Pathogenesis of hyperphosphatemia in lactic acidosis: disparate effects of racemic (DL-) and levo (L-) lactic acid on plasma phosphorus concentration

The mechanism(s) for the hyperphosphatemia associated with lactic acidosis is unknown. Experimental lactate-induced hyperphosphatemia appears to require acidemia because we have shown that prevention of acidemia with NaHCO3 obviates increases in plasma phosphorus concentration ([P]). Since the rate of lactate metabolism (by utilizing NAD or other mechanisms) might modulate transcellular movement of phosphorus, we assessed the plasma [P] response to 3-h infusions of DL-lactic acid versus L-lactic acid. The dog metabolizes primarily the L- moiety of DL-lactic acid (thereby consuming H+), so more L-lactic acid is needed to produce the degree of acidemia attained with DL-lactic acid. Group 1 (n = 6) mongrel dogs received 12 mequiv./kg DL-lactic acid; group 2 (n = 6) 12 mequiv./kg L-lactic acid, and group 3 (n = 7) 16–19 mequiv./kg L-lactic acid. Prior to acid loading, the plasma [P] and acid–base status of the three groups were similar. After 3 h, blood pH and [HCO3] and change from base line in plasma [P], in both milligrams per decilitre and percent, were as follows: group 1: 7.05 ± 0.02, 9 ± 2 mM, 1.9 ± 0.4 mg/dL, 38 ± 10%; group 2: 7.28 ± 0.02, 18 ± 1, 0.9 ± 0.3, 17 ± 6; group 3: 7.06 ± 0.04, 12 ± 1, 1.1 ± 0.3, 26 ± 10, respectively. Thus, there was a tendency for both infusion rates of L-lactic acid to increase [P] less than DL-lactic acid, suggesting the importance of other factors in addition to pH. Also, since presumably more lactate was metabolized in group 3 than in group 2 (but the change in [P] was approximately the same in both), the findings do not support the hypothesis that the rate of lactate utilization is a major modulator of plasma [P] in acute lactic acidosis.