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Both aging and chronic renal failure (especially end-stage renal disease) are characterized by a low bone turnover disorder. In aging, the senile form of osteoporosis may be related to a decrease in stem cells differentiating towards osteoprogenitors, while in CRF there is a decrease in the capacity of the osteoblast differentiation program in the absence of the influence of PTH. In both aging and CRF, secondary hyperparathyroidism is common. Thus, the impact of chronic renal failure on skeletal homeostasis in the elderly may be superimposition of an additional factor producing a deficiency of osteoprogenitors. Compensation through higher PTH levels results in an increase in resorptive activity. The long term clinical result of superimposing CRF on senile osteoporosis is unknown due to shortened survival of the population, but the risk of excess bone resorption is realized as survival is increased. From the above pathogenetic discussion of renal osteodystrophy and senile osteoporosis, the need for improved and specific therapeutic approaches is clear. At the present time, our treatments do not adequately consider the superimposition of chronic renal failure and renal osteodystrophy on the aging skeleton that may have osteoporosis. |
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