Bone Abstracts

Objectives: An increased fracture risk is reported in children requiring recurrent courses of glucocorticoids. Reduced bone mineral density (BMD), particularly in the trabecular compartment, has also been demonstrated in a number of childhood diseases treated with glucocorticoids. The differential contribution of glucocorticoids and underlying inflammatory disease to bone demineralisation is poorly understood. Childhood nephrotic syndrome (NS) often follows a relapsing-remitting course, requiring multiple steroid courses, but with low systemic inflammation during remission. We therefore used peripheral quantitative computed tomography (pQCT) to investigate compartmental volumetric BMD and bone geometry in NS, and evaluated the influence of treatment factors on bone outcomes.

Methods: Children with NS (n=29, 55% males, age 10.7±3.1 years) were compared to healthy controls (n=29, 55% males, age 11.0±3.0 years). Body composition was assessed by whole body DXA. pQCT scans were obtained at metaphyseal (4%) and diaphyseal (66%) sites of the tibia. Lifetime cumulative glucocorticoid exposure was calculated from medical records. Bone outcomes were adjusted for age, gender, height, ethnicity and pubertal status using linear regression.

Results: Children with NS had similar height SDS to controls (P=0.28), but were heavier (0.65±1.28 vs −0.04±0.89 SDS, P=0.022) and had greater body fat SDS (0.31±1.01 vs −0.52±1.10, P=0.008). Tibial trabecular and cortical vBMD were similar between the two groups but bone cross-sectional area (CSA) was significantly greater in children with NS at both the metaphysis (954±234 vs 817±197 mm², P=0.002) and diaphysis (511.0±1.4 vs 442.1±1.4 mm², P=0.006). Endosteal and periosteal circumferences were greater in children with NS than controls (both P<0.01), resulting in reduced cortical thickness (2.4±0.7 vs 2.8±0.7 mm, P=0.018), but similar cortical CSA (P=0.22). The differences in cortical geometry were not statistically significant when weight was included as a confounding factor. There were no associations between cumulative steroid exposure, duration of NS or number of relapses and any bone parameter.

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