Experiences with Furosemide in Renal Disease

Berman, Leonard B.; Ebrahimi, Aziz

doi:10.3181/00379727-118-29835

Cited by 31 publications

(9 citation statements)

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“…Similar findings have been described by many workers (Vorburgher, 1964;Robson, Ashcroft, Kerr & Teasdale, 1964;Bergstrom et al, 1964;Berman & Ebrahimi, 1965;Dettli & Spring, 1966;Laragh et al, 1966;Reubi, 1966;McKenzie et a!., 1966;Muth, 1966Muth, , 1968Heidland et a!., 1969;Gregory et al, 1970), but the magnitude of the response found at low GFR in our studies is amongst the largest yet recorded.…”

Section: Acute Studysupporting

confidence: 92%

Diuretics in Chronic Renal Disease: A Study of High Dosage Frusemide

Allison

Kennedy

1971

Clinical Science

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1. The efficacy and mode of action of frusemide (100-750 mg) have been studied acutely in thirty-four investigations on twenty-four water-loaded subjects with stable, non-oedematous chronic renal disease (GFR 2,3-26'0 ml/min) of varying aetiology (fourteen 'tubular', ten 'glomerular').2. Water loading alone resulted in a slight increase in urine flow rate, a flowdependent rise in electrolyte excretion and a small fall in urine osmolality.3. Basal fractional excretion of fluid and electrolytes was closely related to GFR, increasing as this fell, so that at a GFR of 3·0 ml/min 80% of the fluid filtered, 50-60% of the filtered load of sodium and chloride and 400% of potassium was excreted. 4. After oral or intravenous frusemide, up to 93% of the filtered load of chloride, 87% of sodium and apparently all of the glomerular filtrate could be excreted; the magnitude of the response depended on dose, GFR and basal fractional sodium excretion, being greatest at higher GFR and lowest fractional excretion. Free water clearance increased. 5. No significant change in inulin clearance was found after frusemide and no difference in the response of 'tubular' as opposed to 'glomerular' subjects.6. Long-term treatment of nineteen patients with 'resistant' oedema and chronic renal disease has shown high dosage frusemide (0,12-2,0 gJday) to be an effective diuretic, although significant side effects were found in five patients.In the past, diuretic therapy was considered of little value, and perhaps even harmful. in patients with advanced renal impairment. The organo-mercurials and thiazides are ineffective in patients with glomerular filtration rates (GFR) less than 15-20 nil/min (Reubi & Cottier,

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Section: Acute Studysupporting

confidence: 92%

Diuretics in Chronic Renal Disease: A Study of High Dosage Frusemide

Allison

Kennedy

1971

Clinical Science

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“…When frusemide 40 mg. is injected intravenously, diuresis begins within 5 minutes, reaches its peak in 30 minutes, and is almost complete in 90 minutes (Berman and Ebrahimi, 1965). This coincides narrowly with the action of morphine on pulmonary blood volume (see above), reduction of which takes place within 15 minutes.…”

Section: Discussionsupporting

confidence: 65%

Augmentation of frusemide diuresis by morphine in high altitude pulmonary oedema.

Singh¹,

Lal²,

Khanna³

et al. 1967

Heart

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We have already reported that anxiety, restlessness, and laboured breathing associated with high altitude pulmonary cedema, which did not respond satisfactorily to oxygen therapy, were found to respond dramatically to intravenous morphine . Subsequently, hemodynamic studies in convalescents from high altitude pulmonary oedema suggested that the beneficial effect of intravenous morphine might partly result from reduction of the pulmonary blood volume due to redistribution of blood in the periphery (Roy et al., 1965).We now report that morphine also augments frusemide diuresis in high altitude pulmonary cedema and accelerates recovery. The probable mechanisms are discussed. SUBJECTS AND METHODThere were 98 men, 18 to 38 years old, all plainsmen, of whom 22 were new arrivals at high altitude; 76 had been resident at high altitude for 4 to 17 months, and developed acute pulmonary cedema on their return to high altitude after a sojourn in the plains of 60 to 70 days; none had suffered from pulmonary cedema during their first trip to high altitude. Both new arrivals and former residents developed acute pulmonary cedema 24 to 96 hours after arrival at high altitude. The vulnerable altitude was 11,500 feet. There were 69 out of 98 who were also suffering from acute mountain sickness.All cases were treated locally at the same altitude (11,500 feet). Immediately on arrival at hospital, a pretreatment clinical and radiological examination of the chest was made, and was repeated every 24 hours until the chest was clear.The trial, which was controlled but not blind, then started. Treatment A was administered to 84, and Treatment B, to 14 from a random selection. Treatment A consisted of a single injection of morphine 15 mg. intravenously and frusemide 20 mg. intravenously every 12 hours on the first day, and frusemide 40 mg. orally every 12 hours on the second and third days. Treatment B consisted of Treatment A minus morphine.Received June 23, 1966. 709The patients remained in bed in the same environment throughout these three days. During this period fluid intake consisted of hot sweetened tea and milk from a fixed ration, and additional quantities of water as required. The caloric value (1200 calories) and sodium content (552 mg.) were constant for all patients. The intake of water could not be fixed on account of mountain sickness in the majority of cases.Urine collections were done under supervision and were carefully measured to the millilitre. The difference between the urinary output and the intake of fluid in ml. constituted the effective diuresis.More than one consideration, based on our previous experience, weighed with us in restricting the number in the control group on Treatment B. (1) Most of the cases of high altitude pulmonary cedema occurred under field conditions and were severe. Anxiety, restlessness, and laboured breathing, which had not responded to bed-rest and oxygen therapy, had been specifically relieved with morphine. When morphine was not used, or was used with restraint, there was an associated m...

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“…The use of furosemide (1,2) and the thiazide diuretics (3) results in a loss of potassium as well as sodium and water. In addition, treatment with these diuretics causes an increase in circulating aldosterone levels (3-7).…”

mentioning

confidence: 99%

Inhibition of Furosemide-Induced Kaliuresis in the Rat by Trilostane, an Inhibitor of Adrenal Steroidogenesis

Harding¹,

Creange²,

Potts³

et al. 1984

Experimental Biology and Medicine

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In rats treated with furosemide, urinary losses of water, sodium and potassium were accompanied by increased circulating levels of aldosterone. Trilostane, an inhibitor of adrenal 3/3-hydroxysteroid dehydrogenase activity, prevented furosemide-induced hyperaldosteronism which resulted in a partial inhibition of diuretic-induced kaliuresis without a change in sodium and water excretion. Spironolactone, an antagonist of mineralocorticoid action with inherent diuretic activity, produced qualitatively similar effects to those of trilostane on urinary electrolyte excretion in furosemide-treated intact rats. However, mineralocorticoid-induced potassium loss in adrenalectomized rats was not altered by trilostane but was prevented by spironolactone reflecting the direct effect of spironolactone on the kidney. In addition, furosemide-induced kaliuresis in adrenalectomized rats was not prevented by trilostane. Therefore, although both trilostane and spironolactone reduce diuretic-induced potassium loss, spironolactone acts by competing with aldosterone for the mineralocorticoid receptor while trilostane appears to act exclusively by preventing secondary hyperaldosteronism. o 1984 Society for Experimental Biology and Medicine. 388

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Experiences with Furosemide in Renal Disease

Cited by 31 publications

References 0 publications

Diuretics in Chronic Renal Disease: A Study of High Dosage Frusemide

Diuretics in Chronic Renal Disease: A Study of High Dosage Frusemide

Augmentation of frusemide diuresis by morphine in high altitude pulmonary oedema.

Inhibition of Furosemide-Induced Kaliuresis in the Rat by Trilostane, an Inhibitor of Adrenal Steroidogenesis

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