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Kidney function in very low birth weight infants with furosemide-related renal calcifications at ages 1 to 2 years
G J Downing1, J C Egelhoff, D K Daily
1Department of Pediatrics, Children's Mercy Hospital, University of Missouri-Kansas City School of Medicine, Kansas City, Missouri.
Insights
Long-term furosemide use in preterm infants may cause kidney damage. Infants with furosemide-induced renal calcifications showed impaired kidney function and tubular dysfunction years later.
Area of Science:
- Neonatal Medicine
- Pediatric Nephrology
- Pharmacology
Background:
- Furosemide is commonly used in preterm infants.
- Potential long-term renal effects of furosemide, particularly calcifications, are not fully understood.
Purpose of the Study:
- To investigate long-term renal sequelae in very low birth weight infants exposed to furosemide.
- To assess kidney function in relation to furosemide therapy and renal calcifications.
Main Methods:
- Evaluated renal function in 27 former very low birth weight infants (VLBW) at 1-2 years of age.
- Classified infants into three groups: no furosemide/no calcifications, furosemide/no calcifications, and furosemide/renal calcifications.
- Utilized renal ultrasonography, creatinine clearance, and urine/blood tests to assess glomerular and tubular function.
Main Results:
- Infants with a history of furosemide-related renal calcifications exhibited significantly lower creatinine clearance.
- This group also showed higher urinary calcium/creatinine ratios, increased fractional sodium excretion, and reduced tubular phosphate reabsorption.
- Distal tubular hydrogen ion secretion was impaired in infants with a history of calcifications, especially those with persistent calcifications.
Conclusions:
- Furosemide-induced renal calcifications in VLBW infants can lead to persistent glomerular and tubular dysfunction.
- Long-term monitoring of renal function is crucial for this vulnerable population.
- Further research is needed to elucidate the mechanisms and long-term impact of these findings.
Abstract:
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 (less than 1500 gm) at 1 to 2 years of age. Patients were classified into three groups 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 less than 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 less than 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.