PubMed1998
The effects of aluminum on renal function and phosphate handling were studied using clearance techniques in chronically-intoxicated rats. Rats were given aluminum hydroxide (80 mg/kg b.w., i.p.), three times per week during 6 months. The phosphate tubular transport capacity was evaluated by determining the maximum tubular transport (TmRPi) and the fractional excretion of phosphate (FE% Pi) during the infusion of phosphate solutions with increasing concentrations (0, 9, 18, 33 mM). Parathyroid gland function was studied using indirect methods: calcemia recovery after EDTA administration and the nephrogenic excretion of cAMP as indicative of renal PTH actions, by RIA. The systemic acid base status was determined and food intake and rat growth were controlled in both groups. No changes were observed in the renal function. Pi reabsorption values per ml glomerular filtration rate (TRPi/GFR microg/ml) for different Pi plasmatic concentrations were distributed following a saturation curve compatible with a saturation kinetics. Aluminum increased TmRPi/GFR in treated animals (T) 76+/-4 as compared with control animals (C) 57+/-7 microg/ml, without a statistical modification in the apparent affinity. The FE% Pi and FE% Na were significantly lower in treated animals than in control animals. There were neither systemic variations in the acid-base balance nor in the Ca and Pi concentrations in plasma. The calcemia recovery following a hypocalcemic stimulus and the nephrogenic excretion of cAMP (T: 44+/-4; C: 91+/-7 pmol/min) were diminished. Considering all these facts, it can be postulated that the aluminum renal effect is associated from a decrease in PTH phosphaturic capacity. Nevertheless, other associated factors like minor phosphate intestinal absorption rate may not be disregarded, even though there were no significant intake variations.