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

Heidland, A.; Gerabek, Werner E.; Šebeková, Katarı́na

doi:10.1038/sj.jhh.1001130

Cited by 24 publications

(12 citation statements)

References 40 publications

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“…15,89,[144][145][146] The role of hypertension in the progression of CKD was first described in 1914 by Volhard and Fahr. 13 Subsequently, it was appreciated that hypertension predisposes to kidney failure by inducing renal hypoxia. 147,148 The detrimental effects of hypoxia are exacerbated by hypertension also inducing kidney tissue to generate elevated levels of reactive oxygen species such as superoxide, hydrogen peroxide, peroxynitrite, and hydroxyl radicals.…”

Section: Hypertensionmentioning

confidence: 99%

“…This in turn is driven by a constellation of interlinked risk factors. Primary amongst these factors are anemia, [6][7][8][9] diabetic hyperglycemia, [10][11][12] hypertension, [13][14][15][16][17] hypercholesterolemia, [18][19][20] cigarette smoking, [21][22][23][24][25][26][27] air pollution, [28][29][30][31][32][33][34][35][36][37][38][39][40][41][42] atherosclerosis, [43][44][45][46][47][48][49][50][51][52] repeated episodes of acute kidney injury, [53][54][55][56]…”

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confidence: 99%

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Hypoxia: The Force that Drives Chronic Kidney Disease

Colgan

Shelley

2016

Clinical Medicine & Research

128

111

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In the United States the prevalence of end-stage renal disease (ESRD) reached epidemic proportions in 2012 with over 600,000 patients being treated. The rates of ESRD among the elderly are disproportionally high. Consequently, as life expectancy increases and the baby-boom generation reaches retirement age, the already heavy burden imposed by ESRD on the US health care system is set to increase dramatically. ESRD represents the terminal stage of chronic kidney disease (CKD). A large body of evidence indicating that CKD is driven by renal tissue hypoxia has led to the development of therapeutic strategies that increase kidney oxygenation and the contention that chronic hypoxia is the final common pathway to end-stage renal failure. Numerous studies have demonstrated that one of the most potent means by which hypoxic conditions within the kidney produce CKD is by inducing a sustained inflammatory attack by infiltrating leukocytes. Indispensable to this attack is the acquisition by leukocytes of an adhesive phenotype. It was thought that this process resulted exclusively from leukocytes responding to cytokines released from ischemic renal endothelium. However, recently it has been demonstrated that leukocytes also become activated independent of the hypoxic response of endothelial cells. It was found that this endothelium-independent mechanism involves leukocytes directly sensing hypoxia and responding by transcriptional induction of the genes that encode the β2-integrin family of adhesion molecules. This induction likely maintains the long-term inflammation by which hypoxia drives the pathogenesis of CKD. Consequently, targeting these transcriptional mechanisms would appear to represent a promising new therapeutic strategy.

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Section: Hypertensionmentioning

confidence: 99%

mentioning

confidence: 99%

Hypoxia: The Force that Drives Chronic Kidney Disease

Colgan

Shelley

2016

Clinical Medicine & Research

128

111

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“…The term ‘nephrosclerosis' (‘kidney hardening') was coined in 1918 by the German clinicians and pathologists Franz Volhard and Theodor Fahr [1,2]. The etymology refers to the callous consistence of kidneys cut after removal at autopsy.…”

Section: Introductionmentioning

confidence: 99%

Nephrosclerosis: A Term in Quest of a Disease

Meyrier¹

2015

Nephron

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For a century, nephrosclerosis was ascribed to nonmalignant hypertension and aging. However, it was intuitively perceived that hypertension may follow rather than explain this nephrovasculopathy. Hypertensive nephrosclerosis was long considered a major cause of end-stage renal failure (ESRD). This is especially true in blacks of African descent but not in other ethnic populations. The term ‘nephrosclerosis' is still an easy way out to classify a patient with renal insufficiency. This leads to neglect the possibility of an overlooked nephropathy complicated by hypertension and to believe that drastic blood pressure control may retard the progression to ESRD. Several clinical and experimental lines of evidence lead to the understanding that nephrosclerosis, especially in blacks, is a genetic renovasculopathy that precedes the rise in blood pressure. The identification of coding region variants in APOL1 encoding apolipoprotein L-1 in black but also white and Asians opens new lines of research on the genetics of nephroangiosclerosis and of FSGS. Metabolic derangements, such as obesity, oxidative stress, dyslipidemia and atherosclerosis may be considered confounding factors with regard to nephrosclerosis. Histomorphometric studies led to sorting out the lesions due to aging from those stemming from hypertension. They shed new light not only on glomerular lesions that comprise ischemic obsolescence but also on glomerulomegaly and focal-segmental sclerosis, the latter due to a loss of renal autoregulation. It appears that the control of hypertension is not credited with the expected benefit for slowing the decline of renal function. ‘Nephrosclerosis' can be considered an umbrella term of poor significance that should be replaced by its pathologic description, that is, arterionephrosclerosis and incite to elucidate the various genetic and metabolic factors that lead to a lesion in quest of a specific disease.

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“…In 1918, Volhard recommended that therapy for true uremia include a low protein diet, particularly vegetarian, with a normal energy intake, 2,000 kcal/day [7,9]. He recognized that this diet could reduce serum urea and that this was associated with an improvement in uremic symptoms and sometimes with prolongation of survival.…”

mentioning

confidence: 99%

“…The German clinician, Franz Volhard, recognized in 1914 that the clinical manifestations of renal failure could be categorized into those resulting from the retention of compounds normally excreted in the urine that were retained (true uremia) and symptoms that occurred in individuals with renal failure that were not due to renal retention (pseudouremia; e.g., eclampsia of pregnancy, cardiac asthma, intermittent claudication) [7,8]. In 1918, Volhard recommended that therapy for true uremia include a low protein diet, particularly vegetarian, with a normal energy intake, 2,000 kcal/day [7,9].…”

mentioning

confidence: 99%

History of Dietary Protein Therapy for the Treatment of Chronic Renal Disease from the Mid 1800s until the 1950s

Kopple¹

2002

Am J Nephrol

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

Cited by 24 publications

References 40 publications

Hypoxia: The Force that Drives Chronic Kidney Disease

Hypoxia: The Force that Drives Chronic Kidney Disease

Nephrosclerosis: A Term in Quest of a Disease

History of Dietary Protein Therapy for the Treatment of Chronic Renal Disease from the Mid 1800s until the 1950s

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