Effect of Lactate on the Absorption and Retention of Aluminum in the Remnant Kidney Rat Model

Abstract

In previous investigations we found the gastrointestinal absorption of aluminum (Al) to be enhanced in uremic rats and this phenomenon could not be attributed to either calcitriol deficiency or secondary hyperparathyroidism. The purpose of this study was to examine whether carboxyl ligands such as lactate could affect the absorption of Al in our model and, if so, whether this would impose additional alterations on the Al absorption in uremia. Uremic rats and controls were studied with single oral loads of either Al chloride or Al lactate and, subsequently, urinary Al excretion was measured for 5 days. Compared with Al chloride, administration of Al lactate resulted in significantly higher urinary excretion rates of Al in uremic rats (55.5 ± 22.7 vs. 27.4 ± 7.0 μg; 2.06 ± 0.84 vs. 1.01 ± 0.26 μmol) and in controls (23.6 ± 8.5 vs. 11.9 ± 4.3μg; 0.87 ± 0.31 vs. 0.44 ± 0.16 μmol). However, with either Al load the recovery of Al from urine was substantially higher in uremic animals. In contrast, only in controls was there a more pronounced rise in serum Al concentrations following ingestion of Al lactate, whereas in uremic rats this increase had a similar magnitude following Al chloride and Al lactate, suggesting a larger apparent volume of distribution of the latter. Adjustment of the pH of the Al lactate-containing solution to 7.0 or oral administration of sodium lactate together with Al chloride yielded essentially similar results. These observations indicate that the enhanced intestinal absorption of Al in uremia is further augmented by lactate regardless of the mixture of hydroxolactato complexes employed. By means of a larger apparent volume of distribution Al lactate may accelerate the accumulation of Al in uremia by an increase in both intestinal absorption and tissue distribution.