Effect of lactate on the absorption and retention of aluminum in the remnant kidney rat model.

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 A1 in our model and, if so, whether this would impose additional alterations on the A1 absorption in uremia. Uremic rats and controls were studied with single oral loads of either A1 chloride or A1 lactate and, subsequently, urinary A1 excretion was measured for 5 days. Compared with Al chloride, administration of A1 lactate resulted in significantly higher urinary excretion rates of A1 in uremic rats (55.5 +/- 22.7 vs. 27.4 +/- 7.0 micrograms; 2.06 +/- 0.84 vs. 1.01 +/- 0.26 mumol) and in controls (23.6 +/- 8.5 vs. 11.9 +/- 4.3 micrograms; 0.87 +/- 0.31 vs. 0.44 +/- 0.16 mumol). However, with either A1 load the recovery of A1 from urine was substantially higher in uremic animals. In contrast, only in controls was there a more pronounced rise in serum A1 concentrations following ingestion of A1 lactate, whereas in uremic rats this increase had a similar magnitude following A1 chloride and A1 lactate, suggesting a larger apparent volume of distribution of the latter. Adjustment of the pH of the A1 lactate-containing solution to 7.0 or oral administration of sodium lactate together with A1 chloride yielded essentially similar results. These observations indicate that the enhanced intestinal absorption of A1 in uremia is further augmented by lactate regardless of the mixture of hydroxolactato complexes employed.(ABSTRACT TRUNCATED AT 250 WORDS)