sodium-bicarbonate and Magnesium-Deficiency

Mechanisms of renal potassium excretion and internal potassium balance as the main determinants of serum and/or total body potassium are discussed. Renal handling of potassium is reviewed, with particular attention to the effects of diuretics, acid-base disturbances and aldosterone-deficient states. Among the regulatory processes of internal potassium balance, the importance of adrenergic stimuli/drugs, of acid-base balance, and of magnesium and insulin is stressed. Physiologic and pathophysiologic evidence provides the basis for discussion of relevant clinical implications.

Topics: Acid-Base Equilibrium; Adult; Aged; Alkalosis; Bicarbonates; Biological Transport; Catecholamines; Chlorides; Diuretics; Female; Humans; Hyperkalemia; Hypokalemia; Insulin; Kidney; Kidney Tubules; Magnesium Deficiency; Male; Middle Aged; Potassium; Renin-Angiotensin System; Sodium; Sodium Bicarbonate; Stress, Physiological

Topics: Bicarbonates; Diabetic Ketoacidosis; Diphosphoglyceric Acids; Fluid Therapy; Humans; Hydrogen-Ion Concentration; Hypokalemia; Infusions, Parenteral; Insulin; Magnesium Deficiency; Magnesium Sulfate; Phosphates; Sodium Bicarbonate; Time Factors

Magnesium (Mg) deficiency sometimes causes hypocalcemia with impaired PTH secretion although the precise mechanism remains unclear. We examined the PTH secretion in response to physiological hypocalcemic stimuli in a patient with hypomagnesemic hypocalcemia. We adopted sodium bicarbonate infusion test, which we recently developed, to evaluate the PTH response to acute decrease in plasma ionized Ca. The results showed that, before Mg replacement and when the patient was mildly hypocalcemic, absolutely no PTH release to hypocalcemic stimuli was observed. In contrast, the plasma Ca was promptly normalized following the start of Mg replacement, and brisk PTH response to hypocalcemic stimuli was obtained during the same test carried out a week after the Mg replacement. The data in this case thus suggest that: a) the acute regulation of PTH release by plasma ionized Ca is lost in the patient with hypomagnesemic hypocalcemia, and b) Mg deficiency itself is likely to be a primary cause of this disorder because the hormone response was clearly restored after shortterm Mg replacement alone.

Topics: Adolescent; Adult; Calcium; Dietary Supplements; Eating; Female; Humans; Hypocalcemia; Magnesium; Magnesium Deficiency; Parathyroid Hormone; Sodium Bicarbonate