Abstract
Renal damage from tumor-induced hypercalcemia must be distinguished from renal damage produced directly by the tumor, and more rarely from hypercalcemia accompanying acute renal failure. Calcium salt deposition occurs in arterioles, glomeruli and their capsules, tubular cells and lumena. The accompanying changes include a low glomerular filtration rate, resistance to antidiuretic hormone, hypophosphatemia and metabolic alkalosis. Appropriate treatment includes rehydration, natriuresis, and administration of oral phosphate, calcitonins, steroids, diphosphonates, mithramycin and If possible tumor ablation or removal. The optimal therapy depends on several factors including the verity of the renal failure, the effects of the agents used and the mechanisms of hypercalcemia. The correction of hypophosphatemia enhances the action of endogenous or exogenous calcitonin
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