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  • 1985-1989  (2)
  • Acidosis  (1)
  • Chronic renal failure  (1)
  • Adrenalin
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Pediatric nephrology 3 (1989), S. 397-400 
    ISSN: 1432-198X
    Keywords: Aldosterone ; Atrial natriuretic peptide ; Chronic renal failure ; Dopamine ; Noradrenaline ; Sodium homeostasis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In order to evaluate the possible role of vasoactive hormones in the mechanism of exaggerated sodium loss due to reduced renal mass we measured plasma concentration of atrial natriuretic peptide (ANP), aldosterone, plasma renin activity (PRA), plasma noradrenaline, and dopamine, in 12 children with advanced chronic renal failure (mean CIn17.8-2.6,x± SEM, CPAH93.5±17 ml/min per 1.73 m2, FENa7.0±0.95%). No patient had clinical signs of volume overload. Plasma concentrations of ANP were not significantly different from those of healthy agematched controls (29.2±7.2 vs 23.2±3.1 fmol/ml) and did not correlate with urinary sodium excretion. Plasma concentrations of aldosterone, PRA and noradrenaline, were also within the physiological range, while plasma dopamine levels were elevated (260±36 vs 98±11 pg/ml, 〈0.001). Our data do not support the notion that ANP or the renin-aldosterone axis play a major role in the adaptation of remaining nephrons to maintain long-term sodium balance in normotensive children with chronic renal failure.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-198X
    Keywords: Tubular function ; Atrial natriuretic peptide ; Hypertension ; Acidosis ; Hyperkalaemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A 14-year-old boy with the syndrome of hypertension and hyperkalaemia with normal glomerular filtration rate (Gordon's syndrome) is described. The patient's clinical symptoms consisted of periodic paralysis, slight metabolic acidosis of the proximal type and hypercalciuria. Prostaglandin excretion was normal. Infusion of atrial natriuretic peptide had no effect on electrolyte excretion or glomerular function although a normal increase in cyclic guanosine monophosphate was demonstrated in plasma and urine. This lack of sensitivity to atrial natriuretic peptide offers a new pathophysiological concept in this syndrome. Treatment with hydrochlorothiazide was successful in this case.
    Type of Medium: Electronic Resource
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