UMLS:C0020538 - FACTA Search

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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal transplantation in India costs about US$5000 ($1=Rupees 48.25), azathioprine costs $200 a year and cyclosporine costs $2000. Against this the average per capita income is $279 (Rs. 12989) per year; 36% of the population earn less than $105, and only 2.2% earn more than $1000. The country cannot afford to treat end-stage renal disease. Thirty percent of chronic renal failure is due to diabetic nephropathy, and 10% each to hypertensive nephropathy and chronic pyelonephritis. Social and preventive health workers of the Kidney Help Trust administered a questionnaire at the homes of a study population of 25,000, examined the urine of every individual for albumin and reducing substances, and checked the blood pressure of every person aged over 5; 90% of the population cooperated. Six percent were hypertensive and four percent had diabetes. Eight percent of them subsequently took regular treatment. Using only reserpine, hydrallazine and hydrochlorothiazide for hypertension, and glibenclamide and metformin for diabetes (as these are the cheapest agents available), we were able to control the blood pressure to 140/90 or less in 96% of cases, and to reduce HbAIC by 10% or more of the original reading in 77%. An HbA1C of 7% was achieved in 50% of the diabetic subjects. The total cost amounts to 27 US cents for one year per capita of the study population. The Indian Government now spends $7.67 per capita on health each year, but expects patients to attend its Primary Health Centers. The patients do not attend because in doing so they lose a day's wages. We believe that domiciliary treatment is the solution for these diseases, and expect to see a fall in the incidence of chronic renal failure if this is instituted in the future.
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PMID:Prevention of chronic renal failure at the community level. 1286 81

Hypertensive nephropathy is among the leading causes of end-stage renal disease. Once renal function is severely impaired, the effects of strict control of blood pressure on the recovery of renal function remain elusive. Published case series suggest that optimal control of blood pressure results in regression of renal failure to some extent. In the present case of biopsy-proven hypertensive nephropathy we show that renal function can substantially improve over time if blood pressure is optimally controlled. Glomerula filtration rate continuously improved in our patient from 20 ml/min at presentation to 80 ml/min over a period of three years using a fivefold antihypertensive regimen. Hypertensive retinopathy regressed from stage III to stage I, and left ventricular hypertrophy decreased from an initial septum thickness of 19 mm to 12 mm within that period of time. This case clearly illustrates that optimal control of blood pressure is mandatory in patients with pre-terminal renal failure due to hypertensive nephropathy. Such intervention can lead to a regression of hypertension-associated end-organ injury.
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PMID:Regression of hypertensive nephropathy during three years of optimal blood pressure control. 1291 87

Endothelin (ET)-1 and ET-2 are potent vasoconstrictor peptides with mitogenic activity. In this study, we investigated roles of ET system in renin-angiotensin system (RAS)-mediated hypertension, using transgenic hypertensive mice (THM) with over-expression of both human renin and angiotensinogen genes. In the first step, it was revealed that expression of ET system was locally enhanced, i.e. increases in cardiac preproET-1 mRNA and renal preproET-2 mRNA in THM, compared with the control (wild type) mice. In the next step, we studied the chronic effects of an ET antagonist (SB209670) on THM. Blood pressure (BP) in THM was significantly higher than that in the normal mice during the investigation. However, in the later phase of the study, from 12 to 20 weeks of treatment, THM receiving SB 209670 showed significantly lower BP than that in THM receiving saline. SB 209670 treatment for 20 weeks significantly attenuated phenotypes of cardiac hypertrophy, vascular wall thickening and hypertensive nephropathy observed in THM, suggesting that the ETA/B receptor antagonist is also effective even in the extraordinarily activated RAS condition. These findings suggest that organ specifically activated ET system in THM develops the phenotypes, hypertension, cardiac hypertrophy, and hypertensive nephropathy.
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PMID:The endothelin receptor antagonist ameliorates the hypertensive phenotypes of transgenic hypertensive mice with renin-angiotensin genes and discloses roles of organ specific activation of endothelin system in transgenic mice. 1468 51

Hypertension is more prevalent and severe in African descendent populations living outside Africa than in any other population. Given this greater burden of hypertension in blacks, it is increasingly necessary to refine strategies to prevent the disorder as well as improve its treatment and control. This review assesses results from clinical trials on lifestyle and pharmacologic interventions to identify which approaches most effectively prevent adverse hypertension-related outcomes in African descendent populations. The Dietary Approaches to Stop Hypertension (DASH) study provided evidence that a carefully controlled diet rich in fruits, vegetables, low-fat dairy foods, and reduced in saturated fat, total fat, and cholesterol (i.e., the DASH diet) reduces blood pressure in blacks and is well accepted. The combination of the DASH diet with reduction in dietary sodium below 100 mmol/d may provide a reduction in blood pressure beyond that reached by the DASH diet alone. Physical exercise and interventions to reduce psychological stress may also reduce blood pressure in blacks. Strong evidence from numerous studies is a compelling argument for continuing to recommend diuretics and beta blockers as first-line antihypertensive therapy for persons of all races. Some new studies also favor angiotensin-converting enzyme inhibitors as first-line antihypertensive drugs. The African American Study of Kidney Disease and Hypertension provided evidence that an angiotensin-converting enzyme inhibitor-based treatment program is more beneficial than calcium channel blockers and beta blockers in reducing the progression of renal failure in blacks with hypertensive nephropathy. Studies in patients with diabetes have also shown evidence that both angiotensin-converting enzyme inhibitors and angiotensin receptor antagonists are more effective than other classes of antihypertensives in reducing adverse renal events. Studies to evaluate the effects of the new antihypertensives in improving outcomes in blacks living outside the United States are needed.
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PMID:Meeting the challenge to improve the treatment of hypertension in blacks. 1468 94

The Dahl/Rapp salt-sensitive (S) rat is a model of salt-sensitive hypertension and hypertensive renal disease. This study explored the role of vascular remodeling in the development of renal failure in S rats. Groups of S and Sprague-Dawley rats were given 0.3 and 8.0% NaCl diets for up to 21 days and evidence of smooth muscle proliferation identified using immunohistochemistry that showed nuclear accumulation of proliferating cell nuclear antigen and 5-bromo-2'-deoxy-uridine. Compared with the other three groups, S rats on 8.0% NaCl diet showed increased nuclear labeling of cells of the aorta and arteries and arterioles of the kidney by the end of the first week of study. Progressive luminal narrowing of the interlobular arteries and preglomerular arterioles occurred in S rats over the 3 wk on the 8.0% NaCl diet. Accumulation of pimonidazole adducts and nuclear accumulation of hypoxia-inducible factor-1alpha (HIF-1alpha) were used as markers of tissue hypoxia. By the end of the second week of study, pimonidazole levels increased in S rats on 8.0% NaCl diet and deposition was apparent in tubular cells in the cortex and medulla. At the completion of the experiment, HIF-1alpha levels were increased in nuclear extracts from the cortex and medulla of S rats on this diet, compared with the other three groups of rats. The data demonstrated a disorder of the vascular remodeling process with proliferation of vascular smooth muscle cells temporally followed by development of tissue hypoxia in the hypertensive nephropathy of S rats on 8.0% NaCl diet.
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PMID:Mechanism of hypertensive nephropathy in the Dahl/Rapp rat: a primary disorder of vascular smooth muscle. 1558 17

Renal biopsy is a fundamental tool in the diagnosis and prognostic of multiple nephrological and systemic pathologies. At our institution the first patient submitted to this technique, at 1994, showed Berger disease. Until 2002 we have performed 91 renal biopsies (57 men and 34 women) with the following annual distribution: 1994 (n=3), 1995 (n=3), 1996 (n=3), 1997 (n=15), 1998 (n=5), 1999 (n=23), 2000 (n=13) and 2001 (n=26). Ultrasound guidance was always used and in most of cases the technique was performed with Vim-Silverman (14G) needle. BARD automatic system was employed in only five patients. The clinical diagnosis that lead to renal biopsy were: nephrotic syndrome (n=27), asyntomatic urinary abnormalities (n=25), acute or rapidly progressive renal failure (n=18), chronic renal failure (n=15), hypertension (n=4) and acute nephritis (n=2). The efficacy for optic histological diagnosis was 92.3% (84/91). However, if we include seven cases of presumed IgA nephropathy that don't included fragment for immunofluorescence (IF) analysis the efficacy declined to 84.6% (77/91). The mean number of glomeruli per fragment was 18.3 -/+ 14.2 [0-80]. Histological diagnosis were the following: Berger disease (n=24), idiopathic nephrotic syndrome (n=18), lupus nephritis (n=8), mesangial proliferative glomerulonephritis without glomeruli in the IF fragment (n=6), without glomeruli (n=6), secondary nephrotic syndrome (n=4), tubulointerstitial nephritis or acute tubular necrosis (n=4), diabetic nephropathy (n=3), myeloma kidney (n=3), pauci-imune and crescentic glomerulonephritis (n=3), hypertensive nephropathy (n=2), IgM mesangial proliferative glomerulonephritis (n=2) and various (n=8). Gross hematuria appeared in 9 patients (9.9%). Only in three of these patients it was showed, by ecography, the existence of kidney haematoma. Bleeding throughout the mandrill in four cases, leaded to transfusion in only three patients. We have registered one accidental spleen puncture. Nephrectomy for incontrollable bleeding was never needed. Higher glomerulosclerosis (30% vs 8%; p<0.01) and also a greater extent of tubulointersticial lesions (100% vs 63%; p<0.01), were predictors of progression into end-stage or advanced renal failure. Concluding, renal biopsy with ultrasound guidance was valuable for diagnosis in 84.6% of our proceedings. Our serie is similar to others concerning serious complications. Nephrologists and radiologists improved progressively their coordination performing this technique, improving the results during this period of 8 years.
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PMID:[Percutaneous kidney biopsy: eight years-experience]. 1563 24

Transforming growth factor (TGF)-beta1 has been shown to play a critical role in hypertensive nephropathy. We hypothesized that blocking TGF-beta1 signaling could attenuate renal fibrosis in a rat model of remnant kidney disease. Groups of six rats were subjected to 5/6 nephrectomy and received renal arterial injection of a doxycycline-regulated Smad7 gene or control empty vector using an ultrasound-microbubble-mediated system. Smad7 transgene expression within the kidney was tightly controlled by the addition of doxycycline in the daily drinking water. All animals were euthanized at week 4 for renal functional and histological examination. Hypertension of equivalent magnitude (190 to 200 mmHg) developed in both Smad7- and empty vector-treated rats. However, treatment with Smad7 substantially inhibited Smad2/3 activation and prevented progressive renal injury by inhibiting the rise of 24-hour proteinuria (P < 0.001) and serum creatinine (P < 0.001), preserving creatinine clearance (P < 0.05), and attenuating renal fibrosis and vascular sclerosis such as collagen I and III expression (P < 0.01) and myofibroblast accumulation (P < 0.001). In conclusion, TGF-beta/Smad signaling plays a critical role in renal fibrosis in a rat remnant kidney model. The ability of Smad7 to block Smad2/3 activation and attenuate renal and vascular sclerosis demonstrates that ultrasound-mediated Smad7 gene therapy may be a useful therapeutic strategy for the prevention of renal fibrosis in association with hypertension.
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PMID:Ultrasound-microbubble-mediated gene transfer of inducible Smad7 blocks transforming growth factor-beta signaling and fibrosis in rat remnant kidney. 1574 88

Podocyte loss contributes to the development of glomerulosclerosis. Although podocyte detachment has been recognized as a new mechanism of podocyte loss in glomerular diseases, its time course and relationship to disease activity are not known. Urinary excretion of viable podocytes was quantified in two models of transient glomerular injury, i.e., rats with puromycin aminonucleoside-induced nephrosis (PAN) and mesangioproliferative nephropathy (anti-Thy 1.1 nephritis model), as well as in a model of continuous glomerular injury, i.e., hypertensive nephropathy (5/6-nephrectomy model), and in aging rats. The number of glomerular Wilm's tumor (WT)-1-positive podocytes and the glomerular expression of cell-cycle proteins in vivo were assessed. Urinary podocyte loss occurred in both primary (PAN) and secondary (anti-Thy 1.1 nephritis) in parallel to the onset of proteinuria. However, subsequently proteinuria persisted despite remission of podocyturia. In continuous glomerular injury, i.e., after 5/6-nephrectomy, podocyturia paralleled the course of proteinuria and of systemic hypertension, whereas no podocyturia became detectable during normal aging (up to 12 mo). Despite podocyte detachment of varying degrees, no decrease in glomerular podocyte counts (i.e., WT-1 positive nuclei) was noted in either disease model. Podocyturia in the PAN and anti-Thy 1.1 nephritis model was preceded by entry of glomerular podocytes into the cell cycle, i.e., cyclin D1, cdc2, and/or proliferating cell nuclear antigen (PCNA) expression. Podocyturia is a widespread phenomenon in glomerular disease and not simply a reflection of proteinuria because it is limited to phases of ongoing glomerular injury. The data suggest that podocyturia may become a more sensitive means to assess the activity of glomerular damage than proteinuria.
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PMID:Urinary podocyte loss is a more specific marker of ongoing glomerular damage than proteinuria. 1582 8

Arterial hypertension is a leading contributor to the progression of chronic renal disease. Short-term studies had addressed the role of oxidative stress in hypertensive nephropathy. We have now studied oxidative stress and caspase activation in a long-term model of hypertensive renal injury. Nontreated spontaneously hypertensive rats with uninephrectomy displayed severe arterial hypertension over a 36-week follow-up. Uncontrolled high blood pressure in the context of modest renal mass reduction resulted in significant histological renal injury. Blood pressure control by the angiotensin-converting enzyme (ACE) inhibitor, quinapril, or the AT1 receptor antagonist, losartan, decreased the degree of renal injury. Hypertensive renal injury was associated with evidence of activation of the apoptotic pathway (increased activation of caspase-3) and local renal (increased staining for 4-hydroxy-2-nonenal) and systemic [increased serum levels of 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha)] lipid oxidation when compared with normotensive control rats. In addition, severe hypertension decreased the renal antioxidant defenses, as exemplified by decreased expression of Cu/Zn superoxide dismutase. Treatment with quinapril or losartan decreased caspase-3 activation, 4-hydroxy-2-nonenal staining, and 8-iso-PGF2alpha levels and increased Cu/Zn superoxide dismutase expression. These results suggest that hypertension-associated oxidative stress and its consequences may be decreased by either ACE inhibition or AT1 receptor antagonist, emphasizing the role of angiotensin II in hypertensive renal damage.
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PMID:Long-term blood pressure control prevents oxidative renal injury. 1611 34

The prevalence and incidence of End-Stage Renal Disease (ESRD) have progressively increased in the last 20 years. Hypertension and diabetes are the two most important causes of ESRD, and antihypertensive treatment plays a crucial role in preventing Chronic Renal Failure (CRF) and ESRD. The glomerulus and mesangial extracellular matrix are the principal sources giving rise to hypertensive nephropathy, which is finally characterized by progressive glomerulosclerosis. Several mechanisms are involved in hypertensive nephropathy, including increases in intraglomerular pressure and extracellular matrix production and reactive oxygen species (ROS)-related damage. The various activities of antihypertensive drugs on the kidney are particularly important in understanding their nephroprotective role and in developing new nephroprotective pathways in the future. This paper reviews the main pathophysiological aspects of renal damage in hypertension, the effects of various types of calcium channel blockers (CCBs) on renal function, and their role in nephroprotection.
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PMID:Calcium channel blockers and nephroprotection. 1664 Jan 71

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