The juxtaglomerular apparatus in Bartter's syndrome and related tubulopathies View Full Text


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Article Info

DATE

1988-09

AUTHORS

R. Taugner, R. Waldherr, H. W. Seyberth, E. G. Erdös, J. Menard, D. Schneider

ABSTRACT

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. More... »

PAGES

459-470

References to SciGraph publications

  • 1986-03. Renin activation in juvenile secretory granules? in HISTOCHEMISTRY AND CELL BIOLOGY
  • 1976-06. The structure of the juxtaglomerular apparatus in Addison's disease, Bartter's syndrome, and in Conn's syndrome in VIRCHOWS ARCHIV A PATHOLOGICAL ANATOMY AND HISTOPATHOLOGY
  • 1987-05. The fate of prorenin during granulopoiesis in epithelioid cells in HISTOCHEMISTRY AND CELL BIOLOGY
  • 1979-02. Zur Histopathologie der Niere beim Pseudo-Bartter-Syndrom durch chronischen Diuretikaabusus in JOURNAL OF MOLECULAR MEDICINE
  • 1986-12. Development and fate of the secretory granules of juxtaglomerular epithelioid cells in CELL AND TISSUE RESEARCH
  • 1981-09. Appearance of dense granules in the rough endoplasmic reticulum of the juxtaglomerular cells in mice administered with captopril in CELL AND TISSUE RESEARCH
  • 1983-03. Angiotensin-like activity in resistance vessels in HISTOCHEMISTRY AND CELL BIOLOGY
  • 1984-01. Coexistence of renin and angiotensin II in epitheloid cell secretory granules of rat kidney in HISTOCHEMISTRY AND CELL BIOLOGY
  • 1981-12. Angiotensin II in epitheloid (Renin containing) cells of rat kidney in HISTOCHEMISTRY AND CELL BIOLOGY
  • 1981-03. The distribution of renin in the different segments of the renal arterial tree in HISTOCHEMISTRY AND CELL BIOLOGY
  • 1983-08. Immunocytochemical localization of angiotensinogen in rat liver and kidney in CELL AND TISSUE RESEARCH
  • 1982. Bartter’s Syndrome in ERGEBNISSE DER INNEREN MEDIZIN UND KINDERHEILKUNDE / ADVANCES IN INTERNAL MEDICINE AND PEDIATRICS
  • 1979-01. Immunocytochemical localization of renin in mouse kidney in HISTOCHEMISTRY AND CELL BIOLOGY
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    http://scigraph.springernature.com/pub.10.1007/bf00750580

    DOI

    http://dx.doi.org/10.1007/bf00750580

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1045696657

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/3128915


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    63 conditions
    64 contrast
    65 control
    66 deposits
    67 diseased kidneys
    68 efferent arterioles
    69 electron microscopic study
    70 electron microscopy
    71 epithelial cells
    72 fibrosis
    73 glomerular stalk
    74 granules
    75 hyperplasia
    76 hyperprostaglandin E syndrome
    77 hypertrophy
    78 immune electron microscopy
    79 immunocytochemistry
    80 immunoreactivity
    81 increase
    82 interstitial calcification
    83 interstitial fibrosis
    84 juxtaglomerular apparatus
    85 kidney
    86 length
    87 marked activation
    88 marked hypertrophy
    89 mature secretory granules
    90 mechanism
    91 medium
    92 microscopic study
    93 microscopy
    94 morphological reactions
    95 number
    96 paracrystalline deposits
    97 pathogenetic mechanisms
    98 patients
    99 portion
    100 preglomerular arterioles
    101 previous reports
    102 primary stimulus
    103 protogranules
    104 proximal tubules
    105 reaction
    106 reactivity
    107 renal biopsy
    108 renin
    109 renin synthesis
    110 renin-angiotensin system
    111 renin-positive cells
    112 renin-positive portion
    113 report
    114 results
    115 secretory granules
    116 severe stimulation
    117 stalk
    118 stimulation
    119 stimuli
    120 study
    121 syndrome
    122 synthesis
    123 system
    124 tubular atrophy
    125 tubules
    126 tubulopathy
    127 variants
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