Nephrogenic diabetes insipidus

Brodehl, J

doi:10.1007/978-94-009-7316-9_11

Cited by 8 publications

(2 citation statements)

References 67 publications

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“…Der Kombination von HCT und IN scheint dabei ein additiver Effekt bezüglich der Reduktion der täglichen Ausscheidungsmenge zuzukommen (4, 5, 13, 14). Für die natriuretisch wirksamen Diuretica wird ein paradoxer antidiuretischer Effekt beschrieben; durch Verminderung des Natriumbestands mit nachfolgender gesteigerter Natriumrückresorption im proximalen Tubulus und verringerter Natriumbelastung des distalen Tubulus wird weniger freies Wasser zur Ausscheidung benötigt (4,14). Der therapeutische Einsatz von Prostaglandinsynthesehemmern nutzt den antidiuretischen Effekt durch Erhöhung der ADH-vermittelten c-AMP-Produktion (19), Hemmung der Phosphodiesteraseaktivität (2), Steigerung der proximal tubulären Natriumreabsorption (3,19), Verminderung des corticalen und medullären Blutflusses (9) aus.…”

Section: Diskussionunclassified

Langfristige Verläufe von 6 Jungen mit kongenitalem nephrogenem Diabetes insipidus

Kaulitz

Brodehl²

1989

Klin Padiatr

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From 1975-1986 6 boys with congenital nephrogenic diabetes insipidus were diagnosed at the age of 3 months to 10 years. Symptoms appeared within the first few weeks of life. The diagnosis was confirmed by polyuria, low urinary osmolality (97-225 mosm/kg H20), hypernatraemia (max. 171 mmol/l) and the missing response to vasopressin. The treatment was variable; 4 boys received only hydrochlorothiazide (2-2.5 mg/kg/d) which lead to a reduction of the daily urinary volume of 26-44%. Hyperelectrolytaemia disappeared and a normal thriving could be achieved. Later an additional treatment with indomethacin (2 mg/kg/d) was necessary in 3 boys because of an increase of polyuria; there was a further reduction of the daily urinary volume of 50-60%. The combination of hydrochlorothiazide and indomethacin in the treatment of the congenital nephrogenic diabetes insipidus was well tolerated and seems to be--especially during the first few years of life--a necessary and effective treatment which allows a normal thriving and psychointellectual development.

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Section: Diskussionunclassified

Langfristige Verläufe von 6 Jungen mit kongenitalem nephrogenem Diabetes insipidus

Kaulitz

Brodehl²

1989

Klin Padiatr

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“…Patients with X-linked nephrogenic diabetes insipi dus (N D I) are resistant to the antidiuretic action o f vaso pressin and D D A V P [11], due to a defect either in the renal V , receptor itself or in the process beyond the intracellu lar formation o f cyclic A M P [12], Kobrinsky et al [13] have demonstrated absence o f F V III:C and vW F:Ag responses to D D A V P in 2 N D I patients. From this obser vation, they concluded that the action o f D D A V P on hemostasis is mediated through stimulation o f extrarenal Vs receptors.…”

Section: Introductionmentioning

confidence: 99%

Fibrinolytic Responses to 1-Desamino-8-<i>D</i>-Arginine-Vasopressin in Patients with Congenital Nephrogenic Diabetes insipidus

Knoers

Brommer²,

Willems

et al. 1990

Nephron

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Fibrinolytic responses to infusion of 1-desamino-8-.D-arginine-vasopressin (DDAVP) were assessed in 6 males with congenital nephrogenic diabetes insipidus (NDI), 6 carriers of the NDI gene and 6 normal control subjects. Tissue-type plasminogen activator (t-PA) activity and antigen increased significantly in normal subjects, while plasminogen activator inhibitor (PAI) activity decreased. None of these changes were observed in patients with NDI. In 2 female carriers, normal fibrinolytic responses were seen, while in the other carriers responses were delayed. These findings are consistent with the concept of a general V₂-receptor defect in congenital NDI. DDAVP tests are of limited use in NDI carrier detection.

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