A 10-year-old boy with a past history of progressive renal dysfunction on peritoneal dialysis because of prune belly syndrome was evaluated before renal transplant. Despite treatment with oral phosphate binding agents and 1,25-dihydroxyvitamin D3 analogs, the family described longstanding difficulties complying with a low-phosphorus diet. There was no history of fractures and previous bone densitometry scans had shown his bone mineral density to be normal. Recent complaints centered on worsening lower extremity bone pain and bilateral joint pain affecting the knees and ankles. On examination, the patient was <3rd percentile for stature and weight and exhibited significant genu varus as well profound Trandelenberg gait, resulting in painful ambulation. Laboratory evaluation revealed a low calcium of 2.27 mmol/L (2.4–2.64), elevated phosphorus of 2.13 mmol/L (1.19–1.42), elevated alkaline phosphatase (1648 U/L [415–945]), and parathyroid hormone (64 pmol/L [1–5.2]). Selected radiographs from the patient's skeletal survey are shown. Vertebral endplate sclerosis accounts for the “rugger jersey” appearance of the spine (Fig 1). The patient also exhibited diffuse metaphysical widening, lucency, and fraying with subperiosteal resorption along the middle phalanges of both hands (Fig 2, available at www.us.elsevierhealth.com/jpeds). Despite these and other radiographic findings, a dual energy x-ray absorptiometry (DEXA) scan (GE Lunar Prodigy) at the lumber spine, and both hips showed bone mineral densities within age-reported normal values. Download .jpg (.58 MB) Help with jpg files Fig 2 Renal osteodystrophy is a generic term that describes all skeletal disorders occurring in patients with renal failure. It describes bony changes as a result of phosphate retention, hypocalcemia, and reduced 1,25-dihydroxyvitamin D3 production leading to hyperparathyroidism. In cortical bone, this results in increased resorption at subperiosteal, endocortical, and intracortical sites, whereas thickening and sclerosis occur in trabecular bone.1.Parfitt M. A structural approach to renal bone disease.J Bone Miner Res. 1998; 13: 1213-1220Crossref PubMed Scopus (163) Google Scholar The end result of these changes is impaired bone strength and increased fracture risk, which is not reflected with integrated DEXA bone densitometry measurements.2.Leonard M.B. Bachrach L. Assessment of bone mineralization following renal transplantation in children: limitations of DEXA and confounding effects of delayed growth and development.Am J Transplant. 2001; 1: 193-196Crossref PubMed Scopus (34) Google Scholar This case reinforces the importance of obtaining and evaluating radiographs in patients with metabolic bone disease. These better allow clinicians to directly observe the structural changes of renal osteodystrophy and avoid interpretation of erroneous and conflicting bone densiometry scans.