Tension and the artery: the experimental elucidation of pseudo-uraemia and malignant nephrosclerosis

One of the main obstacles to the understanding of Bright’s disease is the fact that renal damage of many different kinds can cause secondary hypertension which, like some forms of primary hypertension, can impose its own pattern of vascular damage on the final picture. Disentangling cause and effect can come, in the first and last analysis, only from long observation of symptoms, signs and lesions and the first advance, after Bright’s own work, came when Mahomed (1881), Huchard (1889) and in particular Clifford Allbutt (1895) identified ‘hyperpiesia‘ (benign essential hypertension). The next landmark was Volhard & Fahr’s (1914) classification of Bright’s disease, which isolated another entity, malignant nephrosclerosis, which led to early death from renal failure and hypertension. Volhard and Fahr were united in their description of the new syndrome, but differed widely in the interpretation of the picture. Fahr, the histologist, was impressed by the inflammatory reaction surrounding the arterial and glomerular lesions and maintained to the end that this pointed to primary inflammation of the kidney and its vessels caused by a wide range of damaging agents. Volhard, the clinician, on the other hand, was equally insistent that the hypertension was the cause of the renal lesions and that the ‘convulsive uraemia’ which complicated the disease was also hypertensive and should be called pseudouraemia. At a time when Allbutt’s teaching had scarcely been assimilated, Volhard’s revolutionary views, opposed as they were by Fahr, were difficult to grasp, but confirmation by experienced clinicians like Keith (Keith, Wagener & Kernohan, 19281, Fishberg (1925) and Ellis (1938) gradually brought acceptance and Fahr’s dissenting views were in-