Kidney function in very low birth weight infants with furosemide-related renal calcifications at ages 1 to 2 years*,**

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To determine whether long-term renal sequelae follow the use of furosemide in preterm infants, we evaluated renal function in 27 former very low birth weight infants (<1500 gm) at 1 to 2 years of age. Patients were classified into three gorups on the basis of status at the time of discharge from the hospital: group 1 (n=7) had no furosemide treatment or renal calcifications, group 2 (n=10) had furosemide therapy but no calcifications, and group 3 (n=10) had furosemide therapy with renal calcifications. Renal ultrasonography at the time of the study demonstrated resolution of the calcifications in six patients in group 3. No differences in renal function were observed between groups 1 and 2. Creatinine clearance (mean±SEM) in group 3 (83.6±7.8 ml/min per 1.73 m2) was significantly lower than clearance in groups 1 and 2 (103.2±6.5 and 109.1±5.1, respectively; p<0.05). Children in group 3 had significantly higher urinary calcium/creatinine ratios and fractional excretion of sodium and lower tubular reabsorption of phosphate than children in the two other groups had. Urine-blood difference in carbon dioxide tension after oral acetazolamide load, which indicates the ability of the distal tubule to secrete hydrogen ions, was 8.4±3.4 mm Hg in group 3, significantly lower than values in groups 1 and 2 (22.6±3.1 and 28.0±4.3 mm Hg, respectively, p<0.05). Within group 3 the four children with persistent renal calcifications had significantly lower urine-blood carbon dioxide tension differences than did those with resolution of calcifications (p=0.02). We conclude that furosemide-related renal calcifications in very low birth weight infants may lead to glomerular and tubular dysfunction; further long-term follow-up of this population is recommended.

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    Citation Excerpt :

    The clinical implications of this experimental evidence are progressively emerging in the field. In addition, the increased incidence of tubular nephrocalcinosis in preterm infants may possibly occur from exposure of differentiating renal tubular epithelial cells following crystalluria caused by furosemide treatment.140,141 Moreover, tubular nephrocalcinosis has been seen in a large number of renal allografts, suggesting that ischemic injury resulting in increased expression of hyaluronic acid and osteopontin precedes crystal retention.142,143

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*

Supported by Children's Mercy Hospital Research and Education Endowment Fund, Kansas City, Missouri.

**

Presented in part at the Annual Meeting of the American Pediatric Society and the Society for Pediatric Research, New Orleans, La. May 1991.

*

Now at the Children's Rehabilitation Unit, University of Kansas Medical Center, Kansas City, Kan.

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