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Individuals with disorders of bone mineral homeostasis usually pres-ent with abnormalities in serum or urine calcium levels (or both), often accompanied by abnormal serum phosphate levels. These abnormal mineral concentrations may themselves cause symptoms requiring immediate treatment (eg, coma in malignant hypercalce-mia, tetany in hypocalcemia). More commonly, they serve as clues to an underlying disorder in hormonal regulators (eg, primary hyperparathyroidism), target tissue response (eg, chronic kidney disease), or drug misuse (eg, vitamin D intoxication). In such cases, treatment of the underlying disorder is of prime importance.
Since bone and kidney play central roles in bone mineral homeo-stasis, conditions that alter bone mineral homeostasis usually affect one or both of these tissues secondarily. Effects on bone can result in osteoporosis (abnormal loss of bone; remaining bone histologically normal), osteomalacia (abnormal bone formation due to inadequate mineralization), or osteitis fibrosa (excessive bone resorption with fibrotic replacement of resorption cavities and marrow). Biochemical markers of skeletal involvement include changes in serum levels of the skeletal isoenzyme of alkaline phosphatase, osteocalcin, and N- and C- terminal propeptides of type I collagen (reflecting osteo-blastic activity), and serum and urine levels of tartrate-resistant acid phosphatase and collagen breakdown products (reflecting osteoclastic activity). The kidney becomes involved when the calcium × phosphate product in serum rises above the point at which ectopic calcification occurs (nephrocalcinosis) or when the calcium × oxalate (or phos-phate) product in urine exceeds saturation, leading to nephro-lithiasis. Subtle early indicators of such renal involvement include polyuria, nocturia, and hyposthenuria. Radiologic evidence of nephrocalcinosis and stones is not generally observed until later. The degree of the ensuing renal failure is best followed by monitoring the decline in creatinine clearance. On the other hand, chronic kidney disease can be a primary cause of bone disease because of altered handling of calcium and phosphate, decreased 1,25(OH)2D produc-tion, and secondary hyperparathyroidism.
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