sodium-bicarbonate and Hypocalcemia

Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc interval prolongation. The potential impact of regular sodium bicarbonate therapy on worsening vascular calcifications in patients with chronic kidney disease has been insufficiently investigated.

Topics: Acidosis; Clinical Trials as Topic; Disease Progression; Glomerular Filtration Rate; Humans; Hypercapnia; Hypocalcemia; Hypokalemia; Renal Dialysis; Renal Insufficiency, Chronic; Sodium Bicarbonate

Hypocalcemia, transient or permanent, represents a common complication after total thyroidectomy, but data on the secretory capacity of the parathyroid glands in thyroidectomized patients without clinical or biochemical hypocalcemia are limited.. To address this issue, we studied the parathyroid response to acute hypocalcemia induced by iv infusion of sodium bicarbonate in normocalcemic patients submitted to total thyroidectomy at the early postoperative period and 3 months later.. Sixty patients who underwent total thyroidectomy for benign thyroid disease and did not develop clinical or biochemical hypocalcemia and hypoparathyroidism postoperatively and 50 healthy volunteers were included in the study. Patients (at 48 h and 3 months after surgery) and controls (after overnight fast) were subjected to a sodium bicarbonate infusion test.. In healthy volunteers plasma intact PTH increased significantly at 3 min after infusion (4.42 ± 0.15 ng/ml vs. 11.22 ± 0.5 ng/ml, P < 0.001) and gradually returned to baseline values. In the thyroidectomized patients, mean PTH levels were also increased after sodium bicarbonate infusion but to a significantly lesser degree compared with healthy controls (1.77 mean fold increase vs. 2.57 mean fold increase, respectively, P < 0.001). Using as criterion the lowest fold increase of plasma PTH levels at 3 min after infusion observed in healthy volunteers, 38% of the thyroidectomized patients at 48 h after surgery and 6.6% of the patients at 3 months after surgery demonstrated a diminished PTH response to acute hypocalcemia induced by sodium bicarbonate infusion.. In thyroidectomized patients, normal postoperative calcium and PTH values do not exclude a reduced secretory response of the parathyroids to hypocalcemic stimuli.

Topics: Adult; Algorithms; Calcium; Diagnostic Techniques, Endocrine; Female; Humans; Hypocalcemia; Infusions, Intravenous; Male; Middle Aged; Parathyroid Glands; Parathyroid Hormone; Postoperative Period; Reference Values; Sodium Bicarbonate; Thyroid Nodule; Thyroidectomy

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

The case is described of a 29-year-old man with renal failure and recurrent hyperparathyroidism who 3 weeks postparathyroidectomy developed hypocalcemic tetany because he was taking one-half the prescribed dose of calcitriol. He interpreted his symptoms as those of potassium intoxication and self-administered almost 1,500 mEq sodium bicarbonate. The increase in plasma sodium and osmolarity led to increased fluid intake, and at presentation he had an ionized calcium of 0.50 mmol/L, K 5.3 mmol/L, Na 148 mmol/L, total CO2 52.6 mmol/L, pO2 51.2 mm Hg, and pH of 7.61. He had gained 7 kg in weight. All abnormalities were corrected by dialysis, using initially a calcium-free dialyzate with extra calcium infused. The case illustrates the effect of alkalosis in reducing the amount of calcium that exists in ionized form, and it is suggested that complexing of calcium as calcium bicarbonate together with the pH change contributed to the decrease in ionized calcium. It is also an example of the hazards of treating patients who devise their own therapeutic regimens.

Topics: Adult; Alkalosis; Calcitriol; Calcium; Humans; Hyperparathyroidism; Hypocalcemia; Kidney Failure, Chronic; Male; Parathyroidectomy; Postoperative Complications; Renal Dialysis; Self Medication; Sodium Bicarbonate; Tetany

Non-pretrained, randomized adult rats were tested in a panic-inducing model of passive avoidance. Intravenous treatment with alkalinizing agents (sodium lactate 0.5 M, 0.5 ml/100 g b.wt., or NaHCO3, 0.5 mEq/100 g b.wt.), but not with a hypocalcemic dose of EDTA (75 mg/kg) 3 min before testing, significantly increased panic behavior. These data may support the hypothesis that panic attacks are due to alkalosis and not to lactate-induced hypocalcemia.

Topics: Alkalosis; Animals; Behavior, Animal; Bicarbonates; Fear; Female; Hypocalcemia; Lactates; Lactic Acid; Panic; Random Allocation; Rats; Rats, Inbred Strains; Sodium; Sodium Bicarbonate

Hypocalcemia was believed to be the result of aggressive sodium bicarbonate treatment for a cat with aspirin intoxication. The cat developed progressive neuromuscular tetany during the bicarbonate treatment and was determined to have a low serum ionized calcium value.

Topics: Animals; Aspirin; Bicarbonates; Cat Diseases; Cats; Hypocalcemia; Male; Sodium; Sodium Bicarbonate

A 32-year old woman developed severe quadriparesis, hypokalemia, and distal renal tubular acidosis following paint sniffing for one week. A review of literature indicated that a spectrum of renal diseases may develop in association with inhalation of toluene-containing substances. Toluene inhalation should be considered in the differential diagnosis in any young patient who presents with an unexplained renal disorder.

Topics: Acidosis, Renal Tubular; Adhesives; Adolescent; Adult; Bicarbonates; Calcium Gluconate; Female; Humans; Hypocalcemia; Male; Potassium Chloride; Sodium; Sodium Bicarbonate; Substance-Related Disorders; Tetany; Toluene

Topics: Acid-Base Equilibrium; Adolescent; Aspirin; Bicarbonates; Calcium; Humans; Hypocalcemia; Male; Sodium Bicarbonate