Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antihypertensive therapy improves the long-term prognosis of patients with mild to moderate essential hypertension and is able to prevent complications. This is also true for the elderly patient with hypertension. A considerable percentage of patients with mild essential hypertension can be adequately treated without drugs. If drug treatment is required, diuretics, beta-blockers, calcium antagonists, and ACE-inhibitors are the agents of first choice. For the individual patient, the appropriate drug should be chosen on the basis of efficacy, lack of side-effects, and depending upon additional diseases, such as cardiac failure, coronary heart disease and renal failure. Only if these selection criteria are fulfilled should differences in prices of the various groups of antihypertensive agents be considered.
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PMID:[Cost/benefit relations: therapy of hypertension]. 786 89

Although measurement of chromogranin A in the bloodstream is of value in sympathoadrenal investigations, little is systematically known about chromogranin A in cerebrospinal fluid, despite substantial knowledge about its occurrence and distribution in brain. We therefore applied a homologous human chromogranin A radioimmunoassay to cerebrospinal fluid, in order to evaluate the properties and stability of cerebrospinal fluid chomogranin A, as well as its relationship to central noradrenergic neuronal activity, to peripheral (plasma) chromogranin A, and to disease states such as hypertension, renal failure and Parkinsonism. Authentic, physically stable chromogranin A immunoreactivity was found in cerebrospinal fluid (at 37-146 ng/ml; mean, 87.0 +/- 6.0 ng/ml in healthy subjects), and several lines of evidence (including 3.39 +/- 0.27-fold higher chromogranin A in cerebrospinal fluid than in plasma) indicated that it originated from a local central nervous system source, rather than the periphery. Cerebrospinal fluid chromogranin A values were not influenced by administration of effective antihypertensive doses of clonidine or propranolol, and were not related to the cerebrospinal fluid concentrations of norepinephrine, methoxyhydroxyphenylglycol, or dopamine-beta-hydroxylase; thus, cerebrospinal fluid chromogranin A was not closely linked to biochemical or pharmacologic indices of central noradrenergic neuronal activity. Cerebrospinal fluid chromogranin A was not changed (P > 0.1) in essential hypertension (84.2 +/- 14.0 ng/ml) or renal failure (72.2 +/- 13.4 ng/ml), despite a marked (7.1-fold; P < 0.001) increase in plasma chromogranin A in renal failure, and a modest (1.5-fold; P = 0.004) increase in plasma chromogranin A in essential hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chromogranin A immunoreactivity in human cerebrospinal fluid: properties, relationship to noradrenergic neuronal activity, and variation in neurologic disease. 790 34

Proteinuria (protein excretion > 300 mg/d) is an independent risk factor for the development of cardiovascular disease and renal failure. The finding of persistent proteinuria in otherwise asymptomatic patients often precedes the development of arterial hypertension and renal failure. When proteinuria is accompanied by arterial hypertension, blood pressure control can decrease the quantity of protein excretion but not the incidence of proteinuria. In this sense, converting enzyme inhibitors seem to possess a higher capacity to reduce proteinuria. Nevertheless, the effects of reducing proteinuria on renal function and cardiovascular risk remain to be elucidated. Microalbuminuria (urine albumin excretion oscillating between 30 and 300 mg/d) seems to be a predictor of cardiovascular disease in diabetic and nondiabetic subjects and has been established as a predictor for the development of diabetic nephropathy. Blood pressure levels and urinary albumin excretion correlate positively, and antihypertensive therapy of any kind decreases the quantity of albumin present in the urine. The role of increased albumin excretion in essential hypertension and in renal failure remains to be elucidated.
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PMID:Clinical relevance of proteinuria and microalbuminuria. 792 40

The association of excessive lead burden and essential hypertension has been a subject of much dispute. In particular, the potential detrimental effect of low level environmental exposure on BP has caused considerable concern. We studied the urinary excretion of lead following the infusion of EDTA (1 g of calcium disodium edetate) in 12 healthy controls (group I), 10 subjects with essential hypertension alone (Group II) and in 36 subjects with chronic renal insufficiency. Those subjects with renal insufficiency were further divided into three groups: group III, 12 patients with a history of 7-19 years of essential hypertension who subsequently developed into renal failure; group IV, patients with chronic renal failure alone; and group V, patients with chronic renal failure due to causes other than hypertensive nephropathy and associated with secondary hypertension. In comparison with other groups, subjects with hypertensive nephropathy (group III) had significantly elevated lead body burden. In addition, we found that five of the 12 subjects with hypertensive nephropathy had histories of acute gouty attacks after the development of renal function impairment. In conclusion, our observation of a higher EDTA postinfusional urinary lead excretion among some patients with essential hypertension with renal function impairment indicates that lead may play a crucial role in a subgroup of patients with hypertensive nephropathy.
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PMID:Does lead play a role in the development of renal insufficiency in some patients with essential hypertension? 793 12

Heart disease, stroke, and kidney failure are leading causes of death. Essential hypertension is the major predisposing risk factor of cardiovascular disease. Yet, after several decades of intensive investigation, the initiating causative mechanism of essential hypertension is still unknown. However, investigators in the field generally agree that an increased total peripheral resistance (TPR) is the fundamental hemodynamic disorder in essential hypertension. This review addresses the hypothesis that the increased TPR of essential hypertension is due to a defective mechanism in the contractility of arterial smooth muscle. Force-velocity and length-tension studies have shown that both caudal arterial muscle and mesenteric resistance arterial muscle from spontaneously hypertensive rats (SHR) can shorten more and faster than muscle from normotensive control Wistar-Kyoto rats (WKY). In addition, the SHR muscle relaxation rate is slower compared with the WKY muscle. These alterations in mechanical behavior of SHR arterial muscle appear to be primary to the high blood pressure since MK-421 (enalapril maleate)-treated SHR arterial muscle shows the same increased velocity of shortening, increased shortening ability, and decreased relaxation rate as the untreated SHR muscle. MK-421 is an angiotensin-converting enzyme blocker. SHR maintained on MK-421 treatment have normal blood pressures in spite of being of the genetically hypertensive strain. While these findings are encouraging, several other important issues supporting the hypothesis require resolution and warrant review. Firstly, structural alterations of blood vessel walls in hypertension cause the walls to thicken and encroach on the vessel lumens contributing to the increased TPR. Whether such wall thickening is the cause or consequence of high blood pressure has been controversial in the literature. In this report, data are presented from a study in which MK-421-treated SHR were utilized as a model of prehypertensive SHR. Light micrograph observations and morphometric analyses were made of cross-sections of mesenteric resistance arteries from SHR, MK-421-treated SHR, and WKY. Results show that the MK-421-treated SHR resistance arteries had media thicknesses and a number of smooth muscle cell layers that were significantly less than in the untreated SHR and not different from the WKY. Secondly, velocity of shortening is dependent on actomyosin ATPase activity, and, since maximum velocity of shortening has been shown to be increased in SHR arterial muscle, it became necessary to know whether or not an increased actomyosin ATPase activity might be responsible. Therefore, data from a study of SHR and WKY caudal arterial myofibrillar ATPase activities are compared.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Changes in arterial smooth muscle contractility, contractile proteins, and arterial wall structure in spontaneous hypertension. 793 46

End-stage renal disease has become a major and costly public health problem owing primarily to an accelerating incidence of renal failure from hypertension and diabetes. In both disease groups the primary problem appears to be persistent elevation of blood pressure, and there is evidence that early and effective blood pressure control arrests the renal damage and provides continuing protection to the kidney. It is recommended that the blood pressure be controlled to levels below 150/95 mm Hg for essential hypertension and below 140/85 mm Hg for the hypertensive diabetic. Serial monitoring of renal function can be done with a graph of reciprocal (1/serum creatinine) values of annual serum creatinine measurements, particularly in groups at increased risk for end-stage renal disease. High-risk groups include blacks, older individuals, and those with serum creatinine levels > or = 1.5 micrograms/dL.
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PMID:Importance of blood pressure control in the preservation of renal function. 793 17

The development in recent years of sensitive assays specific for albumin has facilitated extensive investigation of the pathophysiology and clinical significance of microalbuminuria. It is now clear that the appearance of microalbuminuria represents a crucial event in the natural histories of diabetes mellitus and essential hypertension. It reflects the presence of generalized vascular damage and is strongly predictive of subsequent renal failure, cardiovascular morbidity, and death. Therapeutic interventions, including strict diabetic and blood-pressure control, can reduce microalbuminuria and improve the overall prognosis. The detection and treatment of microalbuminuria in these high-risk groups should now form an integral part of their management. Large-scale screening programmes are also recommended for insulin-dependent diabetics.
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PMID:Microalbuminuria: pathogenesis, prognosis and management. 795 79

Adrenomedullin is a potent hypotensive peptide newly discovered in pheochromocytoma tissue by monitoring its elevating activity on platelet cAMP. We measured plasma concentration of adrenomedullin in patients with essential hypertension and chronic renal failure. As compared with normal subjects, plasma adrenomedullin was increased by 26% (P < 0.05) in hypertensives without organ damage and by 45% (P < 0.005) in those with organ damage. The increase in plasma adrenomedullin was more prominent in renal failure than in hypertension. Renal failure patients with plasma creatinine of 1.5-3, 3-6, and > 6 mg/dl had higher plasma adrenomedullin levels than healthy subjects by 78% (P < 0.05), 131% (P < 0.001), and 214% (P < 0.001), respectively. Moreover, adrenomedullin showed intimate correlations with norepinephrine, atrial natriuretic peptide, and cAMP in plasma (r = 0.625, P < 0.001; r = 0.656, P < 0.001; and r = 0.462, P < 0.001; respectively). Thus, plasma adrenomedullin is supposed to increase in association with changes in sympathetic nervous activity and body fluid volume in hypertension and renal failure. Considering its potent vasodilator effect, adrenomedullin may be involved in the defense mechanism preserving the integrity of the cardiovascular system in these disorders.
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PMID:Plasma levels of adrenomedullin, a newly identified hypotensive peptide, in patients with hypertension and renal failure. 796 64

In a single-blind trial with a 2-week placebo run-in phase and a 4-week active-treatment period, spirapril at 6 mg once daily was administered to 49 consecutive hypertensive patients (34 men and 15 women). All had pretreatment diastolic blood pressures (DBP) of 95-115 mmHg and varying degrees of renal impairment. At the end of the placebo run-in and at the end of active treatment, renal function was assessed using the following procedures: technetium 99m-DTPA clearance [for glomerular filtration rate (GFR)]; radioiodine (131I)-labelled sodium iodohippurate (Hippuran) clearance [for renal plasma flow (RPF)]; creatinine clearance (Clcr). No statistically significant differences were found in GFR or Clcr during spirapril treatment. In renally impaired patients, RPF remained virtually unchanged whereas, in patients with normal Clcr, there was an increase of around 10% during active treatment. At the end of the study, 48% of the patients with renal failure achieved normalization of DBP (< or = 90 mmHg) and/or a DBP reduction of > or = 10 mmHg; the corresponding rate for patients with normal renal function was 31%. In conclusion, in patients with mild-to-moderate essential hypertension and varying degrees of renal impairment, spirapril at 6 mg once daily is an efficacious and well tolerated antihypertensive therapy.
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PMID:Spirapril in chronic renal failure. 806 47

1. Dopamine beta-hydroxylase is stored and released with catecholamines by exocytosis from secretory vesicles in noradrenergic neurons and chromaffin cells. Although dopamine beta-hydroxylase enzymic activity is measurable in cerebrospinal fluid, such activity is unstable, and its relationship to central noradrenergic neuronal activity in humans is not clearly established. To explore the significance of cerebrospinal fluid dopamine beta-hydroxylase, we applied a homologous human dopamine beta-hydroxylase radioimmunoassay to cerebrospinal fluid, in order to characterize the properties and stability of cerebrospinal fluid dopamine beta-hydroxylase, as well as its relationship to central noradrenergic neuronal activity and its variation in disease states such as hypertension, renal failure, Parkinsonism and congenital dopamine beta-hydroxylase deficiency. 2. Authentic, physically stable dopamine beta-hydroxylase immunoreactivity was present in normal human cerebrospinal fluid at a concentration of 31.3 +/- 1.4 ng/ml (range: 18.5-52.5 ng/ml), but at a 283 +/- 27-fold lower concentration than that found in plasma. Cerebrospinal fluid and plasma dopamine beta-hydroxylase concentrations were correlated (r = 0.67, P = 0.001). Some degree of local central nervous system control of cerebrospinal fluid dopamine beta-hydroxylase was suggested by incomplete correlation with plasma dopamine beta-hydroxylase (with an especially marked dissociation in renal disease) as well as the lack of a ventricular/lumbar cerebrospinal dopamine beta-hydroxylase concentration gradient. 3. Cerebrospinal fluid dopamine beta-hydroxylase was not changed by the central alpha 2-agonist clonidine at a dose that diminished cerebrospinal fluid noradrenaline, nor did cerebrospinal fluid dopamine beta-hydroxylase correspond between subjects to cerebrospinal fluid concentrations of noradrenaline or methoxyhydroxyphenylglycol; thus, cerebrospinal fluid dopamine beta-hydroxylase concentration was not closely linked either pharmacologically or biochemically to central noradrenergic neuronal activity. 4. Cerebrospinal fluid dopamine beta-hydroxylase was not changed in essential hypertension. In Parkinson's disease, cerebrospinal fluid dopamine beta-hydroxylase was markedly diminished (16.3 +/- 2.9 versus 31.3 +/- 1.4 ng/ml, P < 0.001) and rose by 58 +/- 21% (P = 0.02) after adrenal-to-caudate chromaffin cell autografts. In congenital dopamine beta-hydroxylase deficiency, lack of detectable dopamine beta-hydroxylase immunoreactivity in cerebrospinal fluid or plasma suggests absent enzyme (rather than a catalytically defective enzyme) as the origin of the disorder. 5. We conclude that cerebrospinal fluid dopamine beta-hydroxylase immunoreactivity, while not closely linked to central noradrenergic neuronal activity, is at least in part derived from the central nervous system, and that its measurement may be useful in both the diagnosis and treatment of neurological disease.
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PMID:Dopamine beta-hydroxylase immunoreactivity in human cerebrospinal fluid: properties, relationship to central noradrenergic neuronal activity and variation in Parkinson's disease and congenital dopamine beta-hydroxylase deficiency. 814 25


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