Endocrine Abstracts (2013) 33 OC2.2 | DOI: 10.1530/endoabs.33.OC2.2

Increased bone area without reduction in volumetric bone mineral density in children treated with glucocorticoids for nephrotic syndrome

Rebecca Moon1, Rodney Gilbert3, Liam Murphy1, Anna Page1, Pat Taylor4, Cyrus Cooper2, Elaine Dennison2 & Justin Davies1


1Paediatric Endocrinology, University Hospital Southampton NHS Foundation Trust, Southampton, Hampshire, UK; 2MRC Lifecourse Epidemiology Unit, University of Southampton, Southampton, Hampshire, UK; 3Paediatric Nephrology, University Hospital Southampton NHS Foundation Trust, Southampton, Hampshire, UK; 4The Osteoporosis Centre, University Hospital Southampton NHS Foundation Trust, Southampton, Hampshire, UK.


Background: Glucocorticoids are frequently used to treat childhood inflammatory disorders, and may cause increased fracture predisposition with reduced bone mineral density (BMD), particularly from trabecular bone loss. The contribution of the underlying inflammatory disease processes to these outcomes is poorly understood. Childhood nephrotic syndrome (NS) is a useful model to investigate the effects of steroids on bone, as recurrent courses are often required, but systemic inflammation is low during remission.

Methods: Children with NS were compared to age- and sex-matched controls. Body composition and areal BMD were assessed by DXA. Peripheral quantitative computed tomography (pQCT) scans were obtained at the tibial metaphysis (4%) and diaphysis (66%) to determine volumetric BMD and bone geometry. Lifetime cumulative glucocorticoid exposure was calculated from medical records.

Results: 29 children with NS (55% male, age 10.7±3.1 years) were compared to 29 healthy controls (55% male, age 11.0±3.0 years). Children with NS were of similar height SDS to controls (P=0.28), but were heavier (P=0.02) with greater % body fat SDS (P=0.008). Tibial trabecular and cortical vBMD were similar between the two groups but cross-sectional area (CSA) was significantly greater in children with NS at the metaphysis (954±234 vs 817±197 mm2, P=0.002) and diaphysis (535±163 vs 463±156 mm2, P=0.014). Cortical thickness was lower in the children with NS (2.4±0.7 vs 2.8±0.7 mm, P=0.018), but cortical CSA was similar to controls (P=0.22). The differences in geometry were no longer significant when adjusted for weight. Cumulative steroid exposure was not associated with bone outcomes.

Conclusions: Tibial bone CSA is increased in children with NS. We speculate this is a compensatory response to increased body weight. Reductions in vBMD were not identified in this cohort of children with NS.