Abstract
Scleroderma is a disease of mesenchymal tissues characterized by fibrosis and vascular changes which eventually lead to organ insufficiency. Two clinical forms have been recognized, localized and systemic scleroderma. The localized form only affects the skin and the lesions have a tendency to resolve spontaneously. Systemic scleroderma is a progressive, usually irreversible process and the organs most frequently involved are the skin, gastrointestinal tract, lungs and kidneys. The following findings strongly suggest that involvement of small blood vessels (capillaries, arterioles and small size arteries) plays an important role in the pathogenesis of systemic scleroderma: (a) the frequent presence of Raynaud's phenomenon, (b) marked reduction in the number of dermal capillaries, (c) increase in thickness of the basement membrane of muscle capillaries (16), (d) thickening and hyalinization of arterioles (e) intimal proliferation of small size arteries, and (f) eventual ischemic necrosis (2, 3, 17). Small blood vessel changes have been noted in the lungs, heart, gastrointestinal tract, kidneys and striated muscle (19). Further evidence of small blood vessel disease in systemic scleroderma is supported by the high incidence of systemic hypertension, which in some patients develops into the malignant phase (2). The renal vascular lesions in scleroderma may closely resemble those found in essential malignant hypertension (2, 5). The purpose of this study was to measure the serum renin and renin substrate levels in normotensive and hypertensive patients with systemic scleroderma.
Material and methods. Thirty seven subjects were included in this study which were divided into four groups, (a) systemic scleroderma, normotensives, 10 patients, (b) systemic scleroderma, hypertensives, 10 patients, (c) localized scleroderma, 7 patients and, (d) normal controls, 10 volunteers.
In the systemic scleroderma groups, there were 17 females and three males, with ages ranging from 16 to 74 years old.
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