a reduction in the urinary excretion of hydroxyproline, a marker of bone breakdown, and an increase in the serum concentration of osteocalcin, a marker of bone formation. When supplemental potassium bicarbonate was discontinued, the levels of plasma bicarbonate and arterial pH, like those of all other measured variables that had changed with the supplement, returned almost immediately to levels nearly identical to those occurring before the potassium bicarbonate was supplemented. This pattern of results suggests that a state of low-grade metabolic acidosis existed immediately before and after potassium bicarbonate was supplemented; that the acidosis resulted from the endogenous generation of noncarbonic acid at a rate greater than that at which the kidney could excrete it; that the acidosis induced increased bone resorption and reduced bone formation; that the acidosis induced increased renal loss of calcium and phosphate and thereby negative balances of both; and that supplemental potassium bicarbonate reversed each of these metabolic derangements by fully correcting the low-grade metabolic acidosis by titrating endogenously produced noncarbonic acid. Similar results were seen and conclusions drawn in metabolic studies of nonhypertensive young men and women in whom dietary potassium chloride was replaced with potassium bicarbonate, where-upon the urinary excretion of deoxypyridinoline, pyridinoline, and n-telopeptide (markers of bone resorption) promptly decreased (Maurer et al., 2003).

In a pre- and poststudy in which 21 adult patients with calcium urolithiasis were treated with potassium citrate for 11 to 120 months,