tive gains of 3.9 to 12.5 g (100 to 320 mmol), of which about 7.8 g (200 mmol) is destined for the products of conception (Forsum et al., 1988; Hytten and Leitch, 1971; Lindheimer and Katz, 2000). The latter value comes from a review of the literature by Hytten and Leitch (1971), including one serial study that measured total exchangeable potassium (MacGillivray and Buchanan, 1958). Additionally, one report provided estimates of potassium accretion as measured by the 40K naturally present in human tissues (Godfrey and Wordsworth, 1970). The accumulation at birth was 12 g of potassium (307 mmol), while at 1 month of age the total estimated potassium had decreased to 7 g (179 mmol) (Godfrey and Wordsworth, 1970).

A subsequent study, however, suggests that body potassium stores decrease early in gestation and then increase to only 3.9 g (100 mmol) above those present prior to conception (Forsum et al., 1988). Hormonal changes may affect potassium balance and deposition (Ehrlich and Lindheimer, 1972; Lindheimer and Katz, 1985). It has also been noted that pregnant women develop bicarbonaturia at substantially lower plasma bicarbonate levels than do nonpregnant women (Lindheimer and Katz, 2000).

Serum and Plasma Potassium Concentrations. Plasma and serum concentrations of potassium decrease about 0.2 to 0.3 mmol/L, which may not indicate hypokalemia until values decrease by 0.5 mmol, or to below 3 mmol/L. The reason for the decrement in circulating potassium concentrations during gestation is obscure, but could relate to the mild physiologic alkalemia of gestation in which blood concentrations of hydrogen ions have been shown to decrease about 2 to 4 nmol/L (Lindheimer and Katz, 1985).

Urinary Potassium Excretion. Of further interest and in striking contrast to nonpregnant women, pregnant women are resistant to the kaliuresis provoked by a combination of exogenous mineralocorticoids and a high sodium diet (Ehrlich and Lindheimer, 1972). This ability to conserve potassium in the face of high concentrations of potent mineralocorticoids, such as aldosterone or desoxycorticosterone, and the delivery to the distal nephron of substantial quantities of sodium, may be due to the increased concentrations of progesterone, also characteristic of gestation—a view supported by some (Ehrlich and Lindheimer, 1972; Lindheimer et al., 1987; Mujais et al., 1993), but not others (Brown et al., 1986). Of importance, this resistance to the kaliuretic effects may benefit women with certain potassium-losing diseases, such as primary aldoster-