sodium-bicarbonate and Osteomalacia

Metabolic acidosis occurs frequently in small children. The most common causes are hypoxia, sepsis, gastroenteritis and hypovolaemia. Calculation of the anion gap is useful in establishing the cause. An increased anion gap represents unmeasured anions, e.g. lactate in lactic acidosis. Metabolic acidosis was diagnosed in two boys aged one year and six weeks respectively. The first patient had a normal, the second an increased anion gap in blood. By determining the pH and the anion gap in urine it is possible to distinguish between a proximal and a distal tubular disease. The first patient had distal renal tubular acidosis; he recovered after correction of the acidosis. The second patient had a defect in the mitochondrial respiratory chain; he died at the age of seven months.

Topics: Acid-Base Imbalance; Acidosis, Lactic; Acidosis, Renal Tubular; Diagnosis, Differential; Fatal Outcome; Humans; Infant; Male; Mitochondrial Myopathies; Osteomalacia; Sodium Bicarbonate

Renal tubular acidosis represents a heterogenous group of disorders with various etiologies and mechanisms. The physiopathologic basis of each type of renal tubular acidosis is reviewed, focusing on the laboratory investigations necessary to define the nature of the hyperchloremic renal tubular acidosis. Clinically, the four types of renal tubular acidosis can be associated with complications such as osteomalacia, urolithiasis and failure to thrive. Very often, the chronic administration of alkali results in normal growth and development, and greatly reduces the risk of stone formation or nephrocalcinosis.

Topics: Acid-Base Equilibrium; Acidosis, Renal Tubular; Bicarbonates; Child; Female; Growth Disorders; Humans; Infant; Kidney Calculi; Osteomalacia; Sodium; Sodium Bicarbonate

Follow-up of a previously reported family with dominantly inherited adult onset hypophosphatemic osteomalacia with Fanconi syndrome and diabetes mellitus has shown that both the proposita and her affected sister have developed renal glomerular failure. We describe the evolution of renal failure in this family and discuss the possible mechanisms involved. The development of renal tubular acidosis in this condition further impairs renal function and we suggest that correction of systemic acidosis might improve renal function and prevent further decline in these patients.

Topics: Acidosis, Renal Tubular; Adolescent; Adult; Bicarbonates; Child; Child, Preschool; Diabetes Complications; Diabetes Mellitus; Fanconi Syndrome; Female; Follow-Up Studies; Humans; Kidney Failure, Chronic; Male; Osteomalacia; Pedigree; Phosphates; Sodium; Sodium Bicarbonate

A 62-year-old woman was diagnosed with severe osteomalacia caused by renal tubular acidosis associated with Sjögren's syndrome. She was treated with sodium bicarbonate, risedronate, alfacalcidol, and prednisolone (1 mg/kg). By 24 months, renal tubular acidosis was improved and the bone density had normalized. Here we report the successful amelioration of bone lesions through a multidisciplinary approach that improved renal tubular acidosis, with a special focus on treatment of the underlying inflammatory disorder with glucocorticoids.

Topics: Acidosis, Renal Tubular; Bone Density Conservation Agents; Drug Therapy, Combination; Etidronic Acid; Female; Glucocorticoids; Humans; Hydroxycholecalciferols; Middle Aged; Osteomalacia; Prednisolone; Risedronic Acid; Sjogren's Syndrome; Sodium Bicarbonate; Treatment Outcome

We report a 54-year-old man with osteomalacia due to a bladder reconstruction performed 35 years previously. He had had slowly progressive chest and back pain for 18 months. Osteomalacia due to metabolic acidosis was suspected based on hyperalkalinephosphatasemia and a high serum chloride level, and the diagnosis was confirmed by bone scintigraphy. His symptoms and blood electrolyte levels were improved by oral medication, including sodium hydrogen carbonate. Measurement of the serum chloride level is simple and useful for evaluating acidosis, for which a regular blood test is essential in patients who have undergone bladder reconstruction.

Topics: Acidosis; Humans; Male; Middle Aged; Osteomalacia; Sodium Bicarbonate; Sodium Chloride; Time Factors; Tuberculosis, Renal; Urinary Bladder; Urinary Diversion

Topics: Acidosis, Renal Tubular; Female; Humans; Liver Cirrhosis, Biliary; Middle Aged; Osteomalacia; Sodium Bicarbonate; Treatment Outcome

Severe renal tubular acidosis associated with massive osteomalacia is described in a patient with Crohn's disease. To our knowledge this association has not been previously recognized. The possible role of renal tubular acidosis in this patient's osteomalacia is discussed and the factors that could be involved in renal tubular acidosis in the context of Crohn's disease are analyzed.

Topics: Acidosis, Renal Tubular; Administration, Oral; Bicarbonates; Crohn Disease; Gait; Humans; Infusions, Parenteral; Male; Middle Aged; Osteomalacia; Sodium; Sodium Bicarbonate

The case is reported of a woman in whom a chronic hyperchloraemic acidosis and osteomalacia developed follow implantation of her ureters into the rectum. For 14 years she took regular sodium bicarbonate, but a little over four years after discontinuing it she developed clinical, biochemical, radiological and radionuclide evidence of osteomalacia. The latter improved rapidly when sodium bicarbonate was recommenced. This clinical situation is one of the few instances in man where a chronic metabolic acidosis in the context of normal or only mildly impaired renal function can result in osteomalacia.

Topics: Acidosis; Adult; Bicarbonates; Chlorides; Female; Humans; Osteomalacia; Rectum; Sodium; Sodium Bicarbonate; Ureter; Urinary Diversion

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