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

Rapid and dynamic increase of the number of patients that need different forms of renal replacement therapy can be noticed in the developed countries. This increase is associated with increased number of patients with 'diseases of modern civilization', such as diabetes and hypertension, which lead to kidney complications (e.g. diabetic and hypertensive nephropathy). Improved long-term care (especially diabetic and cardiologic) allows these patients to survive longer and to reach the stage of end-stage renal disease. This leads to increasing age and morbidity of patients treated with dialysis. In many cases, due to extremely advanced level of co-morbidity patients on dialysis are exposed to extreme level of suffering and unacceptably low quality of life. Persistent continuing of renal replacement therapy under such circumstances (with no hope for recovery or improvement) raises also some economical issues, especially in the context of permanent crisis and shortage of resources in health systems of most countries in the world. In this review the current practice concerning withdrawal or withholding of renal replacement therapy as well as some legal and ethical issues of this practice are discussed.
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PMID:[Ethical and legal issues concerning renal replacement therapy withdrawal or withholding]. 1720 17

A 75-year old man with long-term arterial hypertension was diagnosed in 1998 with stage 3 chronic kidney disease due to hypertensive nephropathy. Since May 2004 the patient has been treated with intermittent hemodialysis. Since 1998 he has been hospitalized several times because of palpitations in the course of paroxysmal tachycardia with narrow QRS complexes. Initially, class I antiarrhythmic agents were administered; afterwards therapy with beta-adrenolytics was introduced. Because of the ineffectiveness of monotherapy, beta-adrenolytic therapy was combined with amiodarone; however, side effects of this treatment in a form of drug-induced bradycardia appeared. During an invasive electrophysiological investigation, a typical recurrent atrioventricular nodal reentrant tachycardia (AVNRT) was repeatedly released. Subsequently performed percutaneous ablation resulted in effective modification of the slow pathway. During 25 months of follow up after the procedure, recurrence of AVNRT was not observed. Effectiveness of ablation and low risk of adverse effects in non-dialyzed patients encourage us to recommend this method of AVNRT treatment also in patients undergoing intermittent hemodialysis.
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PMID:Recurrent atrioventricular nodal re-entrant tachycardia treated with percutaneous ablation in a 75-year old patient undergoing intermittent hemodialysis. 1819 70

The purpose of this work was to observe the excretion of specific types of urinary proteins and urinary enzymes in elderly essential hypertension patients, for early detection and targeted treatment of hypertensive nephropathy in the elderly. A total of 120 elderly essential hypertensive patients and 38 healthy elderly volunteers were involved. The urinary excretion rate of retinal-binding protein (RBP), transferrin (Tf), albumin (Alb), and urinary enzyme N-acetyl-beta-D-glucosaminidase (NAG) activity were determined. Patients were divided into two groups according to their creatinine clearance (Cockroft-Gault formula). There were 88 patients in group A, whose glomerular filtration rate (GFR) was >or=80 mL/min, and 32 patients in group B with a GFR <80 mL/min. Among the essential hypertensive patients, urinary excretion rates of RBP, Alb, Tf, and NAG were increased in both groups compared with the healthy controls. But the amount of urinary protein differed between group A and group B. The excretion rate of specific urinary protein and urinary enzyme had a positive relationship with the duration of course of hypertension. We believe that specific types of urinary proteins and urinary enzymes may be useful markers for early diagnosis of hypertensive nephropathy; they can also be regarded as a clinical indicator of the progression of hypertensive nephropathy, serving in the assessment of therapeutic effects.
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PMID:Clinical value of urinary kidney biomarkers for estimation of renal impairment in elderly Chinese with essential hypertension. 1820 May 78

The recent discovery of the angiotensin II (Ang II)-breakdown enzyme, angiotensin I converting enzyme (ACE) 2, suggests the importance of Ang II degradation in hypertension. The present study explored the signaling mechanism by which ACE2 is regulated under hypertensive conditions. Real-time PCR and immunohistochemistry showed that ACE2 mRNA and protein expression levels were high, whereas ACE expression levels were moderate in both normal kidney and heart. In contrast, patients with hypertension showed marked ACE up-regulation and ACE2 down-regulation in both hypertensive cardiopathy and, particularly, hypertensive nephropathy. The inhibition of ACE2 expression was shown to be associated with ACE up-regulation and activation of extracellular regulated (ERK)1/2 and p38 mitogen-activated protein (MAP) kinases. In vitro, Ang II was able to up-regulate ACE and down-regulate ACE2 in human kidney tubular cells, which were blocked by an angiotensin II (AT)1 receptor antagonist (losartan), but not by an AT2 receptor blocker (PD123319). Furthermore, blockade of ERK1/2 or p38 MAP kinases by either specific inhibitors or a dominant-negative adenovirus was able to abolish Ang II-induced ACE2 down-regulation in human kidney tubular cells. In conclusion, Ang II is able to up-regulate ACE and down-regulate ACE2 expression levels under hypertensive conditions both in vivo and in vitro. The AT1 receptor-mediated ERK/p38 MAP kinase signaling pathway may be a key mechanism by which Ang II down-regulates ACE2 expression, implicating an ACE/ACE2 imbalance in hypertensive cardiovascular and renal damage.
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PMID:Angiotensin II up-regulates angiotensin I-converting enzyme (ACE), but down-regulates ACE2 via the AT1-ERK/p38 MAP kinase pathway. 1840 95

Hypertension in spontaneously hypertensive rat (SHR) is associated with renal redox stress, and we hypothesized that nephropathy arises in SHR-A3 from altered capacity to mitigate redox stress compared with nephropathy-resistant SHR lines. We measured renal expression of redox genes in distinct lines of the spontaneously hypertensive rat (SHR-A3, SHR-B2, SHR-C) and the normotensive Wistar-Kyoto (WKY) strain. The SHR lines differ in either resisting (SHR-B2, SHR-C) or experiencing hypertensive nephropathy (SHR-A3). Immediately before the emergence of hypertensive renal injury expression of redox genes in SHR-A3 was profoundly altered compared with the injury-resistant SHR lines and WKY. This change appeared to arise in antioxidant genes where 16 of 28 were expressed at 34.3% of the level in the reference strain (WKY). No such change was observed in the injury-resistant SHR lines. We analyzed occurrence of transcription factor matrices in the promoters of the downregulated antioxidant genes. In these genes, the hepatocyte nuclear factor 1 (HNF1) transcription factor matrix was found to be nearly twice as likely to be present and the overall frequency of HNF1 sites was nearly 5 times higher, compared with HNF1 transcription factor matrices in antioxidant genes that were not downregulated. We identified 35 other (nonredox) renal genes regulated by HNF1. These were also significantly downregulated in SHR-A3, but not in SHR-B2 or SHR-C. Finally, expression of genes that comprise HNF1 (Tcf1, Tcf2, and Dcoh) was also downregulated in SHR-A3. The present experiments uncover a major change in transcriptional control by HNF1 that affects redox and other genes and precedes emergence of hypertensive renal injury.
Hypertension 2008 Jun
PMID:Hepatocyte nuclear factor 1 and hypertensive nephropathy. 1844 32

Angiotensin II (Ang II)-induced hypertension is associated with an inflammatory response that may contribute to the development of target organ damage. We tested the hypothesis that, in Ang II-induced hypertension, CC chemokine receptor 2 (CCR2) activation plays an important role in the development of renal fibrosis, damage, and dysfunction by causing oxidative stress, macrophage infiltration, and cell proliferation. To test this hypothesis, we used CCR2 knockout mice (CCR2-/-). The natural ligand of CCR2 is monocyte chemoattractant protein-1, a chemokine important for macrophage recruitment and activation. CCR2-/- and age-matched wild-type (CCR2+/+) C57BL/6J mice were infused continuously with either Ang II (5.2 ng/10 g per minute) or vehicle via osmotic minipumps for 2 or 4 weeks. Ang II infusion caused similar increases in systolic blood pressure and left ventricular hypertrophy in both strains of mice. However, in CCR2-/- mice with Ang II-induced hypertension, oxidative stress, macrophage infiltration, albuminuria, and renal damage were significantly decreased, and glomerular filtration rate was significantly higher than in CCR2+/+ mice. We concluded that, in Ang II-induced hypertension, CCR2 activation plays an important role in the development of hypertensive nephropathy via increased oxidative stress and inflammation.
Hypertension 2008 Aug
PMID:Role of inflammation in the development of renal damage and dysfunction in angiotensin II-induced hypertension. 1883 21

Evaluation of the renal changes by conventional and Doppler ultrasound (US) was performed in patients with hypertension and obesity. 67 persons were examined and divided in 3 groups. Group I includes 27 patients--15 M and 12 F, average age 52+/-4.87 with well controlled diabetes mellitus type II and hypertension, Ccr.--139+/-1.31. Group II includes 20 patients--9 M and 11 F, average age 53+/-7 with well controlled hypertension without diabetes, with Ccr 128+/-7.8. Group III--20) pts. 8 F and 12 M, average age 54+/-5 with uncontrolled hypertension without diabetes, with Ccr 128+/-7.8. All examined pts. were with BMI>30 and hyperlipidemia--total cholesterol>6.5 mmol/l. Tests for microalbuminuria were negative in all 3 groups. In all three groups, using conventional US, the following parameters were detected by Aloca 4000 machine: renal (RV) and parenchyma (PV) volumes as well as Doppler parameters RI, PI, Vmax, Vmin, and Vmean. There were no significant differences between RV and PV of all examined groups: Group I--254+/-53, Group II--238+/-38, Group III--263+/-38, p=0.1. The strong correlation between renal volumes and BMI was found (Pearson's r 0.58). There were no significant differences between Vmax, Vmin, Vmean in all three groups. RI is normal <0.7 in all examined patients: Group I--0.63+/-0.06, Group II--0.61+/-0.02, Group III--0.66+/-0.03. RI in group III was significantly higher, p<0.05 compared to RI indices detected in other two groups but remains at normal levels. Intrarenal hemodynamics exhibited no difference in all examined groups. Analysis of the Doppler spectrum of the intrarenal arteries provides an accurate information about renal vascular changes but has no significant advantages in patients with hypertension and obesity with normal renal function and signs of hypertensive nephropathy "benign nephrosclerosis". Nevertheless Duplex Doppler Ultrasound is a noninvasive method which is an important part of the diagnostic algorithm in patients with diseases characterized by vascular involvement such as hypertension.
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PMID:Renal Doppler ultrasound in patients with hypertension and metabolic syndrom. 1892 66

This review presents data on end-stage renal disease (ESRD) due to diabetes (ESRD-DM) from populations of several racial/ethnic groups and regions; it also identifies factors that may explain differences in risk of ESRD-DM among these groups. Diabetes is a major cause of ESRD in several developed countries, including the United States, England, and Australia. However, in these countries, the incidence is much higher for some groups, such as Blacks and Native Americans in the United States, Blacks and Indo-Asians in England, and indigenous populations in Australia. Despite the worldwide increase in the prevalence of diabetes, in some regions such as South Africa and Brazil, the rates of ESRD attributed to hypertension and glomerulonephritis are even higher than rates attributed to diabetes. High prevalence of accelerated/ malignant hypertension and infection-related glomerulonephritis in addition to a higher risk of early death from diabetes might partially explain the predominance of ESRD attributed to hypertensive nephropathy and glomerulonephitis in South Africa and Brazil. These data call attention to the need to develop more effective strategies to prevent type 2 diabetes and thereby reduce the racial/ethnic gap in ESRD-DM. A greater emphasis on hypertension and diabetes control, particularly in racially and economically disadvantaged populations, is also necessary.
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PMID:End-stage renal disease due to diabetes in racial/ethnic minorities and disadvantaged populations. 1948 75

Nephroangiosclerosis (NAS) is increasingly diagnosed in adult and elderly patients with slowly progressive chronic renal insufficiency. Since these patients usually present with arterial hypertension, this is considered the main cause of NAS (sometimes called, in fact, hypertensive NAS or hypertensive nephropathy). However, there is evidence that other factors such as aging, black race, smoking, and metabolic disturbances contribute to the development and progression of the disease. In some patients, these factors may be prominent while hypertension may be mild or even absent: this form has been denominated ischemic nephropathy (IN). Are NAS and IN really two different diseases or just different presentations of cardiovascular disease involving the kidney? The latter hypothesis is supported by evidence that (a) NAS and IN share a relative aspecificity in their clinical symptoms (low proteinuria, microhematuria, high blood pressure, dyslipidemia) and histopathological features (as determined in the few cases that undergo a kidney biopsy), and (b) there is a high likelihood that atheromatous and hypertensive lesions coexist in the same patient. In this ''Controversy in Nephrology'', Rosario Cianci and Alessandro Zuccala' analyze this issue and try to answer the following questions: 1 - Are NAS and IN two different diseases or two different expressions of the same disease? Rosario Cianci, ''They are two different diseases''. Alessandro Zuccala', ''They represent two different expressions of the same disease''. 2 - Is the pathogenesis different in nephroangiosclerosis and IN? Rosario Cianci, ''The pathogenesis is high blood pressure in NAS and renal ischemia in IN''. Alessandro Zuccala', ''NAS and IN share the same multifactorial pathogenesis: vascular metabolic alterations can cause chronic renal ischemia with or without hypertension''. 3 - Is a biopsy necessary for the diagnosis? Rosario Cianci, ''Yes, it is''. Alessandro Zuccala', ''No, it is not''. 4 - Is it possible to prevent or to slow the progression of the renal damage in this (these) disease(s)? Rosario Cianci, ''Yes it is, by reducing blood pressure''. Alessandro Zuccala', ''Normalization of blood pressure is not enough but all the other risk factors of vascular damage must be addressed, when possible''.
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PMID:[Nephroangiosclerosis and ischemic nephropathy: two different entities or two renal manifestations of the same systemic cardiovascular disease?]. 1955 27

Connective tissue growth factor (CTGF) plays a critical role in angiotensin II (Ang II)-mediated hypertensive nephropathy. The present study investigated the mechanisms and specific roles of individual Smads in Ang II-induced CTGF and collagen I expression in tubular epithelial cells with deletion of transforming growth factor (TGF)-beta1, overexpression of Smad7, or knockdown of Smad2 or Smad3. We found that Ang II-induced tubular CTGF and collagen I mRNA and protein expressions were regulated positively by phosphorylated Smad2/3 but negatively by Smad7 because overexpression of Smad7-abolished Ang II-induced Smad2/3 phosphorylation and upregulation of CTGF and collagen I in vitro and in a rat model of remnant kidney disease. Additional studies revealed that, in addition to a late (24-hour) TGF-beta-dependent Smad2/3 activation, Ang II also induced a rapid activation of Smad2/3 at 15 minutes and expression of CTGF and collagen I in tubular epithelial cells lacking the TGF-beta gene, which was blocked by the addition of an Ang II type 1 receptor antagonist (losartan) and inhibitors to extracellular signal-regulated kinase 1/2 (PD98059) and p38 (SB203580) but not by inhibitors to Ang II type 2 receptor (PD123319) or c-Jun N-terminal kinase (SP600125), demonstrating a TGF-beta-independent, Ang II type 1 receptor-mediated extracellular signal-regulated kinase/p38 mitogen-activated protein kinase cross-talk pathway in Ang II-mediated CTGF and collagen I expression. Importantly, the ability of knockdown of Smad3, but not Smad2, to inhibit Ang II-induced CTGF and collagen I expression further revealed an essential role for Smad3 in Ang II-mediated renal fibrosis. In conclusion, Ang II induces tubular CTGF expression and renal fibrosis via the TGF-beta-dependent and -independent Smad3 signaling pathways, suggesting that targeting Smad3 may have therapeutic potential for hypertensive nephropathy.
Hypertension 2009 Oct
PMID:Angiotensin II induces connective tissue growth factor and collagen I expression via transforming growth factor-beta-dependent and -independent Smad pathways: the role of Smad3. 1966 56


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