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  • Electronic Resource  (3)
  • Bartter's syndrome  (2)
  • Glomerular filtration rate  (1)
  • 1
    ISSN: 1432-1440
    Keywords: Somatostatin ; Glomerular filtration rate ; Vasoactive hormones ; Renal sodium excretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The acute effects of i.v. somatostatin (250 mcg bolus followed by 250 mcg/h continuous infusion for two hours) on renal hemodynamics, renal electrolyte and water handling, and urinary excretion of catecholamines and prostaglandins, as well as on plasma concentrations of arginine vasopressin, atrial natriuretic factor, norepinephrine, epinephrine, dopamine, glucagon, and plasma renin activity were studied in seven normal subjects. Somatostatin decreased effective renal plasma flow and glomerular filtration rate, osmotic and free water clearances, urine volume, and sodium and potassium excretion, while urinary osmolality, fractional excretion of sodium, and phosphate excretion increased significantly. Plasma concentrations of arginine vasopressin, atrial natriuretic factor, norepinephrine, epinephrine, and dopamine remained unchanged, while plasma renin activity (3.0±0.25 vs 2.4±0.2 ng AngI/ml/h;p}〈0.01) and glucagon levels (40±11 vs 20±16 pg/ml;p}〈0.01) decreased. Urinary excretion of norepinephrine, epinephrine, dopamine, PGE2, and PGF2alpha was suppressed under somatostatin. A significant positive correlation was found between urinary dopamine and sodium excretion (r=0.7;p}〈0.001) and urinary postaglandin E2 and glomerular filtration (r=0.52;p}〈0.01). Without accompanying changes in plasma osmolality and vasopressin concentration significant antidiuresis occurred, suggesting a direct tubular effect of somatostatin. However, the hormone-induced changes are due mainly to the decrease in renal plasma flow. The results demonstrate that somatostatin at supraphysiological doses exerts significant effects on the kidney.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2307
    Keywords: Bartter's syndrome ; Hyperprostaglandin E-syndrome ; Juxtaglomerular apparatus ; Renin-angiotensin system ; Immunocytochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A comparative immunocytochemical and electron microscopic study was performed on renal biopsies from two children with classical Bartter's syndrome (BS) and three children with a recently described variant, the so-called hyperprostaglandin E-syndrome (HES). Compared to age-matched controls, kidney specimens from patients with BS and HES disclosed a marked hypertrophy and hyperplasia of the juxtaglomerular apparatus (JGA). In addition, in HES focal tubular and interstitial calcifications accompanied by interstitial fibrosis and tubular atrophy were noted. On immunocytochemistry, chronic stimulation of the JGA in BS and HES was characterized by an increase in the number of renin-positive cells, particularly in the media of afferent arterioles, but also in efferent arterioles and in the glomerular stalk. The length of the renin-positive portion of the preglomerular arterioles was significantly increased when compared to controls (100±32 vs. 49±17 µm;p〈0.001). In addition, the immunoreactivity of individual renin-positive cells was markedly enhanced. On electron microscopy, “hypertrophy” of the RER and of Golgi complexes with paracrystalline deposits in dilated RER cisterns and protogranules indicated an increased renin synthesis. Renin could be identified in mature secretory granules as well as protogranules by immune electron microscopy. Angiotensinogen was present in hypertrophied epithelial cells of Bowman's capsule. Converting-enzyme reactivity was observed in controls as well as in BS and HES in the brush border of the proximal tubule. In contrast to previous reports, Angiotensin II was completely negative in control as well as in diseased kidneys. We conclude from our results that both BS and HES are characterized by a marked activation of the JGA and severe stimulation of the renin-angiotensin system. Since activation of this system, however, leads - independently of the primary stimulus - to qualitatively very similar morphological reactions, these results do not implicate a common pathogenetic mechanism to both conditions.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Pediatric nephrology 8 (1994), S. 407-407 
    ISSN: 1432-198X
    Keywords: Bartter's syndrome ; Hyperprostaglandin E2 syndrome ; Pathophysiology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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