term eprosartan treatment does not seem to have any sympathoinhibitory effects in sodium restricted patients (...) on urinary sodium and lithium excretion, heart rate, blood pressure, and vasoactive hormones was measured during reflex activation of the sympathetic nervous system by a cold pressor test and by a sodium nitroprusside induced 10 mm Hg reduction of the mean arterial pressure. It was a randomized, placebo-controlled, double-blinded, crossover study in 14 patients with essential hypertension. Glomerular filtration rate and renal tubular function were determined with continuous infusion clearance technique

2011 Journal of the American Society of Hypertension : JASH Controlled trial quality: uncertain

176. British guideline on the management of asthma

structured clinical assessment, 3.4 Organisation of diagnostic services 4 Monitoring asthma New: Table 7, 4.1 Targeting care, 4.2 Monitoring current asthma symptom control, 4.3 Predicting future risk of asthma attacks, 4.3.1 Adults, 4.3.2 School-aged children, 4.3.3 Preschool children, 4.3.4 People with severe asthma, 4.4 Physiological measures, 4.4.1 Spirometry and peak expiratory flow, 4.4.2 Fractional exhaled nitric oxide, 4.4.3 Eosinophils, 4.5 Other approaches 5 Supported self management New: 5.2.3

2019 SIGN

177. Acute kidney injury

(including urea and creatinine) ratio of serum urea to creatinine urinalysis urine culture full blood count fractional excretion of sodium fractional excretion of urea urinary eosinophil count venous blood gases fluid challenge bladder catheterisation urine osmolality urine sodium concentration renal ultrasound chest x-ray ECG anti-nuclear antibodies anti-DNA complement (C3, C4, CH50) anti-glomerular basement membrane antibodies anti-neutrophil cytoplasmic antibodies acute hepatitis profile HIV serology (...) obstructive symptoms haematuria fever rash arthralgia/arthritis altered mental status signs of uraemia nausea thirst flank pain abdominal distension abdominal bruit livedo reticularis petechiae ecchymoses advanced age underlying renal disease malignant hypertension diabetes mellitus myeloproliferative disorders, such as multiple myeloma connective tissue disease sodium-retaining states (e.g., congestive heart failure, cirrhosis, nephrotic syndrome) radiocontrast exposure to nephrotoxins (e.g

2019 BMJ Best Practice

178. Hyponatraemia

water excretion fractional excretion of sodium thyroid-stimulating hormone serum cortisol level and/or adrenocorticotrophic hormone test serum lipids and serum protein electrophoresis CT brain, chest, abdomen/pelvis other tests targeted at evaluating the underlying cause Treatment algorithm ACUTE ONGOING Contributors Authors Associate Director Nephrology MedStar Washington Hospital Center Washington DC Disclosures JHV declares that she has no competing interests. Peer reviewers Director Department (...) Hyponatraemia Hyponatraemia - Symptoms, diagnosis and treatment | BMJ Best Practice You'll need a subscription to access all of BMJ Best Practice Search  Hyponatraemia Last reviewed: February 2019 Last updated: January 2019 Summary Defined as a serum sodium concentration of <135 mmol/L. Most common electrolyte disorder encountered in clinical practice. Can occur in settings of volume depletion, volume overload, or euvolaemia. Serum osmolality, urine osmolality, and urine sodium concentration

2019 BMJ Best Practice

180. Guidelines on Diabetes, Pre-Diabetes and Cardiovascular Diseases developed in collaboration with the EASD Full Text available with Trip Pro

rate; GLP1-RA = glucagon-like peptide-1 receptor agonist; HF = heart failure; HFrEF = heart failure with reduced ejection fraction; ICD = implantable cardioverter defibrillator; LEAD = lower extremity artery disease; MRA = mineralocorticoid receptor agonist; o.d. = once daily (omni die); PAD = peripheral arterial disease; PCSK9 = proprotein convertase subtilisin/kexin type 9; RAAS = renin–angiotensin–aldosterone system; SGLT2 = sodium-glucose co-transporter-2; T1DM = type 1 diabetes mellitus T2DM (...) Sulfonylureas 38 8.5.3 Thiazolidinediones 38 8.5.4 Dipeptidyl peptidase-4 inhibitors 38 8.5.5 Glucagon-like peptide-1 receptor agonists 38 8.5.6 Sodium-glucose co-transporter 2 inhibitors 38 9 Arrhythmias: atrial fibrillation, ventricular arrhythmias, and sudden cardiac death 40 9.1 Atrial fibrillation 40 9.1.1 Diabetes and risk of stroke in atrial fibrillation 40 9.2 Ventricular arrhythmias and sudden cardiac death 40 9.2.1 Ventricular premature beats and paroxysmal ventricular tachycardia 40 9.2.2

2019 European Society of Cardiology

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