Inference of the Existence of High Blood Pressure as a Cause of Renal Disease in the Mid-19th Century: Observations on Vascular Structures in the Kidney

Abstract

Histological examination of the kidney was well under way by the mid-19th century. Pathological changes noted to be present in Bright’s disease gave rise to considerable debate in the literature of the time. Toynbee was perhaps the first to note medial hypertrophy and intimal narrowing of blood vessels in the kidney, while Johnson, around the same time, thought that kidney disease was the cause of compressed vessels. Although he later proposed a causal relationship between contraction of vessels and hypertrophy, Johnson never went beyond the insights articulated by Bright himself and failed to make the link between hypertrophy of vessels and persistently raised blood pressure. Traube considered the possibility that cardiac and renal disease could be the consequences of the same unknown disease, but rejected hypertrophy per se as a causal factor. Gull and Sutton disagreed strongly with Johnson and proposed the presence of a general disease which leads to both cardiac hypertrophy and renal disease. But it was Ewald, writing in Germany, who was able to ascribe both cardiac and vascular hypertrophy to increasing tension in the arterial system and he was the first to articulate the effect of hypertension on the kidney.

The Impact of Donor Hypertension on Intragraft Changes in Chronic Rat Cardiac Allograft Rejection

“…It has been shown that hypertension may cause left ventricular hypertrophy and arterial changes throughout the vasculature including heart and kidney. 2,3 Retrospective clinical analyses have recently revealed that hypertension of the donor might lead to inferior graft survival rates following heart and kidney transplantation. 4,5 The experimental data from the present study indicate that hearts from HTN donors may experience severe structur-al changes over time following transplantation, which might contribute, at least in part, to the impaired posttransplant performance of such hearts.…”