Patients with chronic renal failure may present several abnormal findings on chest radiography and CT, due to changes in the phosphorus and calcium metabolism, changes in hemostasis, arterial hypertension, fluid retention, or dialysis. The most frequent abnormalities include interstitial and alveolar edema and cardiomegaly, pleural effusion (Fig. 2), metastatic pulmonary calcifications, and calcifications of the bronchial walls, pleura, and chest wall vessels.

Hematologic abnormalities are among the most consistent manifestations of uremia (Warnock 1992). These abnormalities include anemia, bleeding, and granulocyte and platelet dysfunction. The primary causes of anemia in chronic renal failure are a deficiency of erythropoietin, which is a glycoprotein normally produced by the kidney, and iron deficiency due to reduced iron intake and frequent blood sampling. Erythropoietin therapy has improved the general status of patients with chronic renal failure. In patients with uremic syndrome, the fat bone marrow is progressively replaced by hematopoietic marrow content (Ito et al. 1994) with prolonged T1 relaxation time in various anatomical regions (especially the spine and the upper and lower limb bones). A hemorrhagic diathesis is common in patients with chronic renal failure. Spontaneous nontraumatic bleeding may affect the perinephric and subcapsular spaces, the renal parenchyma, or the collecting system. Gastrointestinal bleeding is also common in uremic patients.

The most common neurologic complications in this patient group include focal white matter lesions, cerebral atrophy, osmotic demyelination syndrome, dialysis encephalopathy, hypertensive encephalopathy, intracranial hemorrhage, infarction, sinus thrombosis, and infection. Peripheral neuropathy is also common in patients with chronic renal failure.

Abnormalities involving the musculoskeletal system are numerous and frequent in patients with chronic renal insufficiency (Murphey et al. 1993). Chronic renal insufficiency, hemodialysis, peritoneal dialysis, renal transplantation, and administration of different medications provoke complex biochemical disturbances of the calcium-phosphate metabolism with wide spectrum of bone and soft tissue abnormalities termed renal osteodystrophy (Jevtic 2003). By the time dialysis is initiated, nearly all patients are affected. Renal osteodystrophy is a global term applied to all pathological features of bone in patients with chronic renal failure and it comprises osteomalacia or rickets according to patient age, secondary hyperparathyroidism with bone resorption (Figs. 3 and 4), pathologic fractures, (Fig. 5), periosteal reaction, osteosclerosis (Fig. 6), osteoporosis, soft tissue and vascular calcifications (Fig. 7), and brown tumors (Fig. 8). Bone resorption typically manifests along the radial aspects of the middle phalanges of the index and middle fingers (Fig. 3), beginning in the proximal metaphyseal region. Additional sites of subperiosteal bone resorption include the upper medial tibia, humerus, and femur; the superior and inferior ribs; and the lamina dura (Murphey et al. 1993). The irregular cortical surface may create a false appearance of periosteal reaction (pseudoperiostitis). Subchondral bone resorption affects the single distal interphalangeal joint (most frequently the fourth and fifth fingers); the metacarpophalangeal joint and the proximal interphalangeal joints; the distal clavicle; the acromioclavicular joint, sacroiliac joint, sternoclavicular joint (Fig. 4); the symphysis pubis, and the posterior patella (Murphey et al. 1993). Subligamentous bone resorption includes the inferior surface of the calcaneus and clavicle (coracoclavicular ligaments), greater and lesser femoral trochanters, anterior inferior iliac spine region, humerus near the insertion of the rotator cuff, ischial tuberosities, and elbow at the level of the extensor surface of the ulna and posterior olecranon (Murphey et al. 1993). Peridiscal destructive arthritis in patients on long-term hemodialysis, especially located on the cervical and dorsal spine, may mimic spondylodiscitis and corresponds to the hemodialysis spondyloarthropathy (Leone et al. 2001). Osteoclastomas or brown tumors (Fig. 8) are caused by localized replacement of bone by vascularized fibrous tissue (osteitis fibrosa cystica) resulting from PTH-stimulated osteoclastic activity. The fibrous tissue contains giant cells, and the lesions may become cystic following necrosis and liquefaction. Radiographically, brown tumors are well-defined lytic lesions, often eccentric or cortical, that may cause endosteal scalloping and osseous expansion (Murphey et al. 1993).

Other abnormalities related to biochemical disturbance of chronic renal failure include soft tissue/vascular or bronchial calcifications (Fig. 7) and crystalline arthropathies. Musculoskeletal sequelae predominantly related to dialysis include aluminum toxicity manifesting as osteomalacia from ingestion of aluminum salts in phosphate-binding antacids used to control hyperphosphatemia, amyloidosis with carpal tunnel syndrome, and destructive spondyloarthropathy (Murphey et al. 1993). Avascular necrosis, osteomyelitis, septic arthritis, tendinosis/tendon rupture, and bursitis/synovitis are caused by a combination of chronic renal failure, steroid/immunosuppressants, and dialysis (Lim and Ong 2013).