Effect of Frusemide Administration on Calcium Excretion

Toft, Henrik; J, Roin

doi:10.1136/bmj.1.5746.437

Cited by 27 publications

(9 citation statements)

References 4 publications

(3 reference statements)

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“…Kleeman et al (1964) showed that there was a positive correlation between clearances of Na and Ca in man. An increase in excretion of Ca was found after the administration of frusemide (Tambyah and Lim, 1969;Toft and Roin, 1971). Davies et al (1974) found that with the administration of bumetanide in adults there was an increase in urinary Ca in the 0to 6-hour period followed by retention in the subsequent 6 to 12 hours, so that over the whole 24 hours excretion was not significantly increased.…”

Section: Discussionmentioning

confidence: 96%

Bumetanide in heart failure in infancy.

Ward¹,

Lam²

1977

Archives of Disease in Childhood

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SUMMARY The effect of bumetanide in infants with congenital heart disease presenting with cardiac failure was studied. The study was divided into acute (3 days) and long-term (mean 10 5 weeks) cases. A total of 12 male infants was included in the acute study and 13 cases were evaluated in the long-term study. The dose used in the acute study (0-015 mg/kg) was suboptimal; notwithstanding, it was found to cause significant natriuresis and chloruresis. Bumetanide in doses varying in different infants from as little as 0 015 mg/kg on alternate days to as much as 0 10 mg/kg daily was shown to be an effective diuretic for long-term use. No side effects were observed in either study.Bumetanide (Burinex) is a potent loop diuretic. Although it bears some structural resemblance to frusemide, unlike the latter which is derived from sulphanilamide, bumetanide is a metanilamide derivative (Feit, 1971). In dogs it is weight for weight 40 to 60 times more active than frusemide when given intravenously and 100 times more active when given orally (Ostergaard et al., 1972). In rats, bumetanide is practically ineffective. In human studies 1 mg bumetanide was equipotent to 40 mg frusemide with regard to urinary excretion of sodium, chloride, potassium, and water (Asbury et al., 1972). In healthy volunteers the major action of bumetanide has been shown to be on the ascending limb of Henle's loop with an additional effect on the proximal tubule but no significant effect on the distal tubule (Bourke et al., 1973). In this study we evaluated the effect of bumetanide in infants with congenital heart disease presenting with cardiac failure. The usual criteria for diagnosis of cardiac failure were used (Lees, 1969 diuretic was given but a preliminary 24-hour collection of urine was obtained. Only male infants were studied in order to facilitate accurate collection of urine samples. The 24-hour urine on day 1 was used as a control and was analysed for volume, sodium, potassium chloride, calcium, magnesium, phosphate, urate, glucose, and osmolality. On day 2 the infant was weighed and a blood sample was obtained and analysed for urea, sodium, potassium, chloride, calcium, magnesium, phosphate, liver function tests (serum proteins, SGOT, SGPT, alkaline phosphatase, bilirubin), haemoglobin, white cell count, and glucose. Immediately after blood sampling bumetanide 0 f015 mg/kg (prepared by dilution of the injectable form in sterile water) was administered orally. Urine was then collected at hourly intervals for 6 hours, followed by a further 18-hour collection to complete the 24-hour urine collection for day 2. On day 3 the infant's weight was recorded again and all the haematological and biochemical tests listed above were repeated.

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Section: Discussionmentioning

confidence: 96%

Bumetanide in heart failure in infancy.

Ward¹,

Lam²

1977

Archives of Disease in Childhood

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“…The development of renal calcification in very low birth weight infants receiving furosemide is presumed to result from the calciuretic effect of furosemide [ 19]. Although infants receiving furo semide have an increment in the urinary calcium excre tion.…”

Section: Discussionmentioning

confidence: 99%

Renal Calcification in Very Low Birth Weight Infants

et al. 1993

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Between January 1990 and December 1991, serial real-time ultrasound examinations and analyses of urine were performed on a total of 50 infants with birth weights less than 1,500 g to assess the incidence of renal calcification. Five infants (10%) developed renal calcification at a mean age of 48.8 ± 14.1 days. These 5 infants with renal calcification had significantly shorter gestations (28.2 ± 0.8 vs. 30.1 ± 1.7 weeks, p < 0.0005) and lower birth weights (934 ± 45 vs. 1,311 ± 188 g, p < 0.0005) when compared with infants without renal calcification. None of the affected infants were treated with furosemide. Affected infants had a mean urine volume of 85.8 ± 11.3 ml/kg/24 h, mean urine calcium level of 5.07 ± 1.18 mg/kg/24 h, mean urine calcium to creatinine (mg/mg) ratio of 0.67 ± 0.09, and a mean urine N-acetyl-β-D-glu-cosaminidase (NAG) to creatinine (U/g) ratio of 259 ± 133. Urinalyses showed that affected infants had significantly higher urine pH values and hematuria. Alkaline phosphatase concentrations and initial parathyroid hormone levels were not different among the two groups. In summary, renal calcification occurred in 10% of very low birth weight infants and multiple risk factors seem to be contributory. The smaller, sicker and more immature infants appear to have increased risk for developing renal calcification. For earlier detection and treatment of renal calcification, follow-up screening by serial ultrasound examinations and assay of urinary excretion of calcium, creatinine and NAG are useful, and a meticulous search for the causes of renal calcification is mandatory.

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“…It is well known that furosemide can increase urinary Ca excretion in human adults (33,34), infants (13), and animals (22); the urinary excretion of Mg also is increased after furosemide administration (22, 28). From our data, it would seem that the urinary losses of Ca and Mg did not result in lowered serum concentrations of Ca and Mg and thus did not stimulate PTH release.…”

Section: Discussionmentioning

confidence: 99%

Growth Failure and Decreased Bone Mineral of Newborn Rats with Chronic Furosemide Therapy

et al. 1986

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ABSTRACT. To test the hypothesis that chronic furosemide treatment in otherwise healthy newborn animals may lead to lowered bone mineral [calcium (Ca) and magnesium (Mg)] content, healthy littermates within each litter of Sprague-Dawley rat pups were randomly assigned to three groups: control, low dose furosemide (5 mg/kg/day), and high dose furosemide (15 mg/kg/day). The pups were treated between days 4 and 28 postnatally. The wet and dry weights of kidneys and tibiae significantly correlated with body weights at sacrifice. Furosemide-treated pups demonstrated a dose-dependent growth delay, decreased total bone (tibiae) Ca and Mg, increased urine Ca and Mg concentration, and a significant inverse correlation between bone Ca and urine Ca concentration. There was no significant difference among the groups when bone Ca and Mg were normalized to per gram of bone dry weight. There were no significant differences among the groups with respect to bone phosphorus or urinary phosphorus concentration; kidney and serum Ca and Mg; or serum sodium, potassium, alkaline phosphatase and immunoreactive parathyroid hormone concentration. We conclude that chronic furosemide therapy leads to growth failure and to increased urinary losses of Ca and Mg. Total bone Ca and Mg in the furosemide-treated pups were diminished in proportion to growth retardation but the bone mineral content per unit of dry weight remained similar to control pups. (Pediatr Res 20: 74-78,1986) Abbreviations Ca, calcium Mg, magnesium P, phosphorus Na, sodium K, potassium PTH, parathyroid hormone Potent "loop" diuretics such as furosemide are frequently used in sick newborn infants. Their role in congestive cardiac failure and acute fluid overload is well established (1-3). These diuretics

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Effect of Frusemide Administration on Calcium Excretion

Cited by 27 publications

References 4 publications

Bumetanide in heart failure in infancy.

Bumetanide in heart failure in infancy.

Renal Calcification in Very Low Birth Weight Infants

Growth Failure and Decreased Bone Mineral of Newborn Rats with Chronic Furosemide Therapy

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