sodium-bicarbonate and Hypercalcemia

Topics: Acidosis, Renal Tubular; Administration, Oral; Ammonia; Diagnosis, Differential; Exome Sequencing; Female; Fluid Therapy; Food Intolerance; Humans; Hyperammonemia; Hypercalcemia; Infant; Metabolism, Inborn Errors; Potassium Citrate; Sodium Bicarbonate; Treatment Outcome; Vacuolar Proton-Translocating ATPases; Weight Gain

Milk-alkali syndrome, once a common cause of hypercalcaemia, is now considered rare. Our aim was to estimate the prevalence of milk-alkali syndrome among hypercalcaemic, non-end-stage renal disease (non-ESRD) inpatients of a University Hospital and identify patients' and syndrome characteristics.. In this retrospective chart review study, we identified patients hospitalized with possible hypercalcaemia between November 1998 and October 2003 by a computer search of admission, discharge and consultation diagnoses. Patients with renal transplantation, stage 5 chronic kidney disease (CKD-5) and those admitted for parathyroidectomy were excluded. The remaining patients' charts were reviewed for confirmation of hypercalcaemia and identification of the cause. In patients with milk-alkali syndrome, additional historical, clinical, laboratory and imaging data were collected.. We identified 125 patients with hypercalcaemia, 11 (8.8%) of whom had milk-alkali syndrome, 42 (33.6%) had malignancy and 37 (29.6%) hyperparathyroidism. Thirty-five patients had severe hypercalcaemia, defined as corrected serum calcium 3.5 mmol/l. Malignancy accounted for 13 of those patients (37.1%) and milk-alkali for nine (25.7%). Conditions prevalent among the milk-alkali inpatients were female gender, hypertension, chronic kidney disease, osteoporosis, upper gastrointestinal diseases, diuretic treatment and vitamin D derivative supplementation. Five of the patients with milk-alkali syndrome were treated with bisphosphonates and all five developed hypocalcaemia, compared to one of the five who received conventional treatment (P = 0.047).. Milk-alkali was the third leading cause of hypercalcaemia of any degree and the second cause of severe hypercalcaemia among inpatients without ESRD. In milk-alkali syndrome, treatment with bisphosphonates contributes to post-treatment hypocalcaemia.

Topics: Adult; Aged; Aged, 80 and over; Calcium Carbonate; Diphosphonates; Diuretics; Female; Humans; Hypercalcemia; Kidney Diseases; Magnesium; Male; Middle Aged; Potassium; Retrospective Studies; Sex Distribution; Sodium Bicarbonate

Topics: Acidosis, Renal Tubular; Humans; Hypercalcemia; Infant; Male; Nephrocalcinosis; Parathyroid Hormone; Sodium Bicarbonate

Topics: Aluminum Hydroxide; Anti-Ulcer Agents; Bismuth; Drug Combinations; Glycyrrhiza; Humans; Hypercalcemia; Magnesium Hydroxide; Male; Middle Aged; Plant Extracts; Sodium Bicarbonate

Three siblings with neonatal familial hyperparathyroidism diagnosed at age 4 months, 2 months, and 5 days, respectively, were treated. Hypercalciuria, nephrocalcinosis, and renal tubular acidosis were present in each child. In all three, there were higher responses of serum parathyroid hormone to serum calcium and higher elevation of serum calcium with oral calcium loading. The metabolism of vitamin D and calcitonin seemed to be intact. Hypercalcemia associated with the abnormal response of parathyroid hormone secretion disappeared when the children passed the age of approximately 2 years, although renal tubular acidosis and nephrocalcinosis remained. An autosomal recessive inheritance seems likely.

Topics: Acidosis, Renal Tubular; Bicarbonates; Calcinosis; Calcium; Calcium, Dietary; Chromosome Aberrations; Chromosome Disorders; Female; Humans; Hypercalcemia; Hyperparathyroidism; Infant, Newborn; Kidney Diseases; Male; Parathyroid Hormone; Sodium; Sodium Bicarbonate; Vitamin D

Chick embryos were injected on the 14th day of incubation with 100 ng calcitriol. The concentration of Ca in their serum rose significantly 4 hours after the injection and the concentration of Pi started to decrease 10 hours after. When embryos of the same age were injected with a solution containing CaCl2, the concentrations of both Ca and P rose significantly 2 hours after the injection and remained high until the end of the experiment. The fact that both treatments produced hypercalcemia but had opposite effects on the concentration of Pi does not agree with the idea that the hypophosphatemic response to calcitriol might be secondary to the hypercalcemia which precedes it. The injection of a solution of NaHCO3 to embryos of the same age failed to produce hypophosphatemia. The fact that calcium salts and bicarbonate, when injected separately, fail to induce hypophosphatemia does not contradict the possibility that the hypophosphatemic response to calcitriol might result from the simultaneous increase in flux of Ca and -HCO3 from the shell. Three days after the injection of calcitriol to 14-day-old embryos, the total amount of Ca and P in the urine was significantly higher than in the controls. The concentration of Ca and P in kidney tissue was also significantly higher in the injected embryos. In addition, calcified precipitates were detected histochemically in the lumen of the kidney tubules from the treated embryos. These results are interpreted as demonstrating that an increase in the excretion of P in the urine is the main mechanism explaining calcitriol-induced hypophosphatemia in the chick embryo.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Bicarbonates; Calcitriol; Calcium; Chick Embryo; Hypercalcemia; Kidney; Muscles; Phosphates; Sodium; Sodium Bicarbonate; Time Factors

Topics: Adult; Alcoholism; Antacids; Bicarbonates; Calcium Carbonate; Humans; Hypercalcemia; Magnesium; Male; Sodium; Sodium Bicarbonate

Topics: Alkalosis; Aluminum Hydroxide; Antacids; Bicarbonates; Brain Diseases; Calcium; Constipation; Diarrhea; Drug Interactions; Humans; Hydrogen-Ion Concentration; Hypercalcemia; Kidney Calculi; Magnesium Hydroxide; Osteomalacia; Phosphates; Sodium; Sodium Bicarbonate; Urine; Water-Electrolyte Imbalance

The effect of changes in bicarbonate ion concentration on calcium ion concentration was examined in vitro in serum and protein-free solution. The findings in this study support the formation of a calcium-bicarbonate complex (CaHCO3+) that has a KA of 5.20 in protein-free solution. [Ca++] varied inversely with [HCO3-] in both serum and protein-free solution. This variation was independent of the known variation of [Ca++] with pH. In serum [Ca++] varied 0.0036 mM Ca++ per 1 mM change in [HCO3-] compared with a variation of 0.0060 mM Ca++ per 0.01 unit change in pH. Addition of bicarbonate to serum (Pco2 constant) produced a 50% greater decrease in [Ca++] than that produced by a reduction in Pco2 which gave the same pH change. These findings indicate that abnormal bicarbonate concentrations should be considered when ionized calcium concentrations are estimated from total plasma calcium values in acid-base disorders. In metabolic acid-base disorders, the bicarbonate effect adds to the pH effect on calcium ion concentration. In compensated respiratory acid-base disorders, the bicarbonate effect subtracts from the pH effect on calcium ion concentration.

Topics: Acid-Base Imbalance; Bicarbonates; Calcium; Carbon Dioxide; Humans; Hydrogen-Ion Concentration; Hypercalcemia; Partial Pressure; Sodium Bicarbonate

Topics: Bicarbonates; Calcium; Calcium Channel Blockers; Cation Exchange Resins; Diuretics; Humans; Hypercalcemia; Hyperkalemia; Insulin; Polystyrenes; Sodium Bicarbonate; Uremia