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PubMed1981

Variability in derived parameters of furosemide pharmacokinetics.

The pharmacokinetics of furosemide in normal man reported from a number of investigators show great discrepancies. We have evaluated the effect on derived pharmacokinetic parameters of furosemide of using different weighting factors or fewer data points to fit the same set of data to an exponential equation, or using noncompartmental analysis. Terminal half-lives of furosemide differed vastly, as did the volume of distribution, but to a lesser extent. The plasma clearance was rather consistent with the different methods used. Thus the discrepancies of the pharmacokinetics of furosemide may, in large part, be due to different methods of analysis of the data. The terminal half-life was most subject to errors of method and the plasma clearance the least.

Furosemide↗
PubMed1977

The effect of indomethacin on kidney function: indomethacin and furosemide antagonism.

The effect of furosemide and indomethacin on renal function was investigated in anesthetized dogs. 1. On infusing 0.05 mg/kg/min furosemide directly into the left renal artery, about 18% of the filtered water and 19% of the filtered sodium was excreted in both non-hydrated and hydrated dogs. 2. Under the effect of 0.1 mg/kg/min indomethacin administered intravenously renal blood flow decreased markedly, glomerular filtration rate remained unchanged, the filtration fraction increased. 3. Indomethacin induced a decrease in water and sodium rejection and water and sodium excretion in both the hydrated and non-hydrated animals. 4. Indomethacin inhibited the diuretic effect of furosemide in the non-hydrated animals. This effect was much weaker in the hydrated group. These data suggest that in the anesthetized dog, endogenous prostaglandins may serve to maintain renal blood flow but not glomerular filtration rate. It is concluded that the indomethacin-induced inhibition of the furosemide effect is the consequence of hemodynamic changes occurring in the kidney. The data do not support the direct physiological role of prostaglandins in regulating tubular function.

Animals↗
PubMed1986

Renal transport kinetics of furosemide in the isolated perfused rat kidney.

Direct quantitative data and corresponding theory are provided for the effect of protein binding on the renal transport of furosemide. Drug studies were performed with various combinations of bovine serum albumin and dextran. This resulted in a percent unbound (fu) of furosemide ranging from 0.785 to 85.8%. The corrected renal (CLr/GFR) and secretion (CLs/GFR) clearances of furosemide were observed to increase with percent free, but in a nonproportional manner. Plots of CLr/GFR or CLs/GFR vs. fu appeared to have a prominent y intercept as well as a convex ascending curve. In addition, the excretion ratio [ER = CLr/(fu . GFR)] was reduced from 60.8 to 8.72 as fu increased. Overall, the data were best fitted to a model in which two Michaelis-Menten terms were used to describe renal tubular transport, and secretion was dependent upon free drug concentrations in the perfusate. The results demonstrate that the renal mechanisms of furosemide excretion are more complex than previously reported and that active secretion may involve two different transport systems over the concentration range studied.

Animals↗
PubMed1975

[Haemodynamic effects of furosemide and ethacrynic acid (author's transl)].

The haemodynamic effects of intravenous injections of furosemide and ethacrynic acid were studied in 12 patients during rest and exercise. Cardiac output, heart rate and arterial blood pressure showed no significant changes after injection of furosemide or ethacrynic acid. Few minutes after injection of furosemide there were significant falls of pulmonary artery diastolic pressure and right atrial pressure, whereas no changes were seen after injection of ethacrynic acid. This initial effect of furosemide apparently is of primarily vascular origin, causing an increased peripheral venous capacitance. Ethacrynic acid failed to exhibit any direct vascular effect.

Acute Disease↗
PubMed1982

Cellular Mechanism of the furosemide sensitive transport system in the kidney.

Experiments were performed in the distal tubule of the doubly-perfused kidney of Amphiuma to determine active and passive forces, involved in the transport processes of potassium, sodium and chloride. Ion-sensitive microelectrodes and conventional microelectrodes were applied to estimate intracellular ion activities, cell membrane potentials and net flux of potassium and chloride under control conditions and during inhibition of active transport. Sodium chloride cotransport, located in the luminal cell membrane is postulated, based on the following observations: Total omission of sodium from the tubular lumen inhibits furosemide sensitive chloride reabsorption, decreases the lumen positive transepithelial potential difference and leads to a dramatic decrease of intracellular chloride. The experiments further suggest that potassium ions are involved in the sodium chloride transport system because potassium reabsorption is inhibited by furosemide and because intracellular sodium falls significantly when potassium ions are removed from the tubular fluid. Furthermore, there is experimental evidence that the luminal potassium uptake mechanism is suppressed after potassium adaptation. Under these conditions potassium transport is found to be insensitive to furosemide. The data suggest a furosemide sensitive cotransport system for sodium, chloride and potassium, operative in the luminal cell membrane. The energy for this carrier-mediated transport process is provided by the large "downhill" gradient of sodium across the luminal cell membrane which is maintained by the sodium pump located in the peritubular cell membrane.

Animals↗
PubMed1984

Prostaglandin excretion after furosemide in normal and low-renin essential hypertension.

We examined the urinary excretion of prostaglandin (PG)E2 and PGF2 alpha before and 15 min after stimulation with the acutely vasodilating agent furosemide in 25 normotensive controls and 81 patients with essential hypertension (EH). After furosemide administration, PGE2 excretion was lower in patients with EH (P less than 0.02). Excretion rates of PGF2 alpha and of sodium, and urinary volume in hypertensive patients were not significantly different from the values found in normotensive controls. Patients with low-renin essential hypertension (LREH) had a significantly reduced excretion of both PGE2 and PGF2 alpha before and after administration of furosemide as compared to controls. The difference in PGF2 alpha excretion was also significant when LREH patients were compared to those with normal-renin essential hypertension (NREH). Patients with LREH were older and excreted less potassium than patients with NREH or normotensive controls. We conclude that the reduced PG excretion immediately after furosemide administration in patients with EH reflects a diminished capacity of the hypertensive kidney to generate prostaglandins which exert an overall vasodilating effect. Since renin secretion is under the control of renal PG formation, the decreased responsiveness of plasma renin activity (PRA) observed in patients with EH and predominantly in those with LREH may be the consequence of a decreased renal cortical PG generation. Alternatively, mechanisms that reduce both PRA and PG generation have to be considered.

Adult↗
PubMed1994

The effects of furosemide and pentoxifylline on the flow properties of equine erythrocytes: in vitro studies.

The effects of various concentrations of furosemide and pentoxifylline on equine RBC in vitro were evaluated to facilitate better understanding of the potential effects of these drugs on blood flow properties. Furosemide induced increased mean cell volume (MCV), increased RBC potassium concentration, increased whole blood viscosity, and decreased the RBC filtrability. These data indicate that furosemide may block the RBC membrane transport pathways resulting in potassium and water retention. The increase in size and the resultant decrease in the surface-area-to-volume ratio may have caused the impaired RBC filtrability and increased blood viscosity. Pentoxifylline improved RBC filtrability without changing the RBC size or the potassium or chloride concentrations, suggesting that pentoxifylline may increase the deformability of the RBC membrane. The study indicated that pentoxifylline has potential therapeutic applications for improving microvascular blood flow but that furosemide may have adverse effects on blood flow.

Animals↗
PubMed1988

Effects of pH, potential, chloride and furosemide on passive Na+ and K+ effluxes from human red blood cells.

Ouabain-resistant effluxes from pretreated cells containing K+/Na+ = 1.5 into K+ and Na+ free media were measured. Furosemide-sensitive cation effluxes from cells with nearly normal membrane potential and pH were lower in NO3- media than in Cl- media; they were reduced when pH was lowered in Cl- media. When the membrane potential was positive inside furosemide increased the effluxes of Na+ and K+ (7 experiments). With inside-positive membrane potential the furosemide-insensitive effluxes were markedly increased, they decreased with decreasing pH at constant internal Cl- and also when internal Cl- was reduced at constant pH. The correlation between cation flux and the membrane potential was different for cells with high or low internal chloride concentrations. The data with chloride greater than or equal to 47 mM showed a better fit with the single-barrier model than with the infinite number-of-barriers model. With low chloride no significant correlation between flux and membrane potential was found. The data are not compatible with pure independent diffusion of Na+ and K+ in the presence of ouabain and furosemide.

Biological Transport↗
PubMed1987

Short lasting increase in urinary specific kallikrein activity during long term administration of furosemide.

Furosemide was administered for seven days to normal rats. Urinary kallikrein excretion showed a biphasic response during the seven consecutive days of study. During the initial three days only the kininogenase activity showed a significant increase without any variation in the excretion of the immunoreactive kallikrein. The specific urinary kininogenase activity was therefore enhanced. After three days of furosemide administration, both the urinary kininogenase activity and urinary immunoreactive kallikrein were augmented. The urinary specific kininogenase activity was that time no more different when compared to the basal value. Considering the delay time of three days, this second part of the response could be a mineralocorticoid mediated effect. In this respect, kidney level of immunoreactive and kininogenase activity of kallikrein are also increased after seven days of furosemide administration. However the short lasting increase in urinary specific kininogenase activity observed during the initial three days is due to a change in the ratio active versus inactive kallikrein without any variation of total kallikrein. It is possible that this immediate response results of a direct effect of furosemide acting either on the preferential excretion of the active form or on the activation of the prokallikrein in the urine.

Animals↗
PubMedDate not supplied

Plasma renin activity and urinary kallikrein excretion in response to intravenous furosemide in diabetic patients.

The responsiveness of renin-angiotensin and kallikrein-kinin systems to furosemide challenge has been investigated in forty-six diabetic patients (34 NIDDM/12 IDDM), subdivided into Group I (uncomplicated DM), Group II (DM with hypertension), Group III (DM with nephropathy), Group IV (DM with hypertension and nephropathy) and a control group of 10 healthy volunteers. Plasma renin activity (PRA) was estimated by radioimmunoassay in blood samples drawn before and 10 min after furosemide administration (0.5 mg/kg i.v.). Urinary kallikrein levels were measured by bioassay using estrogenized rat uterus preparation in 4h urine samples collected before and after the diuretic. Urinary Na+ and K+ were also measured. The basal PRA in diabetics was not significantly different from controls, whereas, urinary kallikrein levels were markedly low in all patients. Both PRA and kallikrein levels increased after furosemide in controls while in diabetics this response was severely blunted. In a subset of Group I, a paradoxical fall in PRA and kallikrein levels was noted after furosemide, an effect similar to that observed in patients with nephropathy (Group III). This response in absence of clinical and biochemical parameters of nephropathy indicates early derangement of renal hemodynamic mechanisms heralding the onset of nephropathy.

Adult↗
PubMed1997

Furosemide and dDAVP for the treatment of pseudohypoaldosteronism type II.

A 27-year-old Turkish male presented with fatigue, long lasting hypertension, hyperkalemia, hyperchloremic metabolic acidosis and normal glomerular filtration rate. His brother also showed hyperkalemia with no other features of the disease. Plasma renin levels were low and serum aldosterone levels were inappropriately low-normal to his hyperkalemia. Plasma cortisol levels were normal. Plasma renin aldosterone levels responded appropriately to postural changes, salt restriction and saline infusion. Fludrocortisone was ineffective in his hyperkalemia. The conditions were consistent with Type II pseudohypoaldosteronism (PHA). Furosemide and sodium bicarbonate were effective to control his hyperchloremia, metabolic acidosis and hypertension but partly effective for his hyperkalemia. dDAVP alone did not control the situation and hypertension and metabolic derangement reoccurred. Adding dDAVP to furosemide and sodium bicarbonate successfully controlled hyperkalemia, hyperchloremic acidosis and hypertension. The patient stayed normotensive with normal metabolic and biochemical parameters after 6 months with furosemide and dADVP although sodium bicarbonate had been discontinued after the first month of therapy. dDAVP is a useful adjunct to furosemide and non chloride anions which altogether successfully reverse the metabolic derangement in Type II PHA.

Adult↗
PubMedDate not supplied

Relationship between kallikrein and PRA after intravenous furosemide.

Interrelationships between plasma renin activity (PRA), urinary kallikrein and sodium excretion were studied before and after furosemide iv administration in nine normal volunteers and in one low renin non hypertensive patient. PRA, urinary kallikrein and sodium excretion increased within 15 min of furosemide injection in nine subjects; kallikrein excretion then decreased sharply, whereas plasma renin activity reached peak values within 15-120 min of stimulation. In low renin subject low basal levels of PRA paralled undetectable values of kallikrein excretion, and PRA and kallikrein excretion showed no increase after furosemide, despite the expected natriuretic response. The following conclusions appear feasible: (i) the natriuretic effect of fuorsemide is direct and independent of the effect on PRA and urinary kallikrein; (ii) in man, furosemide induces an increase in urinary kallikrein excretion which is immediate, of short duration and simultaneous in all the patient studied; (iii) no statistical correlation is demonstrated between the temporal behavior of urinary kallikrein and PRA; it is however possible that, at least for certain stimuli, renin release is in some way correlated with the activation of the renal kallikrein-bradykinin system.

Adult↗
PubMed2004

Differential effects of human atrial natriuretic peptide and furosemide on glomerular filtration rate and renal oxygen consumption in humans.

OBJECTIVE: Imbalance in the renal medullary oxygen supply/demand relationship can cause hypoxic medullary damage and ischemic acute renal failure. Human atrial natriuretic peptide (h-ANP) increases glomerular filtration rate in clinical acute renal failure. This would increase renal oxygen consumption due to increased tubular load of sodium. Loop diuretics are commonly used in acute renal failure. Data on the effects of loop diuretics on glomerular filtration rate and renal oxygen consumption in humans are, however, controversial. We evaluated the effects of h-ANP and furosemide on renal oxygen consumption, glomerular filtration rate, and renal hemodynamics in humans. DESIGN AND SETTING: Prospective two-agent interventional study in a university hospital cardiothoracic ICU. PATIENTS: Nineteen uncomplicated, mechanically ventilated postcardiac surgery patients with normal renal function. INTERVENTIONS: h-ANP (25 and 50 ng/kg per minute, n=10) or furosemide (0.5 mg/kg per hour, n=9). MEASUREMENTS AND RESULTS: Renal plasma flow and glomerular filtration rate were measured using the infusion clearance technique for (51)Cr-labeled EDTA and paraaminohippurate, corrected for by renal extraction of PAH. h-ANP increased glomerular filtration rate, renal filtration fraction, fractional excretion of sodium, and urine flow. This was accompanied by an increase in tubular sodium reabsorption (9%) and renal oxygen consumption (26%). Furosemide infusion caused a 10- and 15-fold increase in urine flow and fractional excretion of sodium, respectively, accompanied by a decrease in tubular sodium reabsorption (-28%), renal oxygen consumption (-23%), glomerular filtration rate and filtration fraction (-12% and -7%, respectively). CONCLUSIONS: The filtered load of sodium is an important determinant of renal oxygen consumption. h-ANP improves glomerular filtration rate but does not have energy-conserving tubular effects. In contrast, furosemide decreases tubular sodium reabsorption and renal oxygen consumption and thus has the potential to improve the oxygen supply/demand relationship in clinical ischemic acute renal failure.

Acute Kidney Injury↗
PubMed2006

Topical furosemide versus oral steroid in preoperative management of nasal polyposis.

The efficacy of topical nasal furosemide treatment has been shown in the protection of nasal polyp recurrence. The aim of the study was to compare the effect of oral steroid, as standard preoperative treatment, and inhaled furosemide, as alternative treatment, for 7 days preoperatively in terms of subjective improvement of nasal symptoms, polyp size reduction, inflammation in the polyp tissue, and intraoperative blood loss. A group of 40 patients with nasal polyposis entered the study and they were randomly allocated to 7-day preoperative treatment with either oral methylprednisolon (1 mg/kg/day) or topical furosemide by inhalation (6.6 mmol/l solution). Subjective scores of rhinosinusitis symptoms, polyp scores at endoscopy, and biopsy of the most superficial polyp were taken at inclusion. All procedures were repeated on day 7. Intraoperative blood loss was estimated (scores 0-10) by the surgeon at the operation. Eosinophils, mastocytes, and oedema were quantified by histomorphometry. Subjective symptoms and endoscopy scores did not differ significantly between the groups after the treatment although improvement of olfaction was insignificantly better in the steroid group. Steroid treatment significantly reduced eosinophil count, with no effect on mastocytes and oedema. Furosemide treatment did not affect inflammatory cells count significantly, but it has significantly reduced oedema in previously unoperated patients. No difference in intraoperative bleeding was observed between the groups.

Administration, Inhalation↗
PubMed1999

Nephrocalcinosis in full-term infants receiving furosemide treatment for congestive heart failure: a study of the incidence and 2-year follow up.

UNLABELLED: In order to study the incidence and course of nephrocalcinosis in full-term infants with congestive heart failure receiving long-term furosemide treatment, 36 such infants (median age 2.9 months, range 1.2-8.0) and 36 full-term control infants not receiving any diuretics (median age 3.4 months, range 1.1-8.4) were studied by renal ultrasonography and random urine calcium variables. The infants with nephrocalcinosis were followed at 3-6 month intervals up to 2 years of age, or until ultrasonic resolution. Nephrocalcinosis was found in 5 out of the 36 (14%) treated infants, but in none of the controls (P = 0.03). The dose of furosemide was higher in the infants with nephrocalcinosis than in those without (1.9+/-0.6 vs. 1.3+/-0.4 mg/kg per day; P = 0.01). The urinary calcium concentration was higher in the infants receiving furosemide than in controls and a similar trend was observed in the urinary calcium/creatinine ratio, but these variables did not differ between the study infants with and without nephrocalcinosis. Ultrasonic resolution of nephrocalcinosis was observed in 3 of the 5 infants at 12 months, but in the other 2 the condition still persisted at 24 months. CONCLUSIONS: Long-term furosemide treatment in full-term infants with congestive heart failure entails a considerable risk of developing nephrocalcinosis. Renal ultrasonography is warranted in these patients within a few months after initiation of the treatment and in the case of nephrocalcinosis alteration of the diuretic regimen is to be considered.

Calcium↗
PubMed2001

Does albumin and furosemide therapy affect plasma volume in nephrotic children?

Albumin infusions transiently increase plasma volume (PV) and oncotic pressure, and may restore diuretic responsiveness in nephrotic edema. To determine if albumin and furosemide therapy have an effect on PV in nephrotic children, 14 severely edematous children with minimal change nephrotic syndrome were evaluated with standard clinical parameters (heart rate, blood pressure, body weight, pretibial edema, abdominal circumference) and echocardiography [inferior vena cava index (IVCI), inferior vena cava collapsibility index (IVCCI)] before, 1 h and 24 h after albumin (20%, 0.5 g/kg, 1 h) and furosemide (2 mg/kg, i.v.) therapy. An increase in IVCI (P < 0.05), decrease in IVCCI (P < 0.05), edema (P < 0.005), and hematocrit (P < 0.005) were statistically significant 1 h after albumin and furosemide therapy, with a transient effect 24 h later. Body weight (P < 0.005), abdominal circumference (P < 0.05), and edema (P < 0.005) decreased significantly at 24 h. It is concluded that albumin and furosemide therapy increases PV transiently in nephrotic edema, returning to baseline values at 24 h with a decrease in body weight, abdominal circumference, and edema.

Child↗
PubMed1981

Acute effects of intravenous furosemide administration on serum digoxin concentration.

The effect of intravenous (IV) furosemide (2.5 mg/kg) on serum digoxin concentration, urine flow rate, and myocardial contractility and rhythm was studied in normal dogs and dogs treated with digoxin. Furosemide IV to animals which had not been receiving digoxin resulted in increased urine flow rate from 0.11 +/- 0.03 to 0.43 +/- 0.1 ml/min/kg, but had no effect on myocardial contractility, blood pressure, or cardiac rhythm. Furosemide IV to animals with steady-state therapeutic serum concentrations of digoxin (2.0 +/- 0.58 ng/ml) increased urine flow similarly but did not significantly alter serum digoxin concentration, blood pressure, myocardial contractility, or cardiac rhythm. Thus, contrary to some previous reports, furosemide does not interact with digoxin to produce an elevation in serum digoxin concentration or enhancement of the glycoside's myocardial action.

Animals↗
PubMed1975

Effect of intrarenal furosemide on renal function and intratenal hemodynamics in acute renal failure.

The ability of short-term furosemide administration to alter intrarenal hemodynamics and to modify the clinical course of acute renal failure was assessed in six patients 2 to 9 days after the onset of acute renal failure. Following renal arterial catheterization, the intraarterial administration of furosemide at a dose of 9.6 mg/min for 30 minutes failed to improve renal function as assessed either by an increase in urine output or a decrease in serum creatinine during the 4 days after administration in the five oliguric patients. In a sixth patient with nonoliguric acute renal failure, urine volume increased with a gradual decrease in blood urea nitrogen and creatinine during the week after study. Furosemide failed to alter either mean renal blood flow or its intrarenal distribution as determined at intervals of 3 to 40 minutes after its infusion. These studies demonstrate that the short-term administration of furosemide in large doses does not improve renal hemodynamics or alter the clinical course of patients with established acute oliguric renal failure.

Acute Kidney Injury↗