Diffuse Osteosclerosis in a Treated Case of Carcinoma Bladder On FDG PET/CT: Lesson to Look Beyond Metastases in Oncology

INTRODUCTION

Renal osteodystrophy is a skeletal complication of chronic kidney disease and part of the CKD–Mineral Bone Disorder spectrum. Although typically characterized by abnormalities in bone turnover and mineralization, diffuse osteosclerosis is a rare manifestation and can mimic skeletal metastases, especially in patients with underlying malignancy. On 18F-FDG PET/CT, it may present as diffuse sclerotic changes without abnormal FDG uptake, posing a diagnostic challenge. We report a case illustrating this potential pitfall and the importance of correlating imaging with biochemical findings to avoid misdiagnosis and unnecessary treatment.

CASE REPORT

A 65-year-old male with a history of high-grade papillary urothelial carcinoma (World Health Organisation 2004) involving the lamina propria and focal detrusor muscle underwent radical cystectomy with ileal conduit urinary diversion and pelvic lymph node dissection. He was kept under regular oncologic surveillance with no evidence of recurrence on imaging. Over the course of follow-up, he progressively developed stage IV chronic kidney disease (CKD). The aetiology was attributed to chronic obstructive uropathy related to ureteroenteric anastomotic complications and progressive parenchymal damage. His renal function gradually deteriorated over 5 years, with persistently elevated serum creatinine levels. The patient later presented with chronic back pain and generalised fatigue. Given his oncologic background, a whole-body 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET)-computed tomography (CT) was performed to evaluate possible metastatic disease. Axial CT and fused PET/CT images [Fig 1a and 1b] show diffuse uniform osteosclerosis involving axial skeleton and proximal appendicular bones bilateral small, shrunken kidneys without evidence of hydronephrosis or nephrolithiasis. No FDG-avid lesions were seen to suggest locoregional recurrence or distant metastases. On further biochemical assessment, serum calcium was 9.4 mg/dl and serum potassium 3.9 mg/dl, both within normal range, with normal values of serum 25(OH) Vitamin D (32 ng/ml). Parathyroid hormone levels were significantly elevated at 165 pg/mL (normal range: 15–65 pg/mL). Since there was a high index of suspicion of secondary hyperparathyroidism, a Tc-99m sestamibi parathyroid scintigraphy with SPECT/CT was performed. On both planar [Fig 2a-c] and SPECT/CT [Fig 3a-c] there was no focus seen in the neck or mediastinum thus ruling out possibility of parathyroid adenoma. Based on the clinical, biochemical, and imaging findings, a diagnosis of renal osteodystrophy with diffuse osteosclerosis secondary to secondary hyperparathyroidism in CKD was established. The patient was managed conservatively with phosphate binders, Vitamin D supplementation, and dietary phosphorus restriction under the care of a nephrologist and endocrinologist. He was advised to undergo regular follow-up to monitor renal function and skeletal symptoms.

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Fig 1:

(a) Sagittal fused and (b) CT images show diffuse osteosclerosis with no significant FDG uptake

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Fig 2:

(a) Whole body planar Tc99 sestamibi, as well as anterior 20-minute and (b) 2 hour (c) images show no focal tracer retention in neck region to suggest parathyroid adenoma

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Fig 3:

Axial CT (a) Tc99m sestamibi axial SPECT/CT, (b) axial SPECT and (c) coronal SPECT images show no focal tracer uptake in the neck region to suggest parathyroid adenoma

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DISCUSSION

Renal osteodystrophy, part of the CKD–mineral bone disorder (CKD–MBD) spectrum, includes a range of skeletal abnormalities secondary to impaired mineral metabolism seen in CKD.^[1,2] The condition encompasses osteitis fibrosa cystica (OFC), osteomalacia (OM), adynamic bone disease (ABD), and mixed uremic osteodystrophy (MUO), each with distinct histologic features and turnover patterns.^[3] Diffuse osteosclerosis is a rare but significant manifestation of renal osteodystrophy. In oncologic patients, especially those with a known history of malignancy, such sclerotic changes may mimic skeletal metastases, prompting extensive metastatic workups and potentially leading to inappropriate management.^[4]

This report presents an unusual case of diffuse osteosclerosis in a bladder cancer survivor with CKD, emphasising the critical need for accurate interpretation of metabolic bone changes on imaging studies. It highlights the essential role of correlating imaging findings with biochemical markers and specialised nuclear medicine investigations to distinguish metabolic from malignant bone disease.

Renal osteodystrophy can be classified into four main subtypes:

1. OFC: Characterised by high bone turnover due to elevated parathyroid hormone (PTH) levels, often showing subperiosteal bone resorption and brown tumours

2. ABD: Features low bone turnover with minimal osteoblastic or osteoclastic activity, often due to over-suppression of PTH

3. OM: Impaired bone mineralisation with increased osteoid volume; historically linked to aluminium toxicity in dialysis patients

4. MUO: Combines features of OFC and OM with high turnover and defective mineralisation.

Radiographically, early skeletal changes involve the radial aspects of the middle phalanges. Additional manifestations include the “rugger jersey spine,” soft-tissue calcifications, and brown tumours, with close differentials being metastatic carcinoma, Paget’s disease, and skeletal fluorosis.^[5]

Our patient’s sclerotic pattern was non-FDG-avid, diffuse, and lacked typical metastatic features. His biochemical profile showed elevated PTH with normal calcium and phosphate levels, supporting the diagnosis of secondary hyperparathyroidism. The negative Tc-99m sestamibi scan effectively ruled out primary hyperparathyroidism. 18F-FDG PET-CT, though not classically used for metabolic bone disease, proved valuable in excluding FDG-avid skeletal metastases.^[6] The combination of negative PET-CT, biochemical markers, and a targeted parathyroid scan helped confirm the benign nature of the skeletal changes.^[7] This case emphasises the importance of a multidisciplinary approach involving nuclear medicine, nephrology, endocrinology, and oncology. Differentiating metabolic bone disease from malignancy in cancer survivors is critical to avoid misdiagnosis and overtreatment.

CONCLUSION

This case highlights diffuse osteosclerosis as a rare manifestation of renal osteodystrophy due to secondary hyperparathyroidism in CKD. In patients with a history of malignancy, this condition can mimic metastatic disease radiologically. Early recognition and differentiation are essential to avoid misdiagnosis and to initiate appropriate CKD–MBD therapy, which may prevent further skeletal complications.