Ageing and changes in phosphate transport: clinical implications.

Hyperphosphatemia is pivotal in some complications secondary to kidney dysfunction. Current guidelines suggest that hyperphosphatemia secondary to kidney dysfunction develops only when glomerular filtration rate is reduced well below the threshold of 60 ml/min. This paper deals with the relationship of age with serum phosphorus and with the possible influences of this relationship on hyperphosphatemia secondary to kidney dysfunction. A recent epidemiologic study shows that serum phosphorus decreases over time not only in pediatric age but also during adulthood. This decrease differs between men and women: continuous in men, but not in women, because of a transitory serum phosphorus increase during climacterics. Data show also that age-associated differences in serum phosphorus among adults are explained by differences in the maximal phosphorus reabsorption in the renal proximal tubule (TmP/GFR). Other studies suggest that the opposite influences on TmP/GFR of growth hormone (stimulation) and estrogen (inhibition) are the determinants of the age-associated changes in TmP/GFR and serum phosphorus. The decline of serum phosphorus with age leads to the hypothesis that, in the presence of a disorder inducing phosphorus retention, the prevalence of hyperphosphatemia should be higher in young adults than in the elderly because the healthy elderly have lower serum phosphorus. A large clinical study supports this hypothesis showing that hyperphosphatemia secondary to kidney dysfunction is approximately 4 times higher at age <65 that at age >65. Data suggest that the relation between kidney function and serum phosphorus should be reevaluated considering the possible confounding effect of age.