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Of 52 cases with 56 affected renal units having symptoms and signs suggestive of Ureteropelvic Junction Obstruction (UPJO) evaluated by conventional (F + 15) diuretic renography where frusemide is given 15 minutes post-injection of radiopharmaceutical m99TC.DTPA.F + 15, twelve (21%) showed a good clearance (group A), 16 (28%) showed partial (group B) and 28 (50%) a poor clearance pattern (group C) indicating a definite obstruction. A high flow (F-15) diuretic renography where frusemide is given 15 minutes prior to the radiopharmaceutical m99TC.DTPA, was done in 23 cases with 27 affected renal units. Eleven renal units showed a good clearance (group A). Of these, 7 (64%) showed a persistent good clearance, 3 (27%) converted to poor clearance and 1 (9%) to partial clearance pattern. Of 8 renal units in group B, 5 (63%) converted to poor clearance and two (25%) to good clearance on F-15 and one remained unchanged. All renal units which presented as poor clearance (group C) on conventional (F + 15) diuretic renography remained unchanged on high flow (F-15) diuretic renography. In majority of cases conventional (F + 15) renography gave a reliable assessment of the upper tract drainage, however, since equivocal group was resolved by the F-15 and the intermittent obstruction group was definitely diagnosed, high flow (F-15) diuretic renography was more conclusive in assessment as compared to F + 15.
It was shown in chronic rat experiments that multiple microinjections of furosemide into the rostral region of the neostriatum facilitated avoidance conditioning in a shuttle box and prevented from GABA-induced deviant freezing, but did not abolish the choreic hyperkinesis produced by picrotoxine (GABA-A receptors antagonist) intrastriatal microinjections. Simultaneous microinjections of furosemide and picrotoxine into the neostriatum increased differences in parameters of picrotoxine-induced hyperkinesis between rat groups capable and incapable (extinct reflex) for conditioned avoidance. These findings point to a certain correlation between the intensity of hyperkinesis, capability for acquisition and realization of avoidance conditioning, and activity of neostriatal neurotransmitter systems involved in neuronal homeostasis. The findings suggest an involvement of neostriatal GABAergic system in conditioning and organization of free locomotor behavioral acts.
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Myo-inositol is a major compatible osmolyte in the renal medulla and is accumulated in cells under hypertonic conditions by uptake via a Na+/myo-inositol cotransporter (SMIT). SMIT is regulated by extracellular osmolarity at the transcription level. We investigated localization of SMIT in rat kidney by immunohistochemical staining using an anti-SMIT-antibody raised against a synthetic peptide corresponding to part of SMIT and by in situ hybridization. SMIT protein localized predominantly to the basolateral membranes of cells of the thick ascending limb of Henle (TAL) and inner medullary collecting duct (IMCD). Macula densa (MD) cells, identified as the Tamm-Horsfall-protein (THP)-unreactive cells surrounded by THP-reactive TAL cells, also stained for anti-SMIT. In situ hybridization yielded the intense SMIT signals in the TAL and IMCD and also in the juxtaglomerular (JG) region. Prior loading of the animal with a high concentration of NaCl rapidly induced SMIT mRNA; furosemide down-regulated it. The high level of SMIT expression suggests that MD cells are exposed to hypertonicity at the basolateral surface. Because SMIT expression seemed to be proportional to the magnitude of NaCl reabsorption, it may be a good marker for examination of the tubuloglomerular feedback mechanism in vivo.
A 13-year-old llama was examined because of lethargy, inappetence, and syncope.
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We assigned heart transplant recipients 18 years of age or older who were oliguric (urine output < 400 ml/day); had volume overload and estimated glomerular filtration rate <60 ml/min/1.73 m(2) of body surface area calculated with the use of the Modification of Diet in Renal Disease equation, to designed initiation of intervention. We followed 30 patients for up to 30 days. The primary outcome was estimated glomerular filtration rate status after intervention.
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This study was designed to assess: (1) whether furosemide modifies the incidence of failure to close a symptomatic patent ductus arteriosus (PDA) in response to indomethacin in premature infants, (2) whether furosemide decreases renal and hydromineral side effects of indomethacin, and (3) whether the effects of furosemide on renal function depend on initial extracellular volume [assessed by blood urea nitrogen (BUN)/creatinine ratio]. We did a systematic review and meta-analysis of all published controlled trials assessing either ductal closure or renal function after randomized allocation to treatment with indomethacin and furosemide versus indomethacin alone. All of the three studies meeting entry criteria were small and had methodological limitations. The number of patients was too small to rule out a 10% risk increase in failure of ductal closure. After the first dose of indomethacin, patients receiving furosemide had higher urine output, fractional excretion of sodium, and osmolar clearance than controls. Among patients with initial BUN/creatinine ratio <20, those on furosemide had a higher glomerular filtration rate (GFR) than controls. Among patients with initial BUN/creatinine of 20-30, those on furosemide had a lower GFR than controls. Thus, dehydration appears to be a contraindication for furosemide administration in premature infants treated with indomethacin for symptomatic PDA. The risk-benefit ratio of administering furosemide in well-hydrated patients treated with indomethacin for symptomatic PDA could only be assessed by a large randomized clinical trial.
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Laparoscopic partial nephrectomy (LPN) has not received widespread clinical application because of its technical challenge. Bovine serum albumin glutaraldehyde (BSAG) is a hemostatic agent that is independent of the clotting cascade. We evaluated the use of BSAG as the sole agent for parenchymal and collecting system closure during LPN in a survival porcine model.
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A 61-year-old man suffering from histologically confirmed amyloidosis associated with coagulation disturbances presented with exercise induced shortness of breath and symptoms of cardiac asthma after four cycles of chemotherapy with melphalan and prednisolone. As a result, treatment with digitoxin was initiated. In addition furosemide and an oral nitrate were administered.
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To determine whether gamma-aminobutyric acid (GABA) affects the contractile properties of airway smooth muscle and, if so, what the mechanism of action is, the authors studied guinea pig tracheal rings under isometric conditions in vitro. GABA and related substances, baclofen and muscimol, had no effect on the resting tension but reversibly depressed contractions induced by electrical field stimulation in a dose-dependent fashion, IC50 values (mean +/- S.E.) being 5.6 +/- 1.4 X 10(-6) M, 6.8 +/- 0.9 X 10(-6) M and 8.5 +/- 1.5 X 10(-5) M, respectively. In contrast, GABA did not alter the response to exogenous acetylcholine or the nonadrenergic noncholinergic inhibitory component. Pretreatment of tissues with bicuculline antagonized the inhibitory effect of GABA as well as that of baclofen. This inhibitory effect was not modified by propranolol, phentolamine, hemicholinium-3 or naloxone, but it was blocked by the Cl channel blocker furosemide and by the substitution of external Cl. These results suggest that GABA decreases the contractile response of airway smooth muscle to cholinergic nerve stimulation by inhibiting the evoked release of acetylcholine and that this effect is exerted by activating Cl-dependent, bicuculline-sensitive GABA receptors.
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To investigate the effect of intravenous normal saline fluid load, with and without furosemide, upon the renal resistive index (RI) of obstructed and nonobstructed kidneys.
The aim of the present study was to investigate the influence of the rate of delivery of frusemide to its site of action on the effect and efficiency of the drug.
Rabbit tracheocytes were isolated by protease treatment and plated onto collagen-treated permeable supports at 1.3 x 10(6) cells/cm2. After 24 hr, cell layers were cultured either air-interfaced (AIC) on their apical surface or under conventional liquid covered conditions (LCC).
To review medications that can affect serum calcium concentrations.
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The experiments were carried out on unanaesthetized dogs with exteriorized ureters. The left kidney was denervated. The function of the left and right kidneys was compared prior to and after furosemide administration, 0.2 mg/kg b. w. The function of the right intact kidney prior to and after left kidney denervation was also compared. The concentrations of sodium, potassium, chloride, calcium, magnesium, zinc, copper, urea, and creatinine in plasma and urine were determined. Denervation of the left kidney was followed by an increase of diuresis, calcium, and copper excretion from the denervated kidney. After furosemide administration the chloride excretion from the side of denervation was also observed to increase. The changes in the excretory function of the left kidney after denervation were not accompanied by changes in excretory function of right (intact) kidney. The excretory function of the intact kidney after denervation of contralateral kidney and furosemide administration did not differ from that prior to denervation and furosemide administration. In unanaesthetized dogs no changes in the excretory function of intact kidney were observed as a result of contralateral kidney denervation.
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Microcapsules with self-microemulsifying core were originated by the vibrating nozzle method. Alginate-pectin (A/P) ratio of the shell forming phase was optimized with regard to core phase retention and drug release kinetics from dried microcapsules. Well shaped microcapsules with high encapsulation efficiency were produced when an A/P composition of 25:75 was used. Microcapsules with higher pectin content exhibited faster drug release, which was additionally enhanced by the addition of sodium chloride to the shell phase.
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The existence of supranormal differential renal function in unilateral hydronephrosis remains controversial. While some authors consider it as fact, others believe that it is just a technical artifact. Within our department, chromium-51 ethylene diamine tetra-acetic acid (Cr-EDTA) renal clearance is systematically performed in conjunction with technetium-99m mercaptoacetyltriglycine (MAG3) renograms to derive an absolute single kidney glomerular filtration rate (SKGFR). Our data allows us to ascertain whether supranormal differential renal function in unilateral hydronephrosis might be due to hypofunction of the contralateral kidney. Children with marked unilateral hydronephrosis were selected from a large database of MAG3 diuretic(s) renograms. We excluded patients with posterior urethral valves, duplex anomalies, neurogenic bladder, solitary kidney, and those who underwent any previous urological surgery. We also excluded children who had an early furosemide injection (F0 procedure), selecting only those having received furosemide at the end of the renogram (F+20 test). Seventy-three patients (92 renograms) fulfilled these criteria. Differential renal function was calculated using the integral method. Hydronephrotic kidney with a relative uptake > or =55% was defined as supranormal. Six renograms (four patients) demonstrated supranormal relative function on the hydronephrotic side. However, the SKGFR of these kidneys was in all cases within the range of normal values, while the contralateral side demonstrated borderline low SKGFR. Increased relative function on the side of the hydronephrotic kidney is relatively infrequent. When it occurs, it may be related to a borderline hypofunction of the contralateral kidney.
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Four patients with thallium toxicity were treated with Prussian blue, 125 mg/kg/day. The diagnosis was made on clinical grounds and confirmed by detection of thallium in the urine. Electromyographic, evoked potentials and electroencephalographic studies confirmed quick clinical and electrophysiologic improvement of the patients.
1. Adriamycin, a commonly used antineoplastic antibiotic, induces glomerular lesions in rats, resulting in persistent proteinuria and glomerulosclerosis. 2. The effect of urine volume on the progression of adriamycin-induced nephropathy was studied in 70 male Wistar rats (180-200 g) observed for 30 weeks and separated into 4 groups: healthy control group (HCG, N = 10) inoculated i.v. with 1 ml of saline, and nephrotic groups inoculated iv with a single dose of adriamycin of 3 mg/kg body weight. The nephrotic rats were separated into 3 groups (N = 20): nephrotic control group (NCG) receiving only adriamycin; dehydrated nephrotic group (DNG) water deprived for 36 h within each 48-h period, and furosemide nephrotic group (FNG) treated with 12 mg/dl furosemide, and 0.9 g/dl NaCl in the drinking water. 3. The 30-week survival rates of the DNG (100%) and HCG (100%) were significantly higher than those of the NCG (85%) and FNG (55%). 4. The proteinuria observed in the HCG (range, 7.38 +/- 0.7 to 13.6 +/- 1.27 mg/24 h) was significantly lower than that observed for all the nephrotic groups throughout the experiment. The DNG presented significantly less proteinuria (range, 42.71 +/- 6.83 to 140.10 +/- 19.22 mg/24 h) than the NCG (range, 35.32 +/- 7.64 to 250.00 +/- 25.91 mg/24 h) from week 10 on. There was no significant difference between the mean 24-h proteinuria of the NCG (range, 35.32 +/- 7.64 to 250.00 +/- 25.91 mg/24 h) and the FNG (range, 35.82 +/- 7.91 to 221.54 +/- 26.74). 5. The mean frequency of damaged glomeruli was 0.3% +/- 0.3 for HCG, 42% +/- 6% for CNG, 40.8% +/- 8% for DNG, and 47% +/- 14% for FNG. The median value of the tubulointerstitial lesion, evaluated by a semiquantitative method, was 0 in HCG, 10 in CNG, 8.5 in DNG and 9.5 in FNG (P < 0.05 for all groups compared to HCG). 6. The data indicate that reduction of urine volume has a protective effect on adriamycin-induced nephropathy.
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These results suggest the presence of an environmental etiology, rather than a genetic one, which is responsible for the development of hepatoblastoma in children of very low birthweight. Close monitoring of the children after being discharged from the neonatal intensive care unit is essential and a case-control study is necessary to identify risk factors for hepatoblastoma in children of very low birthweight.
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Ten consecutive patients with renal calculi underwent a modified four-detector multislice CTU with frusemide, abdominal compression and subsequent injection with contrast medium. After unenhanced CT of the abdomen, a high-resolution contrast-enhanced scan was taken through the kidneys in the pyelographic phase. Data were analysed using multiplanar reconstruction and three-dimensional (3D) reformatting.
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To report a case of presumed furosemide-associated bilateral angle-closure glaucoma.
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This was a retrospective cohort study of patients who received care from a large health system and had a primary hospital discharge diagnosis of HF between Jan 1, 2000 and June 30, 2008. Patients with preexisting end-stage renal disease were excluded. Daily creatinine (Cr) measurements, furosemide dosing (only loop diuretic on hospital formulary), and radiocontrast dye studies were collected using administrative data. Day-to-day changes in Cr and MDRD estimated glomerular filtration (eGFR) were calculated. The first Cr or eGFR value during hospitalization or in the emergency department was considered baseline. Generalized estimating equations were used to test the association furosemide exposure over previous 2 days to the daily change in Cr and eGFR. Covariates included undergoing radiocontrast study, age, race, gender, and baseline Cr or eGFR.
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As part of a prospective, randomised, nonblind study, we assessed the effects of torasemide and furosemide on readmission to hospital in 193 patients treated for CHF at a US urban public healthcare system. We also calculated total direct healthcare costs for the 2 drugs. The perspective of the analysis was that of the healthcare system. Healthcare charge and utilisation data, demographic information, and health status data were obtained from an electronic database containing data for all patients treated within the healthcare system.
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These experiments in isolated mouse cortical thick ascending limbs (cTALH) provide information about: the relative contributions of cellular and paracellular pathways to the transepithelial electrical conductance Ge (mS cm-2); the effects of (CO2 + HCO3-) on Ge; the ratio of net K+ secretion (JKnet) to net Cl- absorption (JClnet); and the K+ requirement for apical membrane furosemide-sensitive NaCl entry. The combination of luminal Ba++, zero K+ reduced Ge; at 5 mM luminal Ba++, the residual conductance was about 75% of the control Ge. The Ba++-insensitive Ge of 73.1 +/- 6.4 mS cm-2 was only slightly greater than the shunt conductance of 57 mS cm-2 computed from the sum of the dissipative bath to lumen fluxes of 22Na+ and 36Cl-. Moreover, luminal 5 mM Ba++, zero K+ had no effect on the Na+/Cl- permselectivity ratio of the paracellular pathway. Thus, Ba++ blockaded transcellular conductance by blocking apical membrane K+ channels. The combination of (CO2 + HCO3-) in external solutions increased Ge solely by augmenting the Ba++-sensitive, that is, transcellular, component of Ge. Finally, in paired experiments, the ratio JKnet/JClnet was 0.27 +/- 0.05; and both Ve, the spontaneous transepithelial voltage (mV), and the equivalent short circuit current Je (pEq sec-1 cm-2) were reduced dramatically by luminal K+ omission. Thus, apical membranes of the cTALH appear to contain a pathway for net K+ secretion, and apical membrane NaCl entry may involve co-transport with K+. Transcellular conductance contributes at least 25% to the total Ge, and the combination (CO2 + HCO3-) augments transcellular conductance.
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Hearing loss in neonatal intensive care unit (NICU) graduates range from 2% to 15% compared to 0.3% in full-term births, and the etiology of this discrepancy remains unknown. The majority of NICU admissions receive potentially ototoxic aminoglycoside therapy, such as gentamicin, for presumed sepsis. Endotoxemia and inflammation are associated with increased cochlear uptake of aminoglycosides and potentiated ototoxicity in mice. We tested the hypothesis that sepsis or systemic inflammatory response syndrome (SIRS) and intravenous gentamicin exposure increases the risk of hearing loss in NICU admissions.
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The median of age was 53+/-18 years old; 53% of the patients were women, and 34% were older than 65 years of age. Sixty-three percent of the patients received one prescription identified as potential D-DI, and 33.5% of these prescriptions were "major D-DIs". The most frequently pairs of drugs prescribed were: fluoroquinolones-hypoglycemics (20.5%), enoxaparin- nonsteroidal antiinflammatory drugs or anticoagulants (18.1%), furosemide- angiotensin converting enzyme inhibitors (ACE inhibitor) (12.2%), alopurinol-ACE inhibitor (9%), and spironolactone-ACE inhibitor (9%). Thirty-three percent of patients older than 65 years of age received a prescription including one potential D-DI. Gender and the number of drugs received were associated factors to the potential D-DI.
What happened to each of the patients? On re-examination, the first person was in tears and unable to lie still, even after 20 mg of i.v. morphine sulfate. Capillary refill was still intact, but he had lost sensation to the dorsum of the foot and was unable to dorsiflex his toes. He had a marked elevation of compartment pressure, and his creatinine phosphokinase (see below) was twice normal. In the OR, a fasciotomy was performed. Some muscle necrosis had occurred. In the second patient, fluids were infused rapidly on arrival at the ED via the i.v. route. He was given morphine sulfate for pain control while we awaited laboratory results. After about 45 minutes, he produced dark red urine. His creatinine phosphokinase (diagnostic muscle enzyme test) was 190,000--nearly 1,000 times above normal. He also had evidence of liver and kidney damage, but no electrolyte abnormalities. With aggressive treatment, including furosemide and sodium bicarbonate, his kidney and liver function returned to normal, he survived the ordeal and was discharged. The group leaders took the third patient to a local ED, where cellulitis was diagnosed and oral antibiotics were prescribed. The pain and fever increased, and significant discoloration began spreading up her hand over the next 24 hours. The second ED visit resulted in an admission. When the findings progressed despite i.v. antibiotics, surgical exploration was performed with drainage, debridement of devitalized tissue and a change in i.v. antibiotics. The common feature of all of these conditions is pain out of proportion to few, if any, findings on physical examination. Swelling that causes much of the damage in each condition is frequently not appreciated clinically until the condition is well advanced. Remember, what you see is not necessarily what you get.
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Prolonged immobilization or physical inactivity has been shown to produce increased bone resorption due to enhanced osteoclastic activity and diminished bone formation. These skeletal changes are a typical complication in tetraplegic patients, who are at risk of developing hypocalcemia. Hypercalciuria is the most characteristic symptom. However, some patients develop hypercalcemia, which is infrequent in these patients, and the hypercalcemia can become a life-threatening complication. Until now, it has been unclear why a small percentage of immobilized patients develop hypercalcemia. Here we present a case of symptomatic hypercalcemia (serum calcium: 3.5 mM/l) following immobilization due to a critical illness polyneuropathy. The diagnosis could be established after malignant hypercalcemia, primary hyperparathyroidism, and other causes of hypercalcemia were excluded. Treatment with intravenous saline, furosemide, and calcitonin was not effective in lowering serum calcium. Treatment with pamidronate (Aredia) was successful and reduced the serum calcium to normal values.
Patients receiving long-term treatment with torasemide had a lower hospitalisation rate (3.6%) compared to patients on furosemide (5.4%). Corresponding hospitalization rates in the German study were 1.4% under torasemide and 2% under furosemide. The higher hospitalisation rates in Swiss patients could be explained by a higher average age (75 years vs. 69 years) and a longer duration of symptomatic heart failure (4.1 yrs vs. 0.7 yrs). Cost estimates based on the average number of hospital days (0.54 under torasemide compared to 1.05 under furosemide) indicated that the financial burden could be halved by a long-term torasemide treatment.
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Therapeutic benefit that can be induced by a pharmaceutical compound partly relies upon the profile of its biological action. Evaluation of the drug-induced effect profile in a given pathological condition begins with the determination of the relevant biological effect related to the therapeutic benefit, which is not always obvious. Evaluation itself is based on dose-effect relationships as a function of time. During chronic treatment, such a kinetic profile oscillates between peak and trough levels. Relationships that can be established between time-dependent effect profile and pharmacokinetic data lead to PK-PD mathematical model, whose main objectives are simulation, prediction of effect and ultimately dose optimisation. The therapeutic implications of the time-dependent effect profile are well illustrated in the cases of antibiotics, diuretics such as furosemide and anti-hypertensive drugs. During drug development, PK-PD approaches can be used in the initial clinical and even pre-clinical phases and can lead to a better definition of effective dose ranges, optimisation of large scale clinical trials or identification of high risk patients. This may favour a reduction of costs and duration of development. Validation of such an approach is easier in well known therapeutic domains but can be more difficult with innovative drugs. The implications of PK-PD approaches can however, be, limited when the relevant biological or clinical parameter cannot be assessed, when the cascade of events leading to pharmacological and therapeutic effects is complex or finally when such PK-PD models require a long time to be established during the early phase of drug development.