Abstract: TH-PO661

Effect of Growth Hormone Therapy on Renal Function in Children Born Small for Gestational Age

Session Information

  • Pediatric Nephrology
    November 02, 2017 | Location: Hall H, Morial Convention Center
    Abstract Time: 10:00 AM - 10:00 AM

Category: Developmental Biology and Inherited Kidney Diseases

  • 403 Pediatric Nephrology

Authors

  • Matsumura, Kazuya, Keio University School of Medicine, Tokyo, Japan
  • Shibata, Hironori, Keio University School of Medicine, Tokyo, Japan
  • Ishii, Tomohiro, Keio University School of Medicine, Tokyo, Japan
  • Hasegawa, Tomonobu, Keio University School of Medicine, Tokyo, Japan
  • Awazu, Midori, Keio University School of Medicine, Tokyo, Japan
Background

Low birth weight infants, especially those born small for gestational age (SGA), are known to have fewer nephrons. Growth hormone (GH) induces catch-up growth in short children born SGA, which is a risk factor for chronic kidney disease (CKD). GH also causes hyperfiltration, which may lead to glomerulosclerosis. We retrospectively examined the effect of GH therapy on renal function in children born SGA.

Methods

Nineteen subjects born SGA (age 3 to 25 years) were studied. Ten were treated with GH and 9 served as controls. Blood pressure, serum creatinine, uric acid, urine microalbumin to creatinine ratio (malb/Cr), and the trajectory of eGFR, calculated by quantic equation for Japanese children (2 to 18 years) or formulas for Japanese adults (≥19 years), were compared.

Results

GH was started at the median age of 4 years (range 3-5). The median dose and duration was 0.25 mg/kg/week (range 0.2-0.3) and 66 months (range 23-95). There were no significant differences in the background characteristics between GH group and controls including age (11 vs 10 years), birth weight (1109 vs 804 g), gestational age (32.3 vs 28.5 weeks), sex, and initial eGFR (107 vs 98 ml/min/1.73 m2). Only one child in each group did not show catch-up growth. eGFR declined in 6 (60%) in GH group and in 1 (11%) in controls (P<0.05). Of 6 GH-treated children whose eGFR declined (107 to 89 ml/min/1.73 m2, P=0.09), eGFR before GH was stable in 2, increasing in 2, and declining in 2. In the remaining children who received GH, eGFR trajectory before and after the start of GH was decline followed by increasing (2), decline followed by stable (1), and continuously increasing (1), suggesting GH-induced hyperfiltration. There was no change in eGFR trajectory in control children; 2 increasing, 6 stable, and 1 decline. Urine malb/Cr (9.7 vs 9.6 mg/g) and the number of children with elevated malb/Cr (6 vs 4) were not different between GH group and controls. One child, however, developed microalbuminuria after GH was started. Hypertension or hyperuricemia was not observed in either group throughout the observation period.

Conclusion

eGFR decline was more frequent in SGA children with GH therapy compared with those not on GH. Initially stable or increasing eGFR followed by decline after the initiation of GH suggests that GH may promote progression of CKD in SGA children.