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

Microalbuminuria is a considerable good indicator of atherogenic disease and cardiovascular risk. In the arterial hypertension, the main centre organ is the kidney. Structural and functional changes that happen in the hypertensive nephropathy are going to cause alterations m the albumin urinary excretion. The authors have done a revision of the main factors which can origin the existence of microalbuminuria in patients with arterial hypertension, and they conclude that this is an useful biochemist indicator in order to evaluate the degree of renal disease in these patients.
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PMID:[Microalbuminuria in arterial hypertension]. 971 Sep 92

ACE inhibitors are well established in the treatment of arterial hypertension, heart failure and diabetic and/or hypertensive nephropathy with albuminuria. The important trials for the various indications are briefly discussed. In Switzerland 11 ACE inhibitors are available for clinical use, differing mainly in their pharmacokinetic and pharmacodynamic properties. The characteristics of practical relevance regarding oral bioavailability, elimination mechanisms and half-life, as well as the necessary dosage modifications in patients with renal, hepatic and cardiac failure, are presented. All ACE inhibitors except captopril and lisinopril are administered as prodrugs. The bioavailability among ACE inhibitors varies widely with a range from 11% (trandolapril) to more than 60% (captopril). The great majority of ACE inhibitors are eliminated predominantly through the kidneys. However, benazepril, fosinopril, ramipril, spirapril and trandolapril also have a hepatic (metabolic) route of elimination. Since half-life varies from 1 h (captopril) to 30 h (spirapril) we drew up, for simplicity, a table of 3 groups with short, medium and long t1/2. In renal insufficiency dose adjustment is required only below a creatinine-clearance level of 30 ml/min. These dosage reductions are not required in liver diseases, but renally excreted drugs such as lisinopril should be preferred. Treatment with ACE inhibitors in severe heart failure should be initiated carefully, with low doses and concomitant diuretic treatment added or maintained. Most common adverse effects of ACE inhibitors are hypotension, cough, hyperkalaemia and renal failure. Less frequent adverse effects are angioedema, bone marrow suppression and also foetal damage. Thus, ACE inhibitors are contraindicated in pregnancy.
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PMID:[Comparative evaluation of ACE inhibitors: which differences are relevant?]. 1046 7

Systemic hypertension is common in patients with acute as well as with chronic renal diseases. Hypertension is an important factor that contributes to the progression of renal failure. Cardiovascular disease is the leading cause of death and disability in patients with chronic renal failure and in those receiving renal replacement therapy. The prevalence of hypertensive nephropathy remains unabated. Hypertension and chronic renal failure are closely interlinked and govern the morbidity and mortality in patients afflicted by these conditions. There is considerable hope that effective control of hypertension may retard the progression of renal disease. Although mere control of hypertension is of paramount importance, specific pharmacologic approaches may offer certain important renal advantages. Angiotensin-converting enzyme (ACE) inhibitors, by the virtue of their intrarenal effects, exert favorable consequences on the kidney function (and structure, to some extent), particularly in patients with diabetic nephropathy and hypertension. Both experimental and clinical studies have demonstrated the renoprotective effects of ACE inhibitors; these drugs slow down the progression of renal disease independent of their antihypertensive actions. More recently, angiotensin-receptor blockers have been shown to exert similar glomerular effects as ACE inhibitors. Preliminary clinical data also suggest a possible role for angiotensin-receptor blockers in the prevention of progression of renal failure. Therapeutic agents that inhibit the renin-angiotensin axis hold considerable promise in the management of patients with renal disease by slowing down the rate of decline in renal function.
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PMID:Role of angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers in the prevention of progression of renal disease. 1098 Nov 2

Tight blood pressure control among diabetic and nondiabetic patients with hypertension is perhaps the single most effective intervention used to delay progression to end-stage renal disease (ESRD). The renoprotective actions of angiotensin-converting enzyme (ACE) inhibitors in patients with diabetic and hypertensive nephropathy is well established. Drugs of this class fairly uniformly reduce glomerulosclerosis, delay the deterioration in renal function, and improve proteinuria, a predictive surrogate marker for renal injury. Calcium- channel blockers (CCBs) in the phenylalkylamine (verapamil) and benzothiazepine (diltiazem) classes also improve proteinuria and delay the progression of renal disease in diabetic and nondiabetic hypertensive nephropathy beyond that attributable to blood pressure control. The short-acting dihydropyridine CCBs worsen proteinuria and accelerate renal injury in both animal models and humans with hypertension or diabetes. A very limited number of studies in animals or humans with hypertension or diabetes have demonstrated at least an additive renoprotective effect when the combination of ACE inhibitors and nondihydropyridine CCBs has been compared with each agent administered as monotherapy. Because patients with impaired renal function and either hypertension or diabetes appear to benefit from aggressive blood pressure reduction, many of these patients will require two or more drugs to achieve the currently recommended blood pressure goals. Combinations of ACE inhibitor and CCB are attractive because they may provide better blood pressure control, appear to be better tolerated with fewer side effects than either drug alone, and may exert a greater renoprotective effect in patients at risk for renal failure than either an ACE inhibitor or a CCB.
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PMID:The case for combining angiotensin-converting enzyme inhibitors and calcium-channel blockers. 1098 Nov 4

Hypertension is a risk factor for the development of end-stage renal disease. The mechanisms underlying hypertensive nephropathy are poorly understood. There is evidence, however, that in hypertension there is an accumulation of partially reduced oxygen and its derivatives, known collectively as reactive oxygen species, which may contribute to progressive renal dysfunction. In the present study, we assess the contribution of oxidative stress in the development of salt-dependent hypertensive nephrosclerosis. Going beyond previous end point studies, which inferred renal function either indirectly or only qualitatively, we have determined oxidative stress concurrently with direct and quantitative measurements of renal function (via inulin and p-aminohippuric acid clearances). Moreover, in this time-dependent study, the measurements have been taken under low- as well as high-salt diets. As was expected from previous studies, in the Dahl salt-sensitive rat, a high-salt diet (8% NaCl) resulted in the development of hypertension, in a decreased glomerular filtration rate, and in a decreased renal plasma flow as compared with the normotensive control, the Dahl salt-resistant rat. In addition, however, we found clear evidence for the accumulation of reactive oxygen species in renal tissue homogenates of Dahl salt-sensitive rats on the high-salt diet. Our time-dependent protocol also indicated that renal oxidative stress follows, in time, the development of hypertension. We also found that after 2 weeks of increased salt loading, Dahl salt-sensitive rats excreted less cyclic guanosine monophosphate and NO(x) than Dahl salt-resistant rats on the same diet. It is known that urinary cyclic guanosine monophosphate and NO(x) represent the activity and stable derivatives of renal NO., respectively, and that they closely correlate with renal vascular resistance. Therefore, our results suggest that, in the Dahl salt-sensitive rat, increased oxidative stress is associated with salt-dependent hypertensive nephrosclerosis and that decreased NO. bioavailability may represent a common factor responsible for the vascular and glomerular dysfunction.
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PMID:Oxidative stress and renal dysfunction in salt-sensitive hypertension. 1143 44

Essential hypertension causes renal injury. Hypertensive nephroangiosclerosis (HN) or hypertensive nephropathy are terms most commonly used to describe this renal pathology. Although specific histological lesions occurring in affected kidneys are well known, pathogenesis of hypertension-related renal scarring is not completely understood. Evidence exists to support the theory that other factors such as aging, black race or smoking, beside blood pressure, contribute to the development and progression of HN. Metabolic disturbances, cocaine and nonsteroidal anti-inflammatory drug abuse, ochratoxin A exposure, dietary salt intake, heavy metal toxicity, hantavirus infection and perinatal programming are also considered risk factors. Renal susceptibility genes may determine whether hypertension-induced progressive renal damage occurs and how severe it is. Determination of all risk factors may identify patients at high risk of renal failure and help tailor an appropriate management. In the present paper, the knowledge available on this clinically important objective is discussed.
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PMID:Multifactorial determination of hypertensive nephroangiosclerosis. 1259 Jan 97

Chronic hypertension leads to renal damage known as hypertensive nephropathy or hypertensive nephrosclerosis. Presently, this renal pathology seems to be one of the most frequent causes of end-stage renal disease requiring chronic dialysis. Unfortunately there are many problems with clinical diagnosis of hypertensive nephropathy which cause overestimation of its prevalence. Renal biopsy and morphological examination which is the gold standard of diagnosis is rarely performed in such patients. Histological lesions in hypertensive nephropathy are well recognised: myointimal hyperplasia of arterioles, hyaline arteriosclerosis, wrinkling of basement membrane, collapse of the glomerular tuft, glomerulosclerosis and tubulointerstitial involvement. These changes are believed to result from ischaemia and hyperfiltration. Genetic susceptibility and enhanced apoptosis could be involved in this process as well. One could hope that adequate treatment of hypertension according to international standards would allow to reduce the still increasing number of patients with hypertensive nephropathy. Pathogenesis, epidemiology, and clinical management of hypertensive nephropathy are currently discussed in this brief review.
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PMID:[Hypertensive nephropathy: pathogenesis, diagnosis and treatment]. 1272 83

Angiotensin II (AngII) has been shown to play a critical role in diabetic nephropathy and vasculopathy. Although it is well recognized that an angiotensin-converting enzyme (ACE)-dependent AngII-generating system is a major source of intrarenal AngII production, it is here reported that the chymase-dependent AngII-generating system is upregulated in the human diabetic kidney. This becomes particularly strong in those with hypertension. In the normal kidney, while ACE was constitutively expressed by most kidney cells, chymase was weakly expressed by mesangial cells (MC) and vascular smooth muscle cells (VSMC) only. In the diabetic kidney, while ACE expression was significantly upregulated (1 to 3-fold) by tubular epithelial cells (TEC) and infiltrating mononuclear cells, there was also markedly increased chymase expression (10 to 15-fold) by both MC and VSMC, with strong deposition in the collagen-rich extracellular matrix including both diffuse and nodular glomerulosclerosis, tubulointerstitial fibrosis, and vascular sclerosis. Interestingly, while ACE expression showed no difference in patients with or without hypertension, upregulation of chymase in hypertensive patients was much stronger than that seen in those without hypertension (4 to 7-fold, P < 0.001). Correlation analysis showed that, in contrast to the ACE expression, upregulation of chymase correlated significantly with the increase in BP and the severity of collagen matrix deposition within the glomerulus, tubulointerstitium, and arterial walls (all with P < 0.001). In conclusion, the present study demonstrates that chymase, as an alternative AngII-generating enzyme, is markedly upregulated in the diabetic kidney and may be associated with the development of diabetic/hypertensive nephropathy. In addition, differential expression of ACE and chymase in the diabetic kidney indicates that both ACE and chymase may be of equal importance for AngII-mediated diabetic nephropathy and vascular disease. Results from this study suggest that blockade of both AngII-generating pathways may provide additional beneficial effect on diabetic nephropathy.
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PMID:Chymase is upregulated in diabetic nephropathy: implications for an alternative pathway of angiotensin II-mediated diabetic renal and vascular disease. 1281 57

Although hypertension is a risk factor for the development of end-stage renal disease, not all hypertensive patients progress to develop renal dysfunction. The mechanisms underlying hypertensive nephropathy are poorly understood. The authors have recently shown that the development of hypertension and renal dysfunction is accompanied by an accumulation of partially reduced oxygen and its derivatives, known collectively as reactive oxygen species. In the present study, the effect of a lipid-soluble antioxidant on the development of salt-dependent hypertensive nephropathy was evaluated in the Dahl rat. It was found that a high-salt diet (8% NaCl) led to the development of hypertension, increased renal oxidative stress (superoxide production and 8-epi-prostaglandin F2alpha), and decreased glomerular filtration rate and renal plasma flow in the Dahl salt-sensitive (DSS) rat, and that these adverse effects of salt were prevented by supplementing the high-salt diet with 1000 U/kg chow of alpha-tocopherol. It is well known that urinary cyclic guanosine monophosphate (cGMP) levels are lower in hypertensive DSS rats than in Dahl salt-resistant (DSR) rats on a high-salt diet. Most surprisingly, when supplemented with alpha-tocopherol, DSS rats on an 8% NaCl diet were able to excrete as much cGMP as DSR rats. Taken together, these findings suggest that, in the DSS rat, salt-dependent hypertensive nephropathy and decreased nitric oxide bioavailability are associated with increased oxidative stress, and that antioxidants can preclude these adverse effects of salt feeding, and consequently, prevent salt-dependent hypertension and nephropathy.
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PMID:Prevention of hypertension and renal dysfunction in Dahl rats by alpha-tocopherol. 1282 31

Hypertensive nephropathy (HN) and focal segmental glomerulosclerosis (FSGS) are significant causes of end-stage renal disease (ESRD), but no genes or loci have been associated with this phenotype among African Americans, a group at high risk. We performed a genomewide linkage scan with approximately 400 microsatellite markers on 23 individuals of a large four-generation African American family with 18 affected individuals (7 with ESRD), in which the 13-year-old proband (also with ESRD) presented with hypertension and proteinuria (2-4 g/day) and underwent a kidney biopsy that revealed FSGS-like lesions with arteriolar thickening. A genomewide scan revealed LOD scores of >2.5 for markers on chromosomes 3 and 9, and fine mapping was performed on 5 additional members (total 28 members) that showed a maximum multipoint LOD score of 5.4 in the 9q31-q32 region, under an autosomal dominant model with 99% penetrance. This 8-cM (6-Mb) region is flanked by markers D9S172 and D9S105, and further candidate gene sequencing studies excluded the coding regions of three genes (ACTL7A, ACTL7B, and CTNNAL1). To our knowledge, this is the first report of a locus, denoted as "HNP1," for the HN/FSGS phenotype in a large African American family with dominantly inherited nephropathy characterized by ESRD, hypertension, and some features of FSGS.
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PMID:African American hypertensive nephropathy maps to a new locus on chromosome 9q31-q32. 1284 Jul 82


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