Metabolic
alkalosis may develop as a consequence of urinary
chloride (and
sodium) wasting, excessive loss of
salt in the sweat, or intestinal
chloride wasting, among other causes. There is also a likely underrecognized association between poor
salt intake and the mentioned
electrolyte and
acid-base abnormality. In patients with excessive loss of
salt in the sweat or poor
salt intake, the maintenance of metabolic
alkalosis is crucially modulated by the
chloride-bicarbonate exchanger pendrin located on the renal tubular membrane of type B intercalated cells. In the late 1970s, recommendations were made to decrease the
salt content of foods as part of an effort to minimize the tendency towards systemic
hypertension. Hence, the baby food industry decided to remove added
salt from formula milk. Some weeks later, approximately 200 infants (fed exclusively with formula milks with a
chloride content of only 2-4 mmol/L), were admitted with
failure to thrive,
constipation, food refusal,
muscular weakness, and delayed psychomotor development. The laboratory work-up disclosed metabolic
alkalosis,
hypokalemia, hypochloremia, and a reduced urinary
chloride excretion. In all cases, both the clinical and the laboratory features remitted in ≤7 days when the infants were fed on formula milk with a normal
chloride content. Since 1982, 13 further publications reported additional cases of dietary
chloride depletion. It is therefore concluded that the dietary intake of
chloride, which was previously considered a "mendicant" ion, plays a crucial role in
acid-base and
salt balance.