Franz Volhard and Theodor Fahr: achievements and controversies in their research in renal disease and hypertension

Citation
A. Heidland et al., Franz Volhard and Theodor Fahr: achievements and controversies in their research in renal disease and hypertension, J HUM HYPER, 15(1), 2001, pp. 5-16
Citations number
78
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
JOURNAL OF HUMAN HYPERTENSION
ISSN journal
09509240 → ACNP
Volume
15
Issue
1
Year of publication
2001
Pages
5 - 16
Database
ISI
SICI code
0950-9240(200101)15:1<5:FVATFA>2.0.ZU;2-G
Abstract
The clinician, Franz Volhard, and the pathologist, Theodor Fahr, worked clo sely together in Mannheim from 1909 until 1915 and introduced a novel class ification of renal diseases. In the monograph entitled 'Die Bright'sche Nie renkrankheit, Klinik, Pathologie und Atlas' (1914) they differentiated betw een degenerative (nephroses), inflammatory (nephritides) and arteriosclerot ic (scleroses) diseases. Nephrosclerosis was divided into the benign and ma lignant form, of which the latter stood the test of time as a new disease e ntity. Fahr further divided benign nephrosclerosis into the compensated and decompensated form - depending on the presence or absence of glomerular in jury. In the pathogenesis of malignant nephrosclerosis, Volhard stressed th e decisive role of severe blood pressure elevation, while Fahr postulated a n inflammatory mechanism, a concept later confirmed by Adalbert Bohle for a t least a minority of patients. A very far reaching concept of Franz Volhar d was his idea that pale (renal) hypertension results from a presser substa nce released from ischaemic kidney(s) contributing - via a vicious circle - to a further rise in blood pressure with subsequent renovascular injury an d aggravation of hypertension. This hypothesis was supported in 1930 by ini tial experiments of his collaborator, Hartwich (demonstrating in dogs a mil d rise in blood pressure after ligation of branches of the renal artery) an d definitively proven by Goldblatt (1934) in dogs by induction of severe an d persistent hypertension after clamping of both renal arteries. The conseq uent detection of the renin angiotensin system was the final confirmation o f Volhard's postulated renal presser substance. In the pathogenesis of red (essential) hypertension, Volhard stressed the role of hereditary factors, age, obesity and potentially of severe alcoholism. He emphasised a prematur e reduction of vascular distensibility (due to elastosis of the prearteriol es), a high cardiac output as well as a dampening of baroceptor function. A dditionally, Volhard made crucial advances in cardiology and pneumology.