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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Clinical and experimental nephrology 4 (2000), S. 313-317 
    ISSN: 1437-7799
    Keywords: Key words Bone mineral density ; Cyclosporin A ; Glucocorticoid ; Nephrotic syndrome ; Osteopenia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background. High doses of cyclosporin A (CsA) produce high-turnover osteopenia in rats. The aim of this study was to determine whether low-dose CsA affects the skeleton in children with nephrotic syndrome. Methods. Biochemical parameters of mineral and skeletal homeostasis, and bone mineral density (BMD) in eight boys with steroid-dependent, frequently relapsing minimal change nephrotic syndrome who had received low-dose CsA (between 1.6 and 3.1 mg/kg per day) for 2 years were compared with measurements in the same patients before CsA therapy and who had received glucocorticoids for long periods, and with measurements in age-matched controls. Results. It was possible to discontinue glucocorticoid therapy within 4 months after the start of CsA therapy. There was a significant increase in the mean serum alka-line phosphatase concentration in CsA therapy patients compared with the same patients before CsA therapy and the controls. Serum osteocalcin and tartrate-resistant acid phosphatase, and urinary deoxypyridinoline concentrations in CsA therapy patients did not differ from those in the controls. BMD in CsA therapy patients was increased significantly compared with values in the same patients before CsA therapy. BMD in CsA therapy patients was lower than that in the controls, but remained within 80% of the overall mean BMD value. Conclusions. Two years of low-dose CsA therapy without glucocorticoids does not appear to induce high-turnover osteopenia in children with steroid-dependent nephrotic syndrome.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Child's nervous system 11 (1995), S. 712-714 
    ISSN: 1433-0350
    Keywords: Hyponatremia ; Central diabetes insipidus ; Osmoreceptor ; Arginine vasopressin ; Hypothalamic tumor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We report the case of a 4-year-old boy with a postoperative hypothalamic tumor, who exhibited unusual water and electrolyte disturbance. This developed as a late manifestation during the course of central diabetes insipidus (DI), which started when the patient was 2 years old. Clinically, hyponatremia and DI appeared alternatlely within 1 day. The hyponatremia (lowest value Na+ 115 mmol/l) was associated with afebrile convulsions. Assessment of fluid status revealed that the patient had a reduced capacity for arginine vasopressin (AVP) secretion (partial DI), which was not physiologically regulated and which was not concomitantly sufficient to produce maximally concentrated urine and allow the production of maximally diluted urine. This defective osmoreceptor function in association with the previously existing reduced capacity for AVP release seemed to be responsible for the fluid disturbance in the patient. The administration of nasal 1-desamino-8d-arginine vasopressin (DDAVP) only when urine output was increased, instead of regular administration at a fixed time, prevented both worsening of hyponatremia and development of DI.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Child's nervous system 8 (1992), S. 81-82 
    ISSN: 1433-0350
    Keywords: Central diabetes insipidus ; Hypernatremia ; Antidiuretic hormone ; Hypoxic brain damage ; Brain death
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We describe two children who after cardiopulmonary arrest developed hypernatremia at the terminal stage. Urinary antidiuretic hormone concentration was very low, indicating central diabetes insipidus. These cases illustrate the necessity of alertness to the development of central diabetes insipidus in patients with severe hypoxic brain damage.
    Type of Medium: Electronic Resource
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