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Osteoporosis and Avascular Necrosis in Renal Transplant Patients: Diagnosis and Management

Learn about glucocorticoid-induced osteoporosis and avascular necrosis, common complications in renal transplant patients. Understand risk factors, assessment methods, diagnostic imaging, and treatment modalities.

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Osteoporosis and Avascular Necrosis in Renal Transplant Patients: Diagnosis and Management

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  1. Case 1 A 55-year-old woman, 6 months after renal transplantation and on corticosteroid treatment, presents with severe back pain after sudden bending. The pain refers into the flanks and anterior abdomen. Movement aggravate the pain. On physical examination, the patient experienced pain upon palpation and percussion of some spinous processes.

  2. Glucocorticoid-induced osteoporosis

  3. INTRODUCTION • GC increase the risk of fracture, particularly vertebral fractures • The incidence of fracture is higher with advanced age, larger dose, and longer duration of GC • The increased risk of fracture has been reported with doses of prednisone as low as 2.5 to 7.5 mg daily • Both high daily and high cumulative GC doses • >10% of patients who receive long-term GC are diagnosed with a fracture

  4. INTRODUCTION • 30–40% have radiographic evidence of vertebral fractures • The highest rate of bone loss occurs within the first 3–6 months • A slower decline continues with persistent use • Potentially reversible

  5. Clinical fracture risk assessment • Details of GC use (dose, duration, pattern of use) • Malnutrition • Significant weight loss or low body weight • Hypogonadism • Secondary hyperparathyroidism • Thyroid disease • Family history of hip fracture • Alcohol use • Smoking • Other comorbidities • Physical examination

  6. Treatment

  7. Case 2 • A 20-year-old woman was with MS since 10 years ago. • Treatment with Interferon • Intravenous Methylprednisolone (1g/day for 5 days) for three attacks • In a few days after her last steroid pulse she complained mild left groin pain. The pain was aggravated by Weightbearing and motion. • Physical findings: limitations of range of motion.

  8. Avascular Necrosis(osteonecrosis)

  9. Definition • Cellular death of bone components secondary to interruption of blood supply • Incidence: 21-37% • Mechanism: • Alterations in circulating lipids >>>> microemboli • Bone marrow adipocyte size and number >>> blocking venous outflow • Prolonged high doses

  10. The most affected sites • Hips • Knees • Shoulders

  11. Examination • Limp • Antalgic gait • Restricted ROM • Tenderness around bone • Joint deformity • Muscle wasting

  12. Imaging: X ray • Initially normal up to 3 months • Sclerosis • Flattening • Crescent sign • Collapse of cortex • OA

  13. Imaging: MRI • 90% sensitive • Reduced subchondral intensity on T1 representing boundary between necrotic and reactive bone • Low signal on T1 and high signal on T2 – reactive zone (diagnostic) • Changes detected early

  14. Radionuclide scan • Donut sign – central reduced uptake with surrounding rim of increased uptake • More sensitive than plain films in early AVN • Less sensitive than MRI • Necrotic zone surrounded by reactive new bone formation

  15. Prevention • Lipid-lowering agent • Anticoagulant

  16. Management principles • Early stages (I & II): • Bisphosphonates prevent collapse • Unloading osteotomies • Medullary decompression + bone grafting • Intermediate stage (III & IV): • Realignment osteototmies, decompression • Arthrodesis • Late stage (V & VI): • Analgesia, activity modification • Arthrodesis • Arthroplasties

  17. Glucocorticoid-induced myopathy

  18. The most common drug-induced myopathy • Dose? Rare in <10 mg/day • Duration? • Glucocorticoid preparation? Fluorinated corticosteroids • Gradual onset • Proximal muscle • Atrophy  • Myalgias ? • Lower extremity • Face, hand, and sphincter muscles are relatively spared • Other features of Cushing's syndrome

  19. Diagnosis? • CK normal • Improved strength within three to four weeks after sufficient dose reduction • Course?

  20. THANK YOU

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