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Frederick Akbar Mahomed was an Englishman of mixed Indian and Irish descent who made substantial contributions to the study of high blood pressure in a short professional life from 1872 to 1884. He was strongly influenced by the previous work of Richard Bright on kidney disease at his own hospital (Guy's Hospital in London) and by the contemporary pathological studies of Gull and Sutton on arteriolar changes in persons with high blood pressure. In detailed clinical studies, he separated chronic nephritis with secondary hypertension from what we now term essential hypertension. He described the constitutional basis and natural history of essential hypertension and pointed out that this disease could terminate with nephrosclerosis and renal failure. His clinical studies were done without the benefit of a sphygmomanometer but with the aid of a quantitative sphygmogram that he had initially developed while a medical student. He described characteristic features of the pressure pulse in patients with high blood pressure and in persons with arteriosclerosis consequent on aging. These pressure wave changes have recently been verified and explained. He contributed to a number of other advances in medical care, including blood transfusion and appendectomy for appendicitis. He initiated the Collective Investigation Record for the British Medical Association; this organization collected data from physicians practicing outside the hospital setting and was the precursor of modern collaborative clinical trials. Mahomed died from typhoid fever, almost certainly contracted from one of his patients, at age 35 at the height of his career.
Hypertension 1992 Feb
PMID:Frederick Akbar Mahomed. 173 55

This article has reviewed the involvement of the kidney as a target organ of essential hypertension. Since Bright first made the association of renal disease and hypertension in 1836, the nature of this relationship has been debated. Although there is evidence implicating abnormalities of renal function in the pathogenesis of essential hypertension, hypertension frequently precedes histologic evidence of alterations in renal structure. Nephrosclerosis, or hardening of the kidney, is the term used to describe the histologic changes occurring in the kidney as the result of hypertension. It can be though of as an acceleration of the normal aging process of the renal vasculature. Glomerular and tubular changes have been traditionally thought to be ischemic in origin. Experimental evidence supports the notion that, as renal function is lost, intraglomerular hypertension develops and may be responsible for additional nephron loss in hypertension. This idea may have therapeutic implications for hypertensive patients with renal insufficiency in that agents that reduce both systemic and intraglomerular pressure may be preferable. Hemodynamically, early hypertension is often characterized by normal peripheral and renal vascular resistance and an increased cardiac output. In established hypertension, cardiac output is usually normal, and peripheral and renal vascular resistances are increased. Renal blood flow is reduced, glomerular filtration rate is maintained, and the filtration fraction rises. In the absence of an accelerated malignant phase, renal failure is uncommon in essential hypertension. Males and blacks are most sensitive to the vascular damage of essential hypertension. Essential hypertension remains an important cause of end-stage renal disease, especially in blacks. Atherosclerotic obstruction of the renal arteries may be a more common cause of renal failure in patients with essential hypertension than has been previously recognized. There are few sensitive markers of early renal involvement in essential hypertension. Several studies of sensitive markers are promising and may detect patients who are prone to renal injury and deserve more aggressive treatment. Malignant hypertension is characterized pathologically by vascular changes of proliferative endarteritis and fibrinoid necrosis. Fortunately, its frequency is decreasing because of early identification and effective treatment of essential hypertension. Effective treatment of severe and malignant hypertension clearly leads to stabilization (and occasionally improvement) of renal function.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Renal parenchymal involvement in essential hypertension. 330 6

The existence of a structural adaptation of the cardiovascular system in hypertension has been known for many years, in fact already since the time of Bright. This paper is concerned with the hemodynamic consequences of the wall thickening of the small arteries and the arterioles. Studies are reported which illustrate the hemodynamic effects of the vascular changes in man, the limited reversibility of these changes and the early occurrence of the wall changes in the course of human hypertension. The pathophysiological role of the structural vascular changes in human hypertension is discussed.
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PMID:Structural adaptation of the cardiovascular system in hypertension. Hemodynamic consequences of vascular wall hypertrophy. 369 54

Chronic Renal Failure is a generalized functional impairment, due to Kidneys inability to maintain volume and composition of body fluids and solutes within normal conditions. In the attempt to point out the pathophysiology of Bright's syndrome, the Authors review the "intact nephron hypothesis" and his functional reserve. The uraemic clinical appearance is a very wide field of investigations and beside their own experience, the Authors present some datas and theories to explain the coming out and the evolution of poliuria and oliguria, hypertension, heart pathology, anemia and bleedings, hormonal and metabolic pathways alterations, calcium and bone diseases and central and peripheral uraemic neuropathy.
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PMID:[Pathogenesis of the uremic syndrome]. 705 15

The pioneering work of Richard Bright, who introduced the concept of the renal origin of cardiovascular disease, initiated the continuous unfolding of knowledge on renal disease and its close interrelationship with arterial hypertension in the 19th century. Hypertension as a clinically and pathologically defined entity, however, was not established. The partial elucidation of the problem that the diseased kidney was sometimes the cause and sometimes the consequence of elevated blood pressure is not only fascinating but also remarkable, given the crude techniques available to physicians at that time. Subsequent workers came to regard 'Bright's disease' as consisting of several conditions differing in clinical manifestation and pathology. In particular, Johnson and Gull and Sutton drew attention to the small blood vessels in renal disease. Only the invention of a clinically applicable method of measuring blood pressure indirectly allowed Mahomed and Allbutt to show that hypertension may occur in the absence of renal disease. They paved the way for a clear separation of hypertensive renal disease from other forms of 'Bright's disease', culminating in the classification introduced by Fahr and Volhard.
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PMID:Hypertension as cause and consequence of renal disease in the 19th century. 784 82

Histological examination of the kidney was well under way by the mid-19th century. Pathological changes noted to be present in Bright's disease gave rise to considerable debate in the literature of the time. Toynbee was perhaps the first to note medial hypertrophy and intimal narrowing of blood vessels in the kidney, while Johnson, around the same time, thought that kidney disease was the cause of compressed vessels. Although he later proposed a causal relationship between contraction of vessels and hypertrophy, Johnson never went beyond the insights articulated by Bright himself and failed to make the link between hypertrophy of vessels and persistently raised blood pressure. Traube considered the possibility that cardiac and renal disease could be the consequences of the same unknown disease, but rejected hypertrophy per se as a causal factor. Gull and Sutton disagreed strongly with Johnson and proposed the presence of a general disease which leads to both cardiac hypertrophy and renal disease. But it was Ewald, writing in Germany, who was able to ascribe both cardiac and vascular hypertrophy to increasing tension in the arterial system and he was the first to articulate the effect of hypertension on the kidney.
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PMID:Inference of the existence of high blood pressure as a cause of renal disease in the mid-19th century: observations on vascular structures in the kidney. 1021 36

Introduction. The relationship between arterial hypertension and renal damage has long been recognized. In 1836, Bright reported an association between cardiac hypertrophy and contraction of the kidney [1] and 40 years later Gull and Sutton [2] suggested that the renal damage in patients with arterial hypertension could be the consequence of vascular hypertensive alterations.
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PMID:Altered circadian blood pressure profile and renal damage. 1023 37

The realization of the key role for raised intra-arterial pressure as a pathogenetic agent in hypertension is usually credited to Ludwig Traube, but Traube in his writings gives credit for the idea to a little-known English doctor, William Senhouse Kirkes (1822-1864). Kirkes' main interest was in cardiology and vascular disease, and he gave the first account of embolism from vegetations in infective endocarditis in 1852. Three years later, he published a study of apoplexy in Bright's disease, in which he pointed clearly to the role of raised intra-arterial tension in the causation of arterial disease, a point that had eluded Bright, Johnson, and other contemporaries. Kirkes died at the age of only 42 while working on a book summarizing his work on cardiology and renal disease, and the neglect of his contribution probably resulted from his early death. We have traced his life history from the few available records; as a boy, Kirkes was apprenticed to become a surgeon and only later trained as a physician. We place his contributions within the setting of the development during the 19th century of understanding of the relationship between the kidney, vascular disease, and high blood pressure.
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PMID:High blood pressure and the kidney: the forgotten contribution of William Senhouse Kirkes. 1097 3

This saga is the story of a scientific development. From the search of a mechanism to explain high blood pressure, research was orientated to the functions of an omnipresent biochemical system. And from the search to elucidate the etiology of arterial hypertension, research has ended up studying the local, functional and structural activity of the renin-angiotensin system and the possibilities of interfering with its actions. Since Bright, left ventricular hypertrophy became associated with nephrosclerosis. Later on, clinical studies led Volhard and Fahr to associate nephrosclerosis to high blood pressure while biochemical research led Tigerstedt and Bergmann to demonstrate that renin was associated to high blood pressure. Two teams of investigators, one in Argentina and one in USA discovered the biochemical mechanism by which renin acted on arterioles and later on, two other teams, one in USA and one in England, discovered the biochemical steps leading to the synthesis of angiotensin II. Since Goldblatt's experimental design resulting in a reliable method to obtain arterial hypertension, more than 20 years had to elapse before renal artery stenosis became established as the main cause of clinical secondary arterial hypertension. The renin-angiotensin system became part of a very complex array of substances able to regulate local circulation directly or indirectly and angiotensin has become involved in the remodeling of the smooth muscles of arterioles and myocardium.
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PMID:[The renin saga]. 1083 99

Stephen Hales was the first to measure blood pressure directly in the horse (1733), and the definitive studies on human nephrins by Richard Bright followed much later (1836). The relation between high blood pressure and renal disease was established by Mahomed (1872). The discovery of renin and its possible link with Bright's disease was made by Tigerstedt and Bergman (1898), but only the experimental production of renal hypertension by Goldblatt and his colleagues (1934) led to the delineation of the role of the kidney in human hypertension by a wide variety of methods.
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PMID:Development of ideas on renovascular hypertension. 1102 90


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