The clinician, Franz Volhard, and the pathologist, Theodor Fahr, worked closely together in Mannheim from 1909 until 1915 and introduced a novel classification of renal diseases. In the monograph entitled 'Die Bright'sche Nierenkrankheit, Klinik, Pathologie und Atlas' (1914) they differentiated between degenerative (nephroses), inflammatory (nephritides) and arteriosclerotic (scleroses) diseases. Nephrosclerosis was divided into the benign and malignant form, of which the latter stood the test of time as a new disease entity. Fahr further divided benign nephrosclerosis into the compensated and decompensated form--depending on the presence or absence of glomerular injury. In the pathogenesis of malignant nephrosclerosis, Volhard stressed the decisive role of severe blood pressure elevation, while Fahr postulated an inflammatory mechanism, a concept later confirmed by Adalbert Bohle for at least a minority of patients. A very far reaching concept of Franz Volhard was his idea that pale (renal) hypertension results from a pressor substance released from ischaemic kidney(s) contributing--via a vicious circle--to a further rise in blood pressure with subsequent renovascular injury and aggravation of hypertension. This hypothesis was supported in 1930 by initial experiments of his collaborator, Hartwich (demonstrating in dogs a mild rise in blood pressure after ligation of branches of the renal artery) and definitively proven by Goldblatt (1934) in dogs by induction of severe and persistent hypertension after clamping of both renal arteries. The consequent detection of the renin angiotensin system was the final confirmation of Volhard's postulated renal pressor 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 premature reduction of vascular distensibility (due to elastosis of the prearterioles), a high cardiac output as well as a dampening of baroceptor function. Additionally, Volhard made crucial advances in cardiology and pneumology. Journal of Human Hypertension (2001) 15, 5-16

中文翻译：

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Franz Volhard和Theodor Fahr：他们在肾脏疾病和高血压研究中的成就和争议。

从1909年到1915年，临床医生Franz Volhard和病理学家Theodor Fahr在曼海姆密切合作，并提出了一种新型的肾脏疾病分类。在名为“ Die Bright'sche Nierenkrankheit，Klinik，Pathologie und Atlas”（1914年）的专着中，他们区分了变性疾病（肾病），炎性疾病（病历）和动脉硬化病（硬化症）。肾硬化分为良性和恶性形式，后者作为新的疾病实体经受了时间的考验。Fahr进一步将良性肾硬化分为补偿型和失代偿型，这取决于肾小球损伤的存在与否。在恶性肾硬化的发病机制中，Volhard强调了严重血压升高的决定性作用，Fahr提出了炎症机制，但后来Adalbert Bohle为至少少数患者证实了这一概念。弗朗兹·沃哈德（Franz Volhard）的一个非常深远的概念是，苍白的（肾性）高血压是由缺血性肾脏释放的加压物质（通过恶性循环）导致血压进一步升高以及随后的肾血管损伤和高血压加剧。这种假设在1930年得到了他的合作者Hartwich（在结扎肾动脉分支后在狗中显示出血压的轻微升高）的初步实验的支持，并由Goldblatt（1934）通过诱发严重和持续性高血压在狗中得到了明确证明。钳住两个肾动脉后。肾素血管紧张素系统的随后检测是Volhard假定的肾脏加压物质的最终确认。在红色（必要性）高血压的发病机制中，Volhard强调了遗传因素，年龄，肥胖症以及潜在的严重酒精中毒的作用。他强调过早降低血管扩张性（由于前小动脉的弹性），高心输​​出量以及抑制压力感受器功能。此外，沃尔哈德（Volhard）在心脏病学和肺病学方面取得了重要进展。人类高血压杂志（2001）15，5-16 他强调过早降低血管扩张性（由于前小动脉的弹性），高心输​​出量以及抑制压力感受器功能。此外，沃尔哈德（Volhard）在心脏病学和肺病学方面取得了重要进展。人类高血压杂志（2001）15，5-16 他强调过早降低血管扩张性（由于前小动脉的弹性），高心输​​出量以及抑制压力感受器功能。此外，沃尔哈德（Volhard）在心脏病学和肺病学方面取得了重要进展。人类高血压杂志（2001）15，5-16