Renal failure is a source of musculoskeletal features, especialy in patients treated by maintenance haemodialysis. In these, bone and joint involvement has become an important limitation of long term prognosis.
Severe secondary hyperparathyroidism can cause osteoarticular pain and an erosive enthesopathy which carries a risk of tendinous rupture.
Urate gout is a classical feature of terminal renal failure which usually does not persist after the onset of haemodialysis, as efficient uric acid clearance is acheived during dialysis sessions.
Periarticular calcifications are usually composed of calcium phosphate crystals and are favoured by hyperphosphataemia and other porly known factors. Deposits are frequently asymptomatic but can grow into tumoral masses or cause acute articular or periarticular flares. Bone erosions, in the vicinity of deposits can be observed. In dialysis patients, secondary oxalosis usually follows vitamin C supplementation of the diet and may be responsible for soft tissue calcification, articular effusion, chondrocalcinosis and a disabling finger flexor contracture.
The incidence of bone and joint infection in haemodialysis patients is 10 to 100 fold the one in the population at large, and this must remain a permanent concern as prompt diagnosis and treatment are required to improve a gloomy prognosis. The leading causative organisms are Staphylococcus species, the usual portal of entry being the arterioveinous fistula. In kidney transplant patients, very unusual pathogens can be identified.
Beta 2-microglobulin amyloidosis has been documented in a few long-standing terminal renal failure patients before the start of dialysis, but most usually develops in long term dialysis patients. Up to 65 p.cent of individuals who have received ten or more years of maintenance haemodialysis using standard cuprophane membranes are affected. Ageing is also an important risk factor. Carpal tunnel syndrome is a prominent feature, although oedema, uremic neuropathy and crystal deposition may play a role in some carpal tunnel syndromes of dialysis patients. A chronic amyloid arthropathy is also frequently observed. Features include chronic arthralgias, particularly of the shoulders, chronic joint swelling, finger tendon synovitis, large subchondral bone erosions which may lead to femoral neck fracture, and destructive arthropathy. Synovial fluid is noninflammatory and may contain numerous blood cells. Destructve spondylarthropathy predominantly affects the cervical spine and can lead to spinal cord and/or nerve root compression, usually through spine instability. Shoulder pain may be related to amyloid synovium involvement and/or amyloid thickening of the cuff tendons and subacromial bursa. Systemic deposits are rare. They can be responsible for intestinal haemorrage or cardiac dysfunction. Lack of β2-microglobulin catabolism by the deficient kidney and unsatisfactory elimination through the dialysis membrane are important in the pathogenesis of the disorders. The use of permeable and biocompatible membranes appears to delay the onset of the disease, but has been thus far unable to totally prevent its development.
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