Hyperplasia of the juxtaglomerular complex with secondary aldosteronism without hypertension (Bartter's Syndrome)

Autor: Russell E. Randall, Marcelo Koppel, William P. Nixon, Newton C. Brackett
Rok vydání: 1968
Předmět:
Pathology
Spironolactone
Kidney Function Tests
urologic and male genital diseases
Plasma renin activity
Norepinephrine
chemistry.chemical_compound
Catecholamines
Renin
Child
Aldosterone
Angiotensin II
Muscles
General Medicine
Water-Electrolyte Balance
Hyperplasia
Hyperaldosteronism
Bartter's syndrome
medicine.anatomical_structure
Female
Kidney Diseases
medicine.medical_specialty
Ammonium Chloride
Adrenocorticotropic Hormone
Chlorides
Internal medicine
Renin–angiotensin system
medicine
Humans
Serum Albumin
business.industry
Body Weight
Sodium
Juxtaglomerular apparatus
Glucose Tolerance Test
Metyrapone
medicine.disease
Body Height
Juxtaglomerular Apparatus
17-Ketosteroids
Diet
Bicarbonates
Microscopy
Electron

Endocrinology
chemistry
Potassium
Pituitary-Adrenal Function Tests
business
Triamterene
Zdroj: The American Journal of Medicine. 44:813-819
ISSN: 0002-9343
DOI: 10.1016/0002-9343(68)90260-x
Popis: Described herein is a ten year old Negro girl with hypertension of the juxtaglomerular complex, an associated increase in plasma renin activity and hyperaldosteronism without hypertension (Bartter's syndrome). In addition to the characteristic histologic findings previously reported by light microscopy, electron photomicrographs confirmed the presence of juxtaglomerular cell hyperplasia and an increased number of mesangial cells morphologically resembling juxtaglomerular cells without granules. The glomerular capillary basement membranes and epithelial cell foot processes appeared normal and the renal arterioles were thickened and sclerotic. Arterioles seen in a gastrocnemius muscle biopsy specimen also appeared thickened. The finding of increased plasma renin levels while the patient was on a normal sodium intake and following expansion of the extracellular fluid volume during infusions of albumin indicates a relative autonomy of the renin-angiotensin mechanism in this syndrome. Suggestions are presented within the framework of available evidence as to the pathogenesis of the disorder.
Databáze: OpenAIRE