CLINICAL PROGRESS Editor: HERRMAN

NO DOCTOR who has had to treat many patients with hypertension can have failed to be exercised by the tragic problem of malignant hypertension. There is now convincing evidence that this syndrome is a simple consequence of the high level of pressure reached in the small arteries and arterioles, and since this hypothesis has a very important therapeutic implication, the evidence on which it is based is assembled here. In their classic work "Die Brightsche Nierenkrankheit" published in 1914, Volhard and Fahr' pointed out that the course of primary or essential hypertension followed one of two paths. In most patients the course was long, and death, when it at length occurred, was due to cardiac failure, cerebral vascular disease or to a disease unrelated to hypertension. The kidneys obtained after death from such patients showed a simple bland sclerosis ("einfache blande Sclerose"), the arteries showing hypertrophy of the elastica, and the arterioles a fatty hyaline change, but apart from the areas of sclerosis the nephrons were well preserved. In some patients, however, mostly younger and with a rather higher diastolic pressure, the onset of a different course was heralded by the appearance of albuminuric retinitis; soon afterwards renal failure appeared and progressed quickly to death in uremia, mostly within the year. In these the kidneys showed not only the changes in the larger and medium sized arteries already described, but intense endarteritis in