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We reviewed baseline and follow-up clinical and echocardiographic data on patients receiving CRT in a single centre. Indices of global left ventricular (LV) function and dyssynchrony before and after CRT were measured. Patients were then divided into those receiving their first device (n = 39) and those receiving CRT as an upgrade to existing RV pacemakers (n = 32). Baseline demographic variables, indices of global LV function, symptomatic status, renal function, hemodynamics, and diuretic requirements were not different between previously paced patients and nonpaced patients. Mean length of RV pacing in the previously paced patients was 59 months (range 12-167 months). Patients in the previously paced group had a broader QRS complex than patients with intrinsic LBBB. Aortopulmonary delay of longer than 40 ms was present in 68% of all subjects, 67% had intraventricular septal and posterior wall motion delay longer than 130 ms, and 59% had an intraventricular delay as measured by tissue Doppler imaging of longer than 65 ms. There was no difference between paced and nonpaced patients for any of these measures of dyssynchrony. QRS duration was reduced to a greater extent in the previously paced patients than those with no previous device therapy. CRT led to important reductions in each dyssynchrony variable in both patients with previous RV pacing and those with intrinsic LBBB. The magnitude of these changes in measures of dyssynchrony was not different between the 2 groups. In all patients undergoing CRT, 50% had a reduction in furosemide dose at 3 months, 56% an improvement of at least 1 grade in New York Heart Association status, and 66% an improvement of at least 5% in LVEF. Divided by group, previously paced patients were no more or less likely than newly implanted patients to achieve one or more of these clinical outcomes.
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Although PTC most frequently occurs in obese females of childbearing age, the syndrome occurs in children as well.(3),(5) Prepubertal children with PTC have a lower incidence of obesity compared with adults and there is no sex predilection. The onset of puberty is best defined by the onset of secondary sexual characteristics such has menarche, pubic hair, and breast development. Children with PTC have a higher incidence of associated conditions and cranial nerve deficits compared with adults. Similar to adult patients, children are at risk for the development of permanent visual loss. In rare instances, children initially diagnosed with PTC will be found to harbor an intracranial neoplasm such as gliomatosis cerebri. An intracranial pressure of 28 cm H2O has recently been established as the upper limit of normal in children.31 Treatment is indicated for the symptomatic management of headaches and to preserve vision. Most children respond to medications such as acetazolamide, furosemide, or topiramate. Surgical treatment such as ONSF and shunting procedures are indicated for children with severe headaches, visual loss, or both despite maximal tolerated medical treatment.
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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.
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There was no significant difference in the mean change in serum creatinine level at the end of 48 h between groups (p = 0.08). There was also no significant difference among groups regarding loss of body weight (p = 0.66). A significantly shorter hospitalization was observed in patients treated with HSS compared with the other groups (cIV group 6.6 ± 3.4 days vs. bI group 7.9 ± 4.1 days vs. HSS group 3.7 ± 1.3 days; p < 0.01).
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To study long-term effects of enalapril, an angiotensin-converting enzyme inhibitor, and hydralazine, an arteriodilator, on renin-angiotensin-aldosterone system and fluid balance before and after administration of furosemide.
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During continuous treatment with diuretics, the kidney adapts to the initial Na loss by activating antinatriuretic mechanisms which serve to prevent further Na and volume losses. To study the renal sites of adaptations to constant diuretic treatment, bendroflumethiazide (4 mg daily), furosemide (8 mg daily) or vehicle (0.24 ml daily) was infused intraperitoneally to female Wistar rats by implanted osmotic minipumps. Half of the animals (groups vol.) were randomized to receive a balanced saline solution to drink in addition to water in order to replace Na, K and volume losses. On the 6th day of treatment, clearances of inulin, Na, and Li were determined during four consecutive 6 hr periods. Circadian changes in renal excretions occurred in all groups with highest excretions of Na, Li and water in the dark period (6 p.m. to 6 a.m.). Renal changes induced by continuous infusion of diuretics were most pronounced in the dark period and would probably not have been disclosed if the clearance experiments had been restricted to the daytime. The average 24-hour clearance for inulin (glomerular filtration rate) was not different among groups, except for a 20% decrease in the furosemide group. The 24-hour fractional Na excretion, being approximately 0.5% in the vehicle group, increased to approximately 0.8% in group (bendroflumethiazide+vol) and to approximately 2.8% in group (furosemide+vol) but was not different from the vehicle group in the diuretic groups without volume replacement.(ABSTRACT TRUNCATED AT 250 WORDS)
The cardiorenal syndrome is not well understood, and a uniform definition is lacking. Worsening renal function as determined by a decline in creatinine clearance in patients with decompensated heart failure is an identifier of patients with this syndrome. Treatment is a challenge. Diuretic therapy is valuable in treating congestion but may worsen renal function. Patients with decompensated heart failure are often refractory to diuretics, in which case higher doses must be used or alternate methods explored to reduce salt and water.
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In paediatrics drugs are prescribed as mg/kg doses to facilitate accurate dosing. Anecdotally, some drugs are prescribed in such a way that the volume to be given is difficult to measure which may lead to inaccuracies and potential for error. Locally, errors have been reported where there has been a misunderstanding of the required dose, especially when decimal points are involved. This audit aimed to evaluate doses prescribed for in-patient children and evaluate whether they can be measured using the printed markings of one oral syringe.
The mechanism of gamma-aminobutyric acid (GABA)-induced suppression of 5-hydroxytryptamine (5HT)-induced contractility of cerebral blood vessels was studied in single smooth muscle cells isolated from the guinea-pig basilar artery. GABA reduced 5HT-induced contraction of single smooth muscle cells, and the effect of GABA was mimicked by muscimol, but not baclofen. The response of muscimol was antagonized by bicuculline, thereby indicating that GABAA receptors exist on the smooth muscle of the basilar artery. Since GABA did not change the contraction induced by the addition of Ca2+ to the Ca2+-free medium in the presence of high K+, it is unlikely that GABA inhibits the influx of extracellular Ca2+. The caffeine-induced contraction in the Ca2+-free medium was reduced by GABA, and the effect of GABA was not obtained by treatment with furosemide and in the Cl- -free medium. These results indicate that GABA acts on the GABAA receptor located on smooth muscle cells and reduces the contractility of the basilar artery by suppression of the mobilization of intracellular Ca2+.
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Contrast medium in combination with NOS and COX inhibition resulted in widespread induction of HIF in the outer and inner medulla that was initiated within 10 minutes, reached the highest levels at 2 hours and diminished 8 hours to 24 hours thereafter. HIF isoforms were expressed in a cell type-specific fashion: HIF-1alpha in tubular and HIF-2alpha in interstitial and endothelial cells. The degree of HIF-1alpha accumulation varied between nephron segments, being much stronger in collecting ducts than in medullary thick ascending limb of the loop of Henle (mTAL). Comparison with pimonidazole staining and the effect of furosemide indicated that HIF induction in mTAL is maximal with moderate hypoxia and declines with increasing severity of hypoxia.
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Amplitude and phase responses of distortion product otoacoustic emissions as a function of stimulus frequency ratio were measured for frequencies between 2 and 48 kHz, in Mongolian gerbils (Meriones unguiculates) aged 15 to 30 days after birth. After baseline measurements, furosemide was administered to distinguish active from passive emissions. At all ages, structure in the form of multiple peaks was observed in the amplitude responses of specific odd-order emissions. This structure depended on the emission frequency, not the stimulus frequency ratio, and did not generally depend on the stimulus amplitude. Nor was it dependent on the functioning of the cochlear amplifier: At moderate stimulus levels, the observed emission distribution simply shifted to lower amplitudes when the cochlear amplifier was made temporarily dysfunctional by furosemide injection. The center frequencies and widths of the peaks in the amplitude response did not generally change with age, except that the relative amplitudes of the higher-frequency peaks were increased in younger animals. At 2 kHz, however, the distribution showed other evidence of maturation, with the frequency of maximum emission moving downward with age. The phase responses yielded estimates of the round trip signal (group or traveling wave) delay. At a given frequency, the active signal delay typically decreased substantially with increasing stimulus level. However, there was a rapid variation in delay as the stimulus level passed the normal active-passive crossover level. At stimulus levels measured relative to the active-passive crossover level, i.e., either 20 or 30 dB lower, the active signal delay decreased only slightly with age. Overall, both filter response and signal delay characteristics were found to be essentially mature near the onset of hearing.
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To retrospectively investigate the effect of carvedilol and spironolactone plus furosemide, administered concomitantly with an angiotensin II converting enzyme inhibitor (ACE-I) or an angiotensin II receptor blocker (ARB) to patients with chronic heart failure (CHF).
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Our results demonstrated that furosemide given as an adjuvant medication in patients with DTC causes a significant decrease in urinary excretion of radioiodine and its higher blood concentration. Therefore, furosemide should not be recommended as an adjuvant therapy to radioiodine ablation in patients with DTC previously iodine depleted by low-iodine diet.
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The study included 34 males and 10 females from 1 to 9 months old (median age 2.6 months) with unilateral congenital hydronephrosis. A 99mtechnetium (Tc) mercaptoacetyltriglycine (MAG3) scan was performed, and regions of interest were drawn on the kidneys, and perirenal and lateral backgrounds. Differential renal function was calculated with and without background subtraction at 30-second intervals from 0.5 to 3 minutes after injection of 99mTc-MAG3. The effects of age, sex, obstruction, site and size of the hydronephrotic kidney were analyzed using the generalized estimating equations method.
Patients with severe left ventricular dysfunction and chronic renal insufficiency who are being considered for procedures that necessitate bowel cleansing with PEG-ELS may be at risk for sodium and water retention and exacerbation of CHF.
In brain slices from young (postnatal day (P) 10--15) rat somatosensory cortex, real-time neuronal intracellular Cl(-) concentration ([Cl(-)](i)) recordings were made by an optical technique measuring 6-methoxy-N-ethlquinolinium iodide (MEQ) fluorescence. Oxygen--glucose deprivation (in vitro model of ischemia) induced a long-lasting [Cl(-)](i) increase preceded by a rapid, transient [Cl(-)](i) decrease that could not be inhibited by blockers of Cl(-) pumps, Cl(-) channels, or Cl(-) antiporters, but was sensitive to cation-Cl(-) cotransporter inhibitors (bumetanide and furosemide). Use of low external Na(+) or high external K(+) revealed that the Na(+),K(+)-2Cl(-) cotransporter was inhibited by bumetanide and furosemide, whereas the K(+)-Cl(-) cotransporter was preferentially inhibited by furosemide under our experimental conditions. With a reduced inward driving force for Na(+) (reducing Na(+),K(+)-2Cl(-) cotransport), the transient [Cl(-)](i) decrease was only rarely induced by oxygen-glucose deprivation. In contrast, with a reduced outward driving force for K(+) (reducing K(+)-Cl(-) cotransport), the transient [Cl(-)](i) decrease still occurred. These results suggest that the transient [Cl(-)](i) decrease was primarily mediated by a rapid inhibition of the inwardly directed Na(+),K(+)-2Cl(-) cotransporter. Reverse transcriptase-polymerase chain reaction (RT-PCR) experiments suggested that the isoform involved is NKCC1. We hypothesize that the initial rapid Cl(-) efflux might effectively delay the irreversible Cl(-) influx that mediates neuronal injury.
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Observational, cross-sectional study.
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It can be concluded that the role of lipids and hydrophilic silica based carrier highlighted in enhancing solubility and permeability, and hence the oral bioavailability of poorly soluble drugs.
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36Cl- uptake was markedly (85 per cent) inhibited by the loop diuretics, furosemide and bumetanide. Partial replacement of Na+ in the incubation medium (from 137 to 5 mM) reduced 36Cl- uptake 30 per cent; total replacement reduced uptake to 40-45 per cent of control values. Partial replacement of K+ (from 5.8 to 1 mM) decreased 36Cl- uptake approx. 45 per cent; complete replacement resulted in minimal levels of 36Cl- uptake (less than 10 per cent of controls). Ouabain reduced 36Cl- uptake approx. 55 per cent in the absence of bumetanide, but was without effect in its presence. 86Rb+ uptake was reduced approx. 85 per cent with bumetanide; complete replacement of Cl- with I- or gluconate-, decreased 86Rb+ uptake by 55 or 40 per cent respectively. The results support the notion that the bulk of Cl- influx in rat parotid acinar cells is via a loop diuretic-sensitive Na+/K+/Cl- co-transport mechanism as may occur in other secretory epithelia.
We microperfused the loop of Henle (LOH) to assess its contribution to urine acidification in vivo. Under control conditions (Na HCO3- = 13 mM, perfusion rate approximately 17 nl/min-1) net bicarbonate transport (JHCO3-) was unsaturated, flow- and concentration-dependent, and increased linearly until a bicarbonate load of 1,400 pmol.min-1 was reached. Methazolamide (2 x 10(-4) M) reduced JHCO3 by 70%; the amiloride analogue ethylisopropylamiloride (EIPA) (2 x 10(-4) M) reduced JHCO3 by 40%; neither methazolamide nor EIPA affected net water flux (Jv). The H(+)-ATPase inhibitor bafilomycin A1 (10(-5) M) reduced JHCO3 by 20%; the Cl- channel inhibitor 5-nitro-2'-(3-phenylpropylamino)-benzoate (2 x 10(-4) M) and the Cl(-)-base exchange inhibitor diisothiocyanato-2,2'-stilbenedisulfonate (5 x 10(-5) M), had no effect on fractional bicarbonate reabsorption. Bumetanide (10(-6) M) stimulated bicarbonate transport (net and fractional JHCO3-) by 20%, whereas furosemide (10(-4) M) had no effect on bicarbonate reabsorption; both diuretics reduced Jv. In summary: (a) the LOH contributes significantly to urine acidification. It normally reabsorbs an amount equivalent to 15% of filtered bicarbonate; (b) bicarbonate reabsorption is not saturated; (c) Na(+)-H+ exchange and an ATP-dependent proton pump are largely responsible for the bulk of LOH bicarbonate transport.
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Both the commonly employed thiazide diuretics and chlorthalidone and the loop diuretics furosemide, piretanide and xipamide lead, to varying extents, to an increase in total and LDL cholesterol as well as triglycerides in subjects with normal metabolism. In addition, some diuretics lower the levels of protective HDL cholesterol. These side effects can be avoided--at least in part--by a combination with such drugs as prazosin, pindolol or captopril, which have a favorable effect on metabolism.
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Few data exist to help physicians in the use of diuretics to provide the greatest symptomatic benefit with the least adverse effect to patients and to select the subset of patients who require a more aggressive diuretic strategy and monitoring. The aim of this study is to identify early predictors of diuretic response in a selected group of patients with acutely decompensated chronic heart failure (ADCHF).
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In CHF, the use of CVVHDF effectively and safely produced greater weight and fluid loss and decreased LOS in the ICU more than the intravenous furosemide with no hemodynamic instability.
Based on five randomized controlled trials (RCTs) involving 1,032 patients treated with i.v. HSS plus furosemide vs. 1,032 patients treated with i.v. furosemide alone, a decrease in all-cause mortality in patients treated with HSS plus furosemide was proven [RR = 0.57; 95 % confidence interval (CI) = 0.44-0.74, p = 0.0003]. Likewise, combined therapy with HSS plus furosemide was shown to be associated with a reduced risk of ADHF-related re-hospitalization (RR = 0.51; 95 % CI = 0.35-0.75, p = 0.001). Besides, combined therapy with HSS plus furosemide was found to be associated with a reduced length of hospital stay (p = 0.0002), greater weight loss (p < 0.00001), and better preservation of renal function (p < 0.00001).
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Cell volume changes critically determine hepatic signal transduction and metabolism. Hepatocyte swelling by insulin contributes to p38(MAPK) activation leading to inhibition of autophagic proteolysis. Recently integrins were shown to sense hypoosmotic hepatocyte swelling. Here the role of integrins, Src, and focal adhesion kinase (FAK) in insulin signaling was investigated using the intact organ model of perfused rat liver. Insulin increases [Tyr(P)(418)]Src, [Tyr(P)(397)]FAK, and dual p38(MAPK) phosphorylation by about 2-fold. Infusion of the integrin-antagonizing hexapeptide GRGDSP or the Src inhibitor PP-2 prevented activation of Src and p38(MAPK) and, consequently, proteolysis inhibition by insulin. However, insulin-induced phosphorylation of IRbeta (Tyr(1158)) and protein kinase B (PKB, Ser(473)), as well as K(+)-uptake and cell swelling, was not reduced by the inhibitors. Both hypoosmotic swelling and insulin increase the plasma membrane levels of activated beta(1) integrin. Inhibition of insulin-induced swelling by furosemide largely abolished activation of beta(1) integrin and phosphorylation of Src, but not of PKB. Rapamycin does not affect either insulin-induced K(+)-retention and cell swelling or proteolysis inhibition, indicating that swelling-dependent proteolysis inhibition occurs independently from the mammalian target of rapamycin. The data suggest that sensing of cell swelling by integrins essentially contributes to insulin signaling, thereby defining a novel way of integrin involvement in growth factor signaling.
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The proposed SIC-FL method features satisfactory sensitivity for AML and FSM in urine samples for the minimum required performance limits recommended by the World Anti-Doping Agency, besides a downscaled consumption of reagents and high rapidity for industrial-scale analysis of pharmaceutical preparations.
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Gout is the most common type of inflammatory arthritis in man caused by deposition of urate crystals into the joints as the result of elevated serum urate levels. A case of a 59-year-old patient with untreated, long-lasting gout and clinical manifestation of decompensated global dilated cardiomyopathy is presented. Examination revealed generalized pitting edema extending from both lower extremities to the sacrum, abdominal, and thoracic wall, with scrotal swelling and upper extremity involvement, an exceptionally vast generalized edema, i.e. anasarca. Proximal and distal interphalangeal joints of the hands and feet were swollen and deformed, with marked yellow tophi nodules. Laboratory studies revealed high serum uric acid concentration (546 micromol/L), decreased creatinine clearance (0.8 mL/s) and albumin concentration (27.4 g/L), as well as increased total urine protein mass (0.35 g/24 h). X-rays of the affected feet and fists showed punched-out lesions of the subchondral bone with overhanging bony margins in the first metatarsophalangeal, proximal, and distal interphalangeal joints of both hands. The extreme clinical presentation resolved upon intravenous administration of diuretics and pleurocentesis, followed by oral medications including furosemide, angiotensin-converting enzyme inhibitor, spironolactone and digoxin. Since serum urate level has been identified as an independent risk factor for the development of ischemic heart and chronic kidney disease, regulation of urate concentration is necessary, especially in patients diagnosed with gout.
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A 53-year-old woman with severe cor pulmonale and generalized edema complicating COPD received low-dose dopamine to stabilize blood pressure and, perhaps, improve cardiac output. Low-dose dopamine also improved her renal function and enhanced the diuretic response to furosemide therapy.
The study included 15 healthy individuals aged 37.3 +/- 7.7 years and 27 patients with the primary uncomplicated blood hypertension (stages I and II according to WHO classification) of the comparable age, untreated and given a diet containing 100-120 nM Na+ daily. Plasma ANP concentrations were measured prior to and after 30, 60, and 90 minutes following 40 mg furosemide intravenously. An increase in 1-minute urine output and 1-minute Na+ excretion in the urine were determined during 90 minutes following furosemide administration. A significant decrease in ANP plasma levels was noted in all examined individuals following furosemide administration in all time intervals comparing with baseline values. An increase in 1-minute urine output and 1-minute sodium excretion with the urine significantly correlated with plasma ANP decrease during 90 minutes following furosemide administration. The obtained results suggest that furosemide inhibits ANP secretion in the patients with uncomplicated primary hypertension similarly to healthy individuals.
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Diuretics are widely used antihypertensive agents, and although their renal actions have been well characterized, the extent of their vascular effects remains to be defined. Because hypertension is associated with numerous vascular complications whose incidences are not always lowered once blood pressure is regulated, this study was undertaken to evaluate the effects of five selected diuretics on capillary permeability to see if they could contribute in some way to these vascular abnormalities. Extravasation of Evans blue dye (EB: 20 mg/kg) injected in the caudal vein of male Wistar rats was used to assess capillary permeability to albumin. Indapamide (0.04 mg/kg), cicletanine (2.0 mg/kg), amiloride (0.3 mg/kg), hydrochlorothiazide (0.5 mg/kg) and furosemide (0.5 mg/kg) were administered by acute i.v. injection or by 10-day "chronic" gavage. EB extravasation was increased in the upper bronchi, lung parenchyma and kidney after acute administration of indapamide (54, 41 and 31%, respectively) and hydrochlorothiazide (45, 41 and 19%, respectively), and increased in all tissues but the duodenum (upper bronchi, lung parenchyma, heart, liver, kidney and muscle; 57-118%) after furosemide. In contrast, capillary permeability was reduced after acute cicletanine in the heart (31%), duodenum (49%) and muscle (58%) and after amiloride in the heart (25%) and muscle (63%). Pretreatment with indomethacin abolished most changes in EB extravasation induced by acute injection of the diuretics. After 10-day gavage, however, changes in capillary permeability were null after amiloride or hydrochlorothiazide treatment, attenuated after cicletanine or furosemide or even reversed after indapamide. Arterial pressure was not affected by diuretic treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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Patients with fluid overloading and hypoalbuminemia who needed diuretic treatment were enrolled and were divided into 2 groups: the first group having clearance of creatinine (CCr) >20 ml/min, and the second group having CCr < or = 20 ml/min. FU (60 mg) mixed with HA (HA group), 60 mg FU mixed with FFP (FFP group) and water (placebo group) were given intravenously to these patients for 60 minutes in random order on the first, third and fifth day. After drug administration, 8-hour urine was collected, and urine amount and urinary sodium excretion were checked.
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Autosomal dominant hypocalcemia type 1 (ADH1) is a relatively rare endocrine disorder characterized by hypocalcemia and inadequate parathyroid hormone secretion. ADH is caused by activating mutations in the calcium-sensing receptor (CaSR) gene, CASR. CaSR plays a crucial role in calcium and magnesium homeostasis in the kidney. ADH may be accompanied by hypokalemia and metabolic alkalosis when it is classified as type V Bartter syndrome. However, the mechanism underlying hypokalemia in this disease is unclear.
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The exploitation of hot-melt extrusion and injection molding for the manufacturing of immediate-release (IR) tablets was preliminarily investigated in view of their special suitability for continuous manufacturing, which represents a current goal of pharmaceutical production because of its possible advantages in terms of improved sustainability. Tablet-forming agents were initially screened based on processability by single-screw extruder and micromolding machine as well as disintegration/dissolution behavior of extruded/molded prototypes. Various polymers, such as low-viscosity hydroxypropylcellulose, polyvinyl alcohol, polyvinyl alcohol-polyethylene glycol graft copolymer, various sodium starch glycolate grades (e.g., Explotab(®) CLV) that could be processed with no need for technological aids, except for a plasticizer, were identified. Furthermore, the feasibility of both extruded and molded IR tablets from low-viscosity hydroxypropylcellulose or Explotab(®) CLV was assessed. Explotab(®) CLV, in particular, showed thermoplastic properties and a very good aptitude as a tablet-forming agent, starting from which disintegrating tablets were successfully obtained by either techniques. Prototypes containing a poorly soluble model drug (furosemide), based on both a simple formulation (Explotab(®) CLV and water/glycerol as plasticizers) and formulations including dissolution/disintegration adjuvants (soluble and effervescent excipients) were shown to fulfill the USP 37 dissolution requirements for furosemide tablets.
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A renal unit was defined as a kidney and its ureter. There were 262 renal units with 4 patients having a solitary kidney. 90 normal and 172 abnormal renal units on sonography were assessed by F+0 diuresis renography. The furosemide clearance half time for the 90 normal renal units was 5.8 +/- 1.4 min. Of the 172 abnormal renal units, 100 were classified as nonobstructed and 72 as obstructed on diuresis renography. All 100 nonobstructed renal units were correctly classified with no false-negative studies; of the 72 renal units classified as obstructed, there were 43 true-positive studies and 29 false-positive studies. The sensitivity was 100%, specificity was 78% and accuracy was 83%.
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The magnesium loading test is a useful tool in the diagnosis of magnesium deficiency. In order to establish a reference range in normal subjects, 88 healthy men and women aged between 18 and 66 years were given 30 mmol magnesium intravenously during eight hours as a loading test, urine was collected from start of infusion for 24 h for measurement of magnesium excretion. The magnesium mean retention was 6.3 +/- 10.3% of the loading dose, and the 0.025 and 0.975 fractiles were -19.5% and 27.5%, respectively. There was no significant difference between the sexes or in the different age groups studied. There was no correlation between the magnesium retention and serum magnesium or with basal urinary magnesium excretion. An excess excretion of magnesium was observed the postload day compared to baseline, but the excretion 24 and 48 h after the magnesium loading were closely correlated, suggesting that 24 h urinary sampling is sufficient. In order to examine the reproducibility of the test 23 of the subjects underwent two magnesium loading tests 4 weeks apart. The mean difference between two repeat magnesium loading tests was 2.0% with a SD of 8.1% and a 95% confidence interval of -1.6-5.5%. Normal saline did not affect baseline magnesium excretion. Concomitant administration of ethanol or physical exercise caused greater variation in magnesium excretion, whereas furosemide was without effect. The 8 h magnesium loading test with 24 h urine sampling seems to be fairly reproducible, is adequate for clinical use, but the normal range is wide.
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Allergy to furosemide is a rare phenomenon. Desensitization to this sulfa-containing drug has not been frequently performed. We describe a patient with severe congestive heart failure and type I allergy to furosemide. Because of the severity of her condition, we decided to use a rapid intravenous desensitization protocol. Following the desensitization, the patient was treated with intravenous and oral furosemide with a dramatic improvement in her clinical state. We suggest that rapid desensitization may be a safe and effective way of introducing furosemide to allergic patients for whom loop diuretics are urgently indicated.
After a mean follow-up of 28 months, two patients showed isolated biochemical recurrence and six patients remained free of recurrence. In seven patients with functional allografts, the creatinine clearance was unimpaired by treatment. However, significant obstruction of the terminal ureter was revealed in two patients by furosemide-stimulated diethylenetriaminepentaacetic acid renograms. The doses delivered to the uretero-neocystostomy were calculated to range from less than 20 Gy to more than 45 Gy depending on bladder repletion.
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Telmisartan 1-O-acylglucuronide, the principal metabolite of telmisartan in humans, was characterized in terms of chemical stability and the structure of its isomerization products was elucidated. In addition, pharmacokinetics of telmisartan 1-O-acylglucuronide were assessed in rats after i.v. dosing. Similar to other acylglucuronides, telmisartan 1-O-acylglucuronide and diclofenac 1-O-acylglucuronide, which was used for comparison, showed the formation of different isomeric acylglucuronides on incubation in aqueous buffer. The isomeric acylglucuronides of telmisartan consisted of the 2-O-, 3-O-, and 4-O-acylglucuronides (alpha,beta-anomers). First order degradation half-lives of 26 and 0. 5 h were observed on incubation in buffer of pH 7.4 for the 1-O-acylglucuronides of telmisartan and diclofenac, respectively. This indicated that the 1-O-acylglucuronide of telmisartan was among the most stable acylglucuronides reported to date. The high stability of telmisartan 1-O-acylglucuronide was confirmed by in vitro experiments that indicated only very low covalent binding of telmisartan acylglucuronide to human serum albumin but a considerable amount of covalently bound radioactivity with the acylglucuronide of diclofenac. After i.v. dosing to rats, telmisartan 1-O-acylglucuronide was rapidly cleared from plasma with a clearance of 180 ml/min/kg, compared with 15.6 ml/min/kg for the parent compound. Because telmisartan 1-O-acylglucuronide exhibited a comparably high chemical stability together with a high clearance that resulted in low systemic exposure, the amount of covalent binding to proteins should be negligible compared with other frequently used drugs, such as furosemide, ibuprofen, or salicylic acid.