Die Brightsche Nierenkrankheit

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

“…'Proteinuria may be completely absent in benign nephrosclerosis over many years and may develop only in traces for years'. 6 This description is truly identical to that of Frederik Akhbar Mahomed, 40,41 who stated in 1874: 'It is very common to meet with people apparently in good health, who have no albumin in the urine or any other sign of organic disease, who constantly present a condition of high arterial tension, when examined by the aid of the sphygmograph'.…”

“…6 The latter signs (eclamptic attack in toxaemia of pregnancy, convulsions, psychosis, claudication intermittens, cardiac asthma, Raynauds disease, transient blindness) were linked to vascular sclerosis (cerebral, coronary and peripheral vessels), but also frequently induced or aggravated by vasospasms.…”

“…6 Interestingly, the majority of these patients were younger (average age 40-50 years, even including children) than those with the benign form, which at first manifests itself at the age of 60-70 (Fahr, 1919). 42 Patients with malignant nephrosclerosis died from renal insufficiency in particular.…”

“…Morphology of malignant nephrosclerosis was characterised by Volhard and Fahr (1914) by severe degenerative changes of afferent arterioles (in particular fibrinoid necrosis), proliferative alterations of interlobular and arcuatae arteries with marked thickening of the intima (oedema and/or concentric onion-skin like alterations), as well as inflammatory and degenerative reactions of many glomeruli. The combination of the severe arteriosclerosis and glomerulitis was defined as 'Kombinationsform' and regarded as a single disease entity.…”

Mechanisms and Treatment of CKD

“…6 three-quarters of the total renal mass in the rat, in addition to increase intraglomerular pressures, 1 led to abnormal glomerular permeability and proteinuria. At that time, proteinuria was considered a marker of the extent of glomerular damage, despite the fact that Franz Volhard and Theodor Fahr in 1914 8 and Wilhelm von Mollendorf and Philipp Stohr in 1924 9 had already found that exuberant protein excretion in the urine could per se promote renal injury. In 1954, Jean Oliver 10 suggested that protein droplets he first recognized in the cytoplasm of tubular cells were possibly due to impairment in the process of reabsorption of plasma proteins normally carried out by the renal tubule and proposed that proteinuria could lead to structural and functional nephron damage.…”