Autoimmunity in the Pathogenesis of Hypertension

Abstract

I want to express my thanks for being selected to present the 2015 Lewis K. Dahl Lecture. This award has a long and proud tradition in the hypertension field, and the list of previous awardees is so impressive that finding myself in their company is an honor indeed. The groundbreaking research of Lewis Kitchener Dahl on the role of salt and genetics in hypertension originated in his earlier interest on the relationship between salt intake and blood pressure,1 and his best known contribution, the salt-resistant and salt-sensitive rat strains,2,3 have been and will continue to be used in hypertension research all over the world. At present, the Dahl’s salt-sensitive (SS) rat is used to examine the genetic characteristics of hypertension using targeted mutagenesis of genes associated with human hypertension.4 Yet, among Dr Dahl’s many seminal contributions, I, as a nephrologist, have a predilection for his studies of cross-transplantation of kidneys between salt-sensitive and salt-resistant rats showing that the high blood pressure and normal blood pressure responses to a high-salt diet travel with the kidney5,6 because these experiments demonstrated that the kidney had a central role in the pathogenesis of hypertension. Less cited among their works, Lewis Dahl and his coworkers also made observations on the histological findings in the kidneys that are of particular relevance to the subject of this conference. They reported that renal lesions did not occur in R (resistant) rats on either diet, were minimum to mild in S (sensitive) rats on the diet low in salt, and were moderate to severe in S rats on the diet high in salt.7 I will take these observations as the starting point to review the evidence that renal inflammation is a key element in the role of the kidney in …