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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Frederick Akbar Mahomed. 173 55

British successors of Richard Bright came to regard the disease which bore his name as consisting of several distinct clinical and pathological types, one of which was referred to as contracted granular kidney. The insidious nature of this form of the disease, the lack of clear-cut precipitating factors and, above all, the associated cardio-circulatory disorders gave rise to much speculation and debate. Whether the renal disease or the vascular disease was the primary and essential change was a question which sharply divided eminent Victorian physicians and gave rise to a bitter quarrel between Sir George Johnson and Sir William Gull. The anser to this conundrum, that the kidney was sometimes the cause and sometimes the consequence of circulatory disease was suggested by Mahomed's discovery of essential hypertension but confirmation had to await the invention of a clinically useful sphygmomanometer.
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PMID:Enigma of contracted granular kidney: a chapter in the history of nephrology. 180 38

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

Elevated arterial pressure had long been surmised from the strength of the pulse. Its association with contracted kidneys and hypertrophied hearts was described by Richard Bright (1789-1858). Microscopic observations of the narrowed and obliterated vasculature initially observed in the kidneys of Bright's disease, and subsequently throughout the body, launched clinical research into hypertension. The description of these findings in the absence of symptoms of kidney disease led to the recognition of primary hypertension. Ultimately, the systematic recording of the blood pressure with a pneumatic cuff and mercury manometer established the significance of hypertension as a distinct disease entity. Subsequent experimental studies established the central role of the kidney in hypertension through the renin-angiotensin system and extracellular volume control. This finding provided the basis for the introduction of diuretics and angiotensin converting enzyme inhibitors, two of the most important and valuable antihypertertensive drugs now available. Thus, the study of kidney disease and function has played a pivotal role in the conceptual evolution of the understanding of hypertension as a disease, the identification of its mechanisms, and the development of clinically useful antihypertensive medications.
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PMID:On the central role of studies on the kidney in the recognition, conceptual evolution, and understanding of hypertension. 1521 90

For several decades clinicians and researchers have come to recognize the crucial role played by the kidney in the control of blood pressure. Richard Bright in the past had noted that patients with chronic kidney disease often showed evidence of left ventricular hypertrophy and arteriosclerosis. Fredrick Mohamed and Sir William Gull later demonstrated that elevation of blood pressure might occur even in patients with no evidence of kidney disease. There are now hypotheses to support the fact that even primary hypertension has its origin in the kidney. The consequence of hypertension of the kidney is chronic renal failure; Prevalence rates of CRF range from 25 -100 per 100,000 populations and the incidence continues to grow increasingly at a rate of about 8-10% per year thereby posing a major public health problem especially in the developing countries. Management of chronic renal diseases is tedious and very costly. The consequence of the association between kidney and hypertension on the patient, the family, the national economy of a country and the society at large is considerable, hence the need to evolve preventive strategies.
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PMID:The relationship between kidney and hypertension: a review. 1675 61

Identification of the genetic influences on human essential hypertension and other complex diseases has proved difficult, partly because of genetic heterogeneity. In many complex-trait resources, additional phenotypic data have been collected, allowing comorbid intermediary phenotypes to be used to characterize more genetically homogeneous subsets. The traditional approach to analyzing covariate-defined subsets has typically depended on researchers' previous expectations for definition of a comorbid subset and leads to smaller data sets, with a concomitant attrition in power. An alternative is to test for dependence between genetic sharing and covariates across the entire data set. This approach offers the advantage of exploiting the full data set and could be widely applied to complex-trait genome scans. However, existing maximum-likelihood methods can be prohibitively computationally expensive, especially since permutation is often required to determine significance. We developed a less computationally intensive score test and applied it to biometric and biochemical covariate data, from 2,044 sibling pairs with severe hypertension, collected by the British Genetics of Hypertension (BRIGHT) study. We found genomewide-significant evidence for linkage with hypertension and several related covariates. The strongest signals were with leaner-body-mass measures on chromosome 20q (maximum LOD = 4.24) and with parameters of renal function on chromosome 5p (maximum LOD = 3.71). After correction for the multiple traits and genetic locations studied, our global genomewide P value was .046. This is the first identity-by-descent regression analysis of hypertension to our knowledge, and it demonstrates the value of this approach for the incorporation of additional phenotypic information in genetic studies of complex traits.
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PMID:Linkage analysis using co-phenotypes in the BRIGHT study reveals novel potential susceptibility loci for hypertension. 1682 22

WNK1--a serine/threonine kinase involved in electrolyte homeostasis and blood pressure (BP) control--is an excellent candidate gene for essential hypertension (EH). We and others have previously reported association between WNK1 and BP variation. Using tag SNPs (tSNPs) that capture 100% of common WNK1 variation in HapMap, we aimed to replicate our findings with BP and to test for association with phenotypes relating to WNK1 function in the British Genetics of Hypertension (BRIGHT) study case-control resource (1700 hypertensive cases and 1700 normotensive controls). We found multiple variants to be associated with systolic blood pressure, SBP (7/28 tSNPs min-p = 0.0005), diastolic blood pressure, DBP (7/28 tSNPs min-p = 0.002) and 24 hour urinary potassium excretion (10/28 tSNPs min-p = 0.0004). Associations with SBP and urine potassium remained significant after correction for multiple testing (p = 0.02 and p = 0.01 respectively). The major allele (A) of rs765250, located in intron 1, demonstrated the strongest evidence for association with SBP, effect size 3.14 mmHg (95%CI:1.23-4.9), DBP 1.9 mmHg (95%CI:0.7-3.2) and hypertension, odds ratio (OR: 1.3 [95%CI: 1.0-1.7]).We genotyped this variant in six independent populations (n = 14,451) and replicated the association between rs765250 and SBP in a meta-analysis (p = 7 x 10(-3), combined with BRIGHT data-set p = 2 x 10(-4), n = 17,851). The associations of WNK1 with DBP and EH were not confirmed. Haplotype analysis revealed striking associations with hypertension and BP variation (global permutation p<10(-7)). We identified several common haplotypes to be associated with increased BP and multiple low frequency haplotypes significantly associated with lower BP (>10 mmHg reduction) and risk for hypertension (OR<0.60). Our data indicates that multiple rare and common WNK1 variants contribute to BP variation and hypertension, and provide compelling evidence to initiate further genetic and functional studies to explore the role of WNK1 in BP regulation and EH.
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PMID:Polymorphisms in the WNK1 gene are associated with blood pressure variation and urinary potassium excretion. 1934 40