Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic kidney disease (CKD), a major worldwide public-health problem which affects about 10% of the population, has an increased annual incidence rate of about 5-8%. This increased incidence is mainly due to type 2 diabetes and hypertension and the increasing incidence of elderly patients with CKD. Although the progression to end-stage renal failure (ESRF) is mainly based upon the underlying disease, comorbid conditions such as an initial low renal function, severe proteinuria, and high levels of blood pressure also play important roles in the development of ESRF. Since experimental and clinical evidence suggest that angiotensin II plays a central role in the progression of CKD, pharmacological inhibition of the renin-angiotensin-aldosteron system (RAAS) with angiotensin converting enzyme inhibitors or angiotensin II receptor antagonists has been suggested as first-line treatment for hypertension and prevention of ESRF in these patients. Aliskiren, a novel renin inhibitor is also a promising medical intervention. However, independently of the category of the drugs used, low target blood pressure levels seem to be equally or more important for the delay or prevention of CKD. In this review the results of studies with pharmacological inhibition of the RAAS in patients with diabetic and nondiabetic nephropathy is discussed.
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PMID:Inhibition of the renin-angiotensin system and chronic kidney disease. 1880 6

Chronic kidney disease (CKD) has been shown to be an independent risk factor for cardiovascular disease (CVD) in a number of recent epidemiological studies. There are possible explanations for the independent association of CKD with CVD. Reduced renal function is associated with a high prevalence of traditional CVD risk factors, such as hypertension, diabetes, dyslipidemia, and left ventricular hypertrophy. In addition, reduced renal function may be associated with increased levels of nontraditional risk factors, such as inflammation and oxidative stress. Subjects with CKD should be considered a high-risk population for CVD and be recommended for more intensive preventive management of CVD, including active detection and strict treatment of CVD risk factors.
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PMID:[Chronic kidney disease (CKD) as an independent risk factor for cardiovascular disease (CVD)]. 1878 91

Chronic kidney disease (CKD) is common in Japan and worldwide. The estimated prevalence of CKD in Japanese adults was 10.6% in 2005, based on the survey conducted by the Japanese Society of Nephrology. The most common risk factors for CKD include diabetes, hypertension and cardiovascular disease. Major outcomes of CKD include progression to kidney failure and increased risk for cardiovascular disease. CKD is usually silent until its late stages, thus many patients with CKD are detected only shortly before the onset of symptomatic kidney failure, when there are few opportunities to prevent adverse outcomes. Earlier detection allows for more time for evaluation and treatment but requires explicit testing strategies for asymptomatic individuals at increased risk. Understanding the strengths and limitations of CKD testing and risk factors of CKD is critical for appropriate management of CKD patients. The goal of this paper is to discuss CKD testing and early detection in clinical practice and its application to public health initiatives, with attention to limitations and appropriate interpretation.
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PMID:[Causes and characteristics of CKD]. 1878 92

Chronic kidney disease (CKD) is a major risk factor for the development of cardiovascular disease (CVD). Abnormalities of renal hemodynamics are associated with CKD. Abnormalities in renal hemodynamics include blood flow into glomeruli, and tubulointerstitial tissue. Renin-angiotensin system, oxidative stress and NOS system affect abnormalities of renal hemodynamics in CKD. Further, intrarenal hemodynamic abnormalities are strongly associated with systemic arteriosclerosis. Appropriate regulation of renal hemodynamics and controls of hypertension and diabetes mellitus retard the progression of both CKD and CVD.
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PMID:[Abnormalities in renal hemodynamics]. 1878 95

Chronic kidney disease (CKD) is characterized by proteinuria and kidney dysfunction caused by multiple factors. Metabolic disorders such as diabetes, dyslipidemia and hypertension are involved in the underlying pathological mechanisms of CKD and cardiovascular disease (CVD). In patients with CKD, CVD is a major cause of morbidity and mortality. Recent clinical studies have revealed that intervention by angiotensin II blockade with ARB and ACEI reduces CKD and CVD. Accordingly, earlier intervention to metabolic disorders with blockers for angiotensin II and aldosterone may prevent CKD as well as CVD associated with CKD.
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PMID:[Prevention of CVD in patients with CKD]. 1878 4

Chronic kidney disease (CKD), like other chronic diseases, is a serious public health problem because of both its high incidence and prevalence and its significant morbidity and mortality and socioeconomic cost. Advanced chronic kidney disease (ACKD) includes stages 4 and 5 of the CKD classification. It is defined as chronic kidney disease in which there is a severe reduction in glomerular filtration rate (GFR < 30 ml/min). The treatment goals are to reduce and treat the complications associated with chronic kidney failure and to prepare the patient adequately and sufficiently in advance for kidney replacement therapy. The prevalence of ACKD is 0.2-0.6% of the adult population. This prevalence increases with age and in Spain is 1.6% in persons older than 64 years. - CKD is easily detected in clinical practice with simple tests (GFR estimated by equations based on serum creatinine, albuminuria and urine sediment) (Strength of Recommendation B). - It is recommended to detect the presence of CKD in all persons older than 60 years or with hypertension, diabetes or cardiovascular disease (Strength of Recommendation B). - Early detection and appropriate referral to the nephrology of patients with ACKD improves long-term morbidity and reduces costs for both the patient and the health care system (Strength of Recommendation B). Adequate communication and coordination between the primary care and nephrology is essential for this early detection: - Referral to nephrology should be made based on the stage of CKD, age of the patient, rate of progression of kidney failure, degree of albuminuria and presence or appearance of early warning signs.All patients with CKD stages 4-5 should be referred to nephrology (Strength of Recommendation C). - A protocol should be established in each health area for joint follow-up between primary care and nephrology (Strength of Recommendation C). - The creation of multidisciplinary ACKD units including a nephrologist, nephrology nurse, dietitian and social worker allows an integrated approach to the different aspects of management of patients with ACKD and is cost-effective (Strength of Recommendation B).
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PMID:[Advanced chronic kidney disease]. 1901 31

Chronic kidney disease (CKD) is common after hematopoietic cell transplantation (HCT). We prospectively measured the urinary albumin:creatinine ratio (ACR) in 142 patients. Total (intact) monomeric albumin was determined by liquid chromatography of untreated urine samples collected weekly to day 100 after HCT. Albuminuria was defined as ACR (mg/g creatinine) > 30; proteinuria, as ACR >300. Cox and logistic regression analyses evaluated ACR as a risk factor for clinical events. The prevalence of albuminuria was 37% at baseline, 64% at day 100, and 50% at 1 year. Proteinuria occurred in 4% of patients at baseline, in 15% at day 100, and in 4% at 1 year. Characteristics associated with albuminuria include age, sex, donor type, hypertension, and sinusoidal obstruction syndrome (SOS). Albuminuria was associated with an increased risk of acute graft-versus-host disease (aGVHD) and bacteremia, but not acute kidney injury (AKI). Albuminuria at day 100 was associated with CKD at 1 year (odds ratio = 4.0; 95% confidence interval [CI] = 1.1 to 14.6). Nonrelapse mortality (NRM) risk was elevated (hazard ratio = 6.8; 95% CI = 1.1 to 41.5) in patients with overt proteinuria at day 100. Albuminuria occurs frequently after HCT and is correlated with aGVHD, bacteremia, hypertension, and progression of renal disease. Proteinuria at day 100 is associated with an 6-fold increased risk of NRM by 1 year after HCT.
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PMID:Albuminuria in hematopoietic cell transplantation patients: prevalence, clinical associations, and impact on survival. 1904 Oct 58

Chronic kidney disease (CKD) in ageing is a burden on health systems worldwide. Rat models of age-related CKD linked with obesity and hypertension were used to investigate alterations in oxidant handling and energy metabolism to identify gene targets or markers for age-related CKD. Young adult (3 months) and old (21-24 months) spontaneously-hypertensive (SHR), normotensive Wistar-Kyoto (WKY) and Wistar rats (normotensive, obese in ageing) were compared for renal functional and physiological parameters, renal fibrosis and inflammation, oxidative stress (hemeoxygenase-1/HO-1), apoptosis and cell injury (including Bax:Bcl-2), phosphorylated and non-phosphorylated forms of oxidant and energy sensing proteins (p66Shc, AMPK), signal transduction proteins (ERK1/2, PKB), and transcription factors (NF-kappaB, FoxO1). All old rats were normoglycemic. Renal fibrosis, tubular epithelial apoptosis, interstitial macrophages and myofibroblasts (all p<0.05), p66Shc/phospho-p66 (p<0.05), Bax/Bcl-2 ratio (p<0.05) and NF-kappaB expression (p<0.01) were highest in old obese Wistars. Expression of phospho-FoxO/FoxO was elevated in old Wistars (p<0.001) and WKYs (p<0.01). SHRs had high levels in young and old rats. Expression of PKB, phospho-PKB, ERK1/2 and phospho-ERK1/2 were significantly elevated in all aged animals. These results suggest that obesity and hypertension have differing oxidant handling and signalling pathways that act in the pathogenesis of age-related CKD.
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PMID:Obesity and hypertension have differing oxidant handling molecular pathways in age-related chronic kidney disease. 1904 34

The presence of kidney disease, manifested by low glomerular filtration rates (GFR) and/or large amounts of protein in the urine, is independently associated with increased rates of cardiovascular disease (CVD). The severity of kidney disease is associated with graded increases in risk for CVD and death. Chronic kidney disease (CKD) should be recognized and treatment initiated early to maximize the chances for slowing nephropathy progression and reducing proteinuria. We recommend screening for CKD in all patients with CVD, including computing an estimated GFR and evaluating for proteinuria using a spot urine albumin:creatinine ratio. Aggressive management of traditional cardiovascular risk factors should be employed in this high-risk population, specifically rigorous hypertension control (including the use of angiotensin-converting enzyme inhibitors (ACEI)/angiotensin receptor blocking agents (ARB)), management of hyperglycemia, hyperlipidemia and smoking cessation. Further studies are needed to identify the unique renal failure-related (non-traditional) risk factors that contribute to accelerated atherosclerosis in this population and performance of randomized trials to assess the effects of cardiovascular interventions in individuals with CKD.
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PMID:Cardiovascular disease in chronic kidney disease. 1912 39

Accelerated cardiovascular disease (CVD) is a frequent complication of renal disease. Chronic kidney disease (CKD) develops hypertension and dyslipidemia, which in turn can contribute to the progression of renal failure. There is general agreement that endothelin-1 (ET-1), which acts through the two subtypes of receptor ET(A) and ET(B), plays important physiological roles in the regulation of normal cardiovascular function and that excessive ET-1 production is linked to CVD and CKD. Although selective ET(A) or nonselective ET(A)/ET(B) receptor antagonisms have been recognized as a potential strategy for treatment of several cardiovascular disease, it remains unclear which of the antagonisms is suitable for the individuals with CKD because upregulation of the nitric oxide (NO) system via ET(B) receptor is responsible for renal function such as natriuresis, diuresis, and glomerular hemodynamics. Our findings clearly indicate that the blockade of ET receptors, in particular ET(A)-receptor antagonism, not only produces a potential renoprotective effect in CKD but also reduces the risk of CVD. In contrast, pharmacological blockade or genetic deficiency of ET(B) receptor seems to aggravate CKD and CVD in several experimental models of rats. Moreover, preliminary evidence in patients with CKD also suggests that both selective ET(A)- and nonselective ET(A)/ET(B)-receptor blockade decreases blood pressure but that selective ET(A) blockade has additional desirable effects on renal hemodynamics. Thus, at least in CKD, these findings support the notion that ET(B) receptor-mediated actions produce a renoprotective effect and that nonselective ET(A)/ET(B)-receptors blockade seem to offer no advantage over selective ET(A) antagonism, and if anything may potentially reduce the benefits.
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PMID:Drug discovery for overcoming chronic kidney disease (CKD): the endothelin ET B receptor/nitric oxide system functions as a protective factor in CKD. 1915 34


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