Dietary Chloride Deficiency Syndrome: Pathophysiology, History, and Systematic Literature Review.

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.

Dietary acid load in early life and bone health in childhood: the Generation R Study.

BACKGROUND: Dietary contribution to acid-base balance in early life may influence subsequent bone mineralization. Previous studies reported inconsistent results regarding the associations between dietary acid load and bone mass. OBJECTIVE: We examined the associations of dietary acid load in early life with bone health in childhood. DESIGN: In a prospective, multiethnic, population-based cohort study of 2850 children, we estimated dietary acid load as dietary potential renal acid load (dPRAL), based on dietary intakes of calcium, magnesium, phosphorus, potassium, and protein, and as a protein intake to potassium intake ratio (Pro:K) at 1 y of age and in a subgroup at 2 y of age : Bone mineral density, bone mineral content (BMC), area-adjusted BMC, and bone area were assessed by dual-energy X-ray absorptiometry at the median age of 6 y. Data were analyzed by using multivariable linear regression models. RESULTS: After adjusting for relevant maternal and child factors, dietary acid load estimated as either dPRAL or Pro:K ratio was not consistently associated with childhood bone health. Associations did not differ by sex, ethnicity, weight status, or vitamin D supplementation. Only in those children with high protein intake in our population (i.e., >42 g/d), a 1-unit increase in dPRAL (mEq/d) was inversely associated with BMC (difference: -0.32 g; 95% CI: -0.64, -0.01 g). CONCLUSIONS: Dietary acid load in early life was not consistently associated with bone health in childhood. Further research is needed to explore the extent to which dietary acid load in later childhood may affect current and future bone health.

Acid-base disorder analysis during diabetic ketoacidosis using the Stewart approach--a case report.

This case report presents a 49 year-old female with type 1 diabetes admitted to the intensive care unit with acute respiratory failure and severe diabetic ketoacidosis with an initial measurement of blood glucose level of 1,200 mg L⁻¹, pH 6.78, serum HCO3 ⁻ 3.2 mmoL L⁻¹ and BE -31.2 mmoL L⁻¹. Analysis of the blood gasometric parameters with the Stewart approach and the traditional Henderson-Hasselbalch concept enabled the discovery of metabolic acidosis caused by unidentified anions (mainly ketons). A treatment protocol with intensive fluid management with 0.9% NaCl, intensive intravenous insulin therapy, and potassium supplementation was administered. Analysis of the gasometric parameters after 12 hours of treatment according to the Stewart approach compared to the Henderson-Hasselbalch concept disclosed that metabolic acidosis caused by the unidentified anions has resolved almost completely and been replaced by metabolic hyperchloremic acidosis. The hyperchloremic acidosis was caused by the intensive fluid resuscitation with 0.9% NaCl, which contains a high chloride load, exceeding the chloride levels observed in human serum. Fluid management with balanced fluids other than saline was continued, together with intravenous insulin infusion, potassium supplementation, and 5% glucose administration. Analysis of this case study revealed the advantages of the Stewart approach to acid base abnormalities compared to the traditional Henderson-Hasselbalch concept. The Stewart approach allows the diagnosis of the exact causes of severe life-threatening metabolic acidosis and the appropriate modification of the therapeutic mangement of patients with diabetic ketoacidosis.

Electrolyte disorders and substitution fluid in continuous renal replacement therapy.

Electrolyte balances during acute renal failure treated with continuous convective techniques, such as continuous arteriovenous hemofiltration (CAVH) and its pumped variants, are largely dependent on the eloctrolyte plasma concentration available for ultrafiltration, the ultrafiltration rate and the composition of the replacement solution. As blood sodium concentrations measured by potentiometry (Na +P) and the total ultrafiltrate sodium concentration are very similar, Na +P can be taken as the value of ultrafilterable sodium when choosing the correct sodium concentration in the substitution fluid. In CAVH, the ultrafiltrate contains about 3 m Eq/liter of calcium and 1 m Eq/liter of magnesium that must be replaced by the substitution fluid in order to prevent hypocalcemia and hypomagnesemia. In addition, if plasma potassium levels are normal, 3 to 4 mEq/liter of potassium should be added to the replacement fluid to avoid hypokalemia. Although convection and diffusion are combined in continuous hemodialysis, solute transport is largely mediated by convection; however, the net removal of sodium and calcium is significantly influenced by their concentrations in the dialysate, and the risk of hypomagnesemia and hypokalemia can be attenuated by adjusting magnesium and potassium concentrations in the dialysis solution to levels near to the plasma water values. Since critically ill patients are prone to developing dialysis-induced hypophosphatemia, phosphorous must be monitored and supplemented if necessary, Since CRRT works continuously, serious derangement in fluid and electrolyte homeostasis may occur in the absence of careful prescription and extremely vigilant monitoring.

The nature of the renal response to chronic disorders of acid-base equilibrium.

The rate of acid excretion by the kidney appears to be determined by factors regulating the site and the rate of sodium reabsorption, rather than by a homeostatic mechanism that responds to systemic pH. This hypothesis, although unconventional, is supported by much experimental evidence, and it accounts for a wide variety of clinical and physiologic findings that heretofore have been difficult or impossible to explain.