Renal Calcifications: A Complication of Long-Term Furosemide Therapy in Preterm Infants

Hufnagle, Karen G.; Khan, Shadid N.; Penn, Duna; Cacciarelli, Alexander; Williams, Paul

doi:10.1016/s0022-5347(17)52290-9

Cited by 64 publications

(115 citation statements)

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“…When the function of this transporter is inhibited by furosemide or decreased by a genetic defect as is observed in Bartter syndrome, sodium loss is accompanied by increased potassium and Ca 2ϩ loss (31,32), because Ca 2ϩ transport passively follows that of sodium in this segment. As a result of hypercalciuria, nephrocalcinosis is frequently observed in patients with Bartter syndrome or in neonates treated with furosemide (33).…”

Section: Discussionmentioning

confidence: 99%

Modulation of Renal Calcium Handling by 11β-Hydroxysteroid Dehydrogenase Type 2

Ferrari

Bianchetti²,

Sansonnens³

et al. 2002

Journal of the American Society of Nephrology

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Abstract. Reduced concentration of serum ionized calcium and increased urinary calcium excretion have been reported in primary aldosteronism and glucocorticoid-treated patients. A reduced activity of the 11␤-hydroxysteroid dehydrogenase type 2 (11␤HSD2) results in overstimulation of the mineralocorticoid receptor by cortisol. Whether inhibition of the 11␤HSD2 by glycyrrhetinic acid (GA) may increase renal calcium excretion is unknown. Serum and urinary electrolyte and creatinine, serum ionized calcium, urinary calcium excretion, and the steroid metabolites (THFϩ5␣THF)/THE as a parameter of 11␤HSD2 activity were repeatedly measured in 20 healthy subjects during baseline conditions and during 1 wk of 500 mg/d GA. One week of GA induced a maximal increment of 93% in (THFϩ5␣THF)/THE. Ambulatory BP was significantly higher at day 7 of GA than at baseline (126/77 Ϯ 10/7 versus 115/73 Ϯ 8/6 mmHg; P Ͻ 0.001 for systolic; P Ͻ 0.05 for diastolic). During GA administration, serum ionized calcium decreased from 1.26 Ϯ 0.05 to 1.18 Ϯ 0.04 mmol/L (P Ͻ 0.0001), and absolute urinary calcium excretion was enhanced from 29.2 Ϯ 3.6 to 31.9 Ϯ 3.1 mol/L GFR (P Ͻ 0.01). Fractional calcium excretion increased from 2.4 Ϯ 0.3 to 2.7 Ϯ 0.3% (P Ͻ 0.01) and was negatively correlated to the fractional sodium excretion during GA (R ϭ Ϫ0.35; P Ͻ 0.001). Moreover, serum potassium correlated positively with serum ionized calcium (R ϭ 0.66; P Ͻ 0.0001). Inhibition of 11␤HSD2 activity is sufficient to significantly increase the fractional excretion of calcium and decrease serum ionized calcium, suggesting decreased tubular reabsorption of this divalent cation under conditions of renal glucocorticoid/mineralocorticoid excess. The likely site of steroid-regulated renal calcium handling appears to be the distal tubule.

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Section: Discussionmentioning

confidence: 99%

Modulation of Renal Calcium Handling by 11β-Hydroxysteroid Dehydrogenase Type 2

Ferrari

Bianchetti²,

Sansonnens³

et al. 2002

Journal of the American Society of Nephrology

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show abstract

“…5 It has been suggested that furosemide therapy should be discontinued when nephrocalcinosis is identified on a renal ultrasound, or that thiazide be added to blunt the hypercalciuric effect of furosemide. 6 Based on the results of this study, caution should be used before diuretic therapy is changed based on a single ultrasound reading by an individual radiologist who may "over-read" subtle ultrasound findings.…”

Section: Discussionmentioning

confidence: 95%

Nephrocalcinosis in Premature Infants

et al. 1999

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“…As a result, the most common cause of echogenic foci in neonates relates to this widespread use of furosemide therapy and caldum supplementation.s, 6 The differential diagnosis of acoustic shadowing within the kidney is limited to renal calculi or intrarenal gas (introduced via retrograde catheterization, antegrade pyelography, or surgery).' The sanagraphic appearance of these two entities, however, can be indistinguishable.s-1o According to Rubin and coworkers,& differences in shadowing ("clean" versus "dirty") are primarily related to the properties of the surface of the shadowing object and are not pathognomonic of the entity itself.…”

Section: Discussionmentioning

confidence: 99%