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  • 1985-1989  (2)
  • Atrial natriuretic peptide  (1)
  • Glomerular basement membrane  (1)
  • 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
    Electronic Resource
    Electronic Resource
    Springer
    Pediatric nephrology 1 (1987), S. 428-435 
    ISSN: 1432-198X
    Keywords: Glomerular basement membrane ; Type IV collagen ; Alport's syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Urinary excretion of glomerular basement membrane (GBM)-related peptides was analysed in 72 patients with a variety of renal diseases by immunoblotting using polyclonal antibodies against either collagenase or pepsin digests of human GBM. The specificity of the antibodies was verified by elution of antibodies bound to urinary GBM-related peptides on nitrocellulose blots and demonstration of reactivity of the eluted antibodies with the respective GBM digests. Furthermore, six mice immunized with urinary GBM-related peptides all developed focal linear deposits of mouse IgG along their GBM, linear and mesangial deposits of C3 in the glomeruli and serum antibodies reactive with human GBM. Monoclonal antibodies against urinary GBM-related peptides of one of the mice reacted with different peptides of the non-collagenous and collagenous domains of type IV collagen, the major structural protein of GBM. In the majority of the 75 patients' urines tested, excretion of GBM-related peptides with molecular weights of 33, 50, 80 and 150 kilodaltons (kD) was detectable. Patients with a diminished glomerular filtration rate (GFR) demonstrated excretion of the 33 kD peptide more frequently (91%) and never of the 80 kD peptide as compared with patients with normal GFR (33 kD [42%] 80 kD [87%]). The pattern of urinary GBM-related peptides was not specific for the underlying renal disease as in Alport's syndrome.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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