What types of crystal deposition diseases occur in patients with renal disease?
• Monosodium urate arthritis (gouty arthritis) occurs occasionally, although less frequently than one would expect considering how common hyperuricemia is in patients with chronic renal failure. There is increased GI excretion of uric acid when patients are in renal failure. Uric acid is extensively removed during hemodialysis.
• CPDD is seen occasionally in secondary hyperparathyroidism (although less common than in primary hyperparathyroidism). CPDD is manifested by chondrocalcinosis (knee, wrist, and symphysis pubis), acute pseudogout, and/or a degenerative arthritis.
• Hydroxyapatite arthropathy can present as acute episodes of joint pain or as a chronic periarthropathy resulting from calcium hydroxyapatite deposits. This arthropathy is strongly correlated with a high calcium–phosphate product. Periarticular and subcutaneous deposits may become quite large (tumoral calcinosis), particularly around the hips, knees, shoulders, and wrists, where they may cause pain, reduce range of motion, and predispose to infection.
• Secondary oxalosis rarely develops in long-standing renal failure. It is marked by oxalate deposition in visceral organs, blood vessels, bones, and articular cartilage where it may contribute to chronic polyarthralgias. Oxalate is produced from ascorbic acid and is cleared very poorly in chronic renal failure (GFR <20 mL/minute) and dialysis. Most cases of oxalosis can be prevented by limiting ascorbic acid (vitamin C) and oxalate intake (tea, spinach, okra, sweet potatoes, nuts, and soy products). Treatment of established calcium oxalate arthropathy with nonsteroidal antiinflammatory drugs (NSAIDs), colchicine, intraarticular corticosteroids, or increased dialysis has produced only slight improvement.
