Ultrastructural examinations of 32 cases of various forms of fibrousmuscular dysplasia (FMD) of renal arteries showed the lesions at the subcellular level to be identical in all these forms and to differ only in their intensity and localization. As the disease progresses, smooth muscle cells (SMC) show signs of activation accompanied by an increased collagen synthesis. In this, the cells exhibit large multiblade nuclei, intensive proliferation of the granular endoplasmic reticulum, hypertrophy of the Golgi complex. In cases of intensive fibrous changes, occasional fibroblasts appear in the arterial media. As collagen accumulates in intercellular spaces, signs of involution of various degrees are found in SMC. The number of elastic fibers in the media of the affected arteries decreases markedly as compared with the control. The inner elastic membrane of the arteries is frequently destroyed, particularly in the intimal form of the lesions. The study suggests that all forms of FMD represent a single process in the morphogenesis of which the leading role is played by fibroblast-like transformation of SMC.