Rheumatologic manifestations of renal diseases
Julie T. Li-Yu, MD, FPCP, FPRA
University of Santo Tomas Hospital
Manila, Philippines
Musculoskeletal complaints among patients undergoing hemodialysis are commonly encountered. These appear to be major limiting factors in the quality of life in long term survivors. It might be considered a trade off for prolonged lifespan of patients kept on chronic hemodialysis that bone abnormalities are considered important in clinical management of these patients.
The variation as to the nature and type of bone disease is related to patient’s age, duration of renal disease, variation of the pathogenic processes involved, type of therapy, differences in diet, and type and duration of dialysis therapy.Abnormal metabolism or action of vitamin D is responsible for defective mineralization of bone in renal failure.
There is enhanced osteoclastic activities with increased bone resorption surfaces due to high circulating levels of parathyroid hormone. Skeletal findings in uremic patients are rarely pure osteomalacia or osteitis fibrosa. There is some degree of admixture of impaired mineralization and enhanced osteoclastic activity, with one process predominating over the other. Immobilization, calcium deficiency, chronic protein depletion maybe causes of osteoporosis in renal osteodystrophy. A peculiar feature of renal osteodystrophy is osteosclerosis which appears as increased bone density on radiograph most often seen in trabecular/cancellous bones. Radiographic features of hyperparathyroidism, osteoporosis, and osteomalacia have also been observed in patients with chronic renal failure.
Arthralgias and joint erosions are classical features of severe hyperparathyroidism. Bone pains and talalgias are most prominent on weight bearing. Erosive enthesopathy occur in the insertion of Achilles tendon, biceps tendon, and the knee or finger tendons. Aluminum intoxication has been a cause of bone pain and proximal muscle weakness in the past. This has been effectively controlled through avoidance of aluminum phosphate binders in the dialysate. _2 microglobulin amyloid deposits have been reported in chronic renal failure patients who have not received dialytic therapy, not necessarily a consequence of dialysis treatment alone. However, they are most commonly reported among long survivors of dialysis, with predilection to deposit along the articular cartilage, muscle, ligament, and synovium, occasionally blood vessels too. Multiple joints of the extremities are often affected with
deposits in and around the shoulders, wrists, and hands. Among patients on hemodialysis for 10 years or longer, prevalence of shoulder pain ranged from 34% to 84%; prevalence of carpal tunnel syndrome from 9% to 73%.
Diagnosis of dialysis-related amyloidiosis is made by suggested clinical presentation. Radiographic findings such asbone cysts, arrowed intervertebral disc space, and vertebral endplate erosion corroborate the diagnosis. However, histological identification of _2M amyloid by Congo red and immunohistological stain in biopsy specimens is considered the “gold standard” in the diagnosis of amyloidosis.
Prevalence of peri-articular calcification in uremic patients ranged from 7.5% to 44%, seen in both hemodialysis and peritoneal dialysis patients. Most of these calcifications contain carbonate substituted apatites and other calcium phosphates, as are found in patients with normal renal functions. Risk factors for peri-articular calcifications include hyperphosphatemia, secondary yperparathyroidism, magnesium retention, increased plasma vitamin K level, and iatrogenic factors. Aging and aluminum related bone disease have also been implicated to contribute to its formation. These deposits can occasionally cause inflammatory peri-arthritides, but not account for chronic arthropathy seen in amyloid arthropathy. Calcium pyrophosphate dihydrate (CPPD) crystals have been demonstrated in patients during attacks of pseudogout. Secondary oxalosis caused by calcium oxalate crystals is due to insufficient removal of oxalates during dialysis. Acute attacks of gout can occur in chronic renal failure due to underexcretion of uric acid. Upon institution of dialysis, attacks become rare because of removal of uric acid during dialysis.
Incidence of bone as well as joint infection is increased in patients undergoing dialysis. Immune defense of these patients are impaired, and the arterio-venous fistula is considered a potential source of hematogenous spread of bacterial infection. Septic arthritis is most often polyarticular and can be sub-acute. Bacteriological studies should be performed at all times to identify the usual and uncommon pathogens. Septic discitis is a consideration in destructive spondyloarthropathy among patients undergoing dialysis.
Miscellaneous disorders include olecranon bursitis, avascular necrosis most especially among patients on chronic steroid therapy following transplantation. Erosive arthritis of the finger joints is commonly as a well-recognized feature of dialysis arthropathy. Involvement of trapeziometacarpal joint that mimic clinical picture of osteoarthritis of this joint can also cause localized pain.
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