Paradoxic acuduria can be a feature of a primary metabolic alkalosis due to vomiting or sequestration of hydrochloric acid-rich gastric contents in all species, but particularly ruminants. In this example of a ruminant with abomasal displacement, hydrochloric acid-rich and water-rich secretions are sequestered in the displaced abomasum. Due to hypochloremia, more sodium is delivered to the late distal tubule and collecting ducts, resulting in increased sodium absorption in these segments. The sodium absorption makes the lumen more negative, which drives hydrogen excretion via a sodium-dependent hydrogen pump (not shown). In addition, hypochloremia (reduces salt sensing in the macula densa, not shown) and hypovolemia stimulates aldosterone, which promotes sodium absorption in the distal convoluted tubules of the kidney. Normally sodium is exchanged for potassium, however potassium is concurrently depleted (moves intracellularly in exchange for hydrogen in an alkalemia, lost in gastric secretions, decreased intake in ruminants that are anorectic) so sodium is exchanged (resorbed) for hydrogen (excreted) resulting in a paradoxic aciduria.