Much is known about the renin-angiotensin system during cyclosporine treatment: plasma renin or prorenin activity seems to be raised in man and animals; hyperplasia of the juxtaglomerular apparatus has been reported in man and animals; renin concentration is known to be increased in animal kidneys; renin-angiotensin-like alterations in vascular contractility have been identified in animal vessels. Since the major functional side effects of cyclosporine are systemic vasoconstriction and renal vasoconstriction, the renin-angiotensin system could be involved. Also, an infrequent complication in man, vasculopathy, develops only in the afferent arteriole, where renin production is most abundant. Hence, this information is now reviewed and incorporated into a single pathophysiological concept, with the implication that renin activation plays a central role in the pathogenesis of cyclosporine-induced functional and structural lesions, merits further attention.
|Original language||English (US)|
|Issue number||SUPPL. 32|
|State||Published - Jan 1 1991|
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