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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to establish morbidity and mortality in treated patients with essential hypertension, a prospective study was started in 1974. 714 patients were followed for 15 years. Admission criteria included diastolic blood pressure over 95 mmHg during one month on placebo, absence of malignant or accelerated hypertension and no recent (6 month) cardiovascular complication. According to target organ damage, 51% of patients were in WHO stage I, 35% in stage II and 14% in stage III. There were 342 males and 372 females, with mean age 58.7 +/- 9.8 years. Mean initial blood pressure was 181/110 +/- 12/8.9 mmHg. Treatment schedules included diuretics alone (23%), beta blockers alone (32%), diuretic and betablocker (38%), combined therapy with vasodilators (9%) and other forms of therapy (5%). 75 subjects failed to comply with therapy but were maintained in the analysis (intention to treat). A significant reduction in blood pressure was observed in the group as a whole (154/93 +/- 7/9 mmHg). Sustained normalization of BP (< 90 mmHg) was obtained in 40.2% of patients, reductions to between 91 and 100 mmHg in 37.2% and reductions to over 101 mmHg in 22.5% 47 patients died from cerebro vascular complications (15-year cumulative death rate of 12.3%). Total morbidity rate was 40.1% (232 events) with 61 coronary events (13.3%), 43 cerebrovascular events (8.7%), 30 cases of heart failure (12.9%) and 21 cases of renal failure (4.3%). These figures are in agreement with internationally reported ones with the exception of coronary morbidity which appears lower in this study.
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PMID:[Morbidity and mortality of essential arterial hypertension treated in Chile: a 15 years' follow-up study]. 184 49

The discovery and clinical availability of ACE inhibitor drugs is a triumph of rational drug development and a land-mark in biochemical pharmacology and hypertension research. The clinical pharmacological properties and haemodynamics of the clinically available drugs, captopril and enalapril, are reviewed, as is their therapeutic efficacy in African patients with essential and renal hypertension and chronic congestive heart failure. ACE inhibitors act as balanced arteriolar vasodilators and venular dilators and do not excite a reflex tachycardia in contrast to other vasodilator drugs. Their efficacy is, at least in part, dependent on plasma renin activity, which is low in Blacks and in Africans. Consistent with this, is the poor response to ACE inhibitor monotherapy of essential hypertension in controlled studies in Africans. However, the compensatory neuroendocrine activation which occurs in malignant hypertension, renal failure and congestive heart failure and concurrent diuretic therapy appears to enhance the clinical response to ACE inhibitors in African patients.
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PMID:Angiotensin converting enzyme inhibitors in cardiovascular and renal disease in Africans: a review. 190 20

To determine how frequently essential hypertension results in significant renal impairment we undertook a follow-up study of 176 patients with well documented essential hypertension first seen in 1975-1977. Six patients were Asian, two Negro, and the remainder Europid. Follow-up was achieved in 92% of the cohort at five years and in 87% at 12-14 years. At five years 13 (7%) patients had moved away or were lost, and 15 (9%) patients had died (11 cardiovascular deaths). Treated blood pressure was greater than 160/95 mmHg in 60/148 patients and greater than 200/100 mmHg in 16 patients. Despite this, no significant change in serum creatinine was detected in the group as a whole. Increments in serum creatinine of at least 35 mumol/l occurred in six patients. Over the ensuing 6-9 years serum creatinine had returned to normal in three of these patients and stabilized in two; the sixth patient died from myocardial infarction. No patient reached end-stage renal failure. We conclude that progressive deterioration in renal function in essential hypertension is rarely a significant problem in Caucasian patients. A decline in renal function should prompt a search for underlying primary renal disease.
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PMID:Does treated essential hypertension result in renal impairment? A cohort study. 192 Mar 41

To document the clinical presentation of malignant accelerated hypertension in Nigerians, 56 patients were studied between 1987 and 1989 (30 months). Age range was 16 to 55 years with 59% in the range of 30-49 years; 47 were male. Mean systolic and diastolic blood pressures were 217 mmHg and 146 mmHg, respectively. Thirty patients had grade III and 26 grade IV hypertensive retinopathy. Mean body mass index was only 22.4 in the 21 patients who had no evidence of fluid retention. Seventy-five percent of patients had no awareness of hypertension. Essential hypertension accounted for 66%, chronic renal disease 32% and renal artery stenosis 2% of cases. The most common clinical features were headaches (80%), fatigue (68%), oliguria (52%), heart failure (46%), weight loss (41%), and poor vision (21%). Multiple symptoms were common and 24 patients had both renal and cardiac failure. Laboratory features included microscopic haematuria (100%) and proteinuria (100%). In 37 patients with essential hypertension, renal failure was a complication in 60%. Microangiopathic haemolytic anaemia was present in 23 patients. In addition to eight deaths from renal failure in the acute stage, 23 of these patients required long-term dialysis. Thus, malignant accelerated hypertension was associated with high morbidity, especially renal failure; it primarily afflicted patients in their prime years. Known survival at one year was 37.5%, but some patients were lost to follow-up.
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PMID:The clinical presentation of malignant hypertension in Nigerians. 195 31

Chromogranin A, co-stored and co-released with catecholamines from adrenal medullary and sympathetic neuronal vesicles, is elevated in the plasma of patients with pheochromocytoma. The usefulness of the hormone in the differential diagnosis of hypertension is examined. An elevated level of chromogranin A had comparable diagnostic sensitivity (83%, 24/29) to, but greater diagnostic specificity (96%, 86/90) than the level of plasma catecholamines when subjects with pheochromocytoma (n = 29) were evaluated in comparison to several reference groups, including normotensive controls (n = 49), subjects with essential hypertension (n = 28), subjects with renovascular hypertension (n = 5), and subjects with primary aldosteronism (n = 3). Subjects with signs or symptoms suggesting pheochromocytoma, but in whom the diagnosis was ultimately ruled out (n = 5) had normal plasma levels of chromogranin A. A modest rise in chromogranin A in those with essential hypertension, and correlation of chromogranin A with diastolic blood pressure in normotensive patients and patients with essential hypertension did not impair the diagnostic usefulness of chromogranin A for pheochromocytoma. Renal failure was associated with an elevated plasma chromogranin A independently of blood pressure. Plasma chromogranin A correlated with tumor mass, tumor chromogranin A content, tumor norepinephrine content, and urinary vanillylmandelic acid excretion; it did not correlate with plasma or urinary catecholamines, nor with blood pressure in patients with pheochromocytoma. Plasma chromogranin A levels did not differ in subjects with pheochromocytoma when stratified by age, sex, tumor location, or tumor pathology. Several drugs used in the diagnosis or treatment of pheochromocytoma (clonidine, metoprolol, phentolamine, and tyramine) had little effect on plasma chromogranin A concentration. Within the pheochromocytoma, chromogranin A was localized along with catecholamines to the soluble core of chromaffin granules, where it accounted for 18 +/- 5% of vesicle soluble protein. We conclude that 1) chromogranin A emerges along with catecholamines from pheochromocytoma chromaffin granules; 2) plasma chromogranin A is a sensitive and specific diagnostic tool in evaluation of actual or suspected pheochromocytoma; 3) plasma chromogranin A predicts pheochromocytoma tumor size and overall catecholamine production; and 4) drugs commonly employed in the diagnosis or treatment of pheochromocytoma have little effect on plasma chromogranin A level, preserving the usefulness of chromogranin A in evaluating pheochromocytoma. Thus, measurement of chromogranin A provides a useful adjunct to the diagnosis of pheochromocytoma.
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PMID:Chromogranin A storage and secretion: sensitivity and specificity for the diagnosis of pheochromocytoma. 198 65

The metabolic changes which accompany hyperglycemia in a person with diabetes are thought to cause renal hyperperfusion and intraglomerular hypertension, especially in the person with a predisposition to essential hypertension. Intraglomerular hypertension causing deposition of protein in the mesangium leads to glomerulosclerosis and renal failure. Screening for microalbuminuria can predict which type I diabetic patients will develop nephropathy. The decline in renal function in established diabetic nephropathy can be slowed with aggressive treatment of hypertension. The use of ACE inhibitors may also decrease intraglomerular hypertension. Whether similar treatment in the person with preclinical diabetic nephropathy would delay or prevent the onset of diabetic nephropathy is being investigated. Restricted protein intake, anti-platelet and rheolitic drugs may have a role in the treatment of established diabetic nephropathy. In end stage renal failure, renal transplantation is the treatment of choice. When transplantation cannot be performed, chronic ambulatory peritoneal dialysis is preferable to hemodialysis.
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PMID:Diabetic nephropathy: changing concepts of pathogenesis and treatment. 200 Aug 93

The common association between diabetes mellitus and hypertension may be promoted by several mechanisms. Patients with insulin-dependent (type I) diabetes and prone to develop nephropathy often have a familial predisposition for essential hypertension, whereas normotensive healthy offspring of nondiabetic essential hypertensive parents tend to have a reduced insulin sensitivity and increased plasma insulin levels. Na+ retention occurs as a characteristic alteration in type I or non-insulin-dependent (type II) diabetes; exchangeable body Na+ (Naex) is increased by 10% on average. This abnormality develops in the uncomplicated stage of diabetes and differentiates diabetic from nondiabetic essential hypertensive subjects. Possible Na(+)- retaining mechanisms include increased glomerular filtration of glucose leading to enhanced proximal tubular Na(+)-glucose cotransport, hyperinsulinemia (which activates several tubular Na+ transporters), an extravascular shift of fluid with Na+, and, once it occurs, renal failure. The pathogenetic role of Na+ retention in diabetes-associated hypertension is supported by positive correlations between systolic or mean blood pressure and Naex and by normalization of blood pressure after removal of excess Na+ by diuretic treatment in hypertensive diabetic subjects. The latter may also have an enhanced sensitivity of blood pressure to Na+. Plasma levels of active renin, angiotensin II, aldosterone, and catecholamines are usually normal or low in metabolically stable type I or type II diabetes. However, an exaggerated vascular reactivity to norepinephrine and angiotensin II commonly occurs already at uncomplicated stages of type I or type II diabetes. This may be a manifestation of functional (i.e., intracellular electrolytes) and/or morphological (proliferation, narrowing, and stiffening) vasculopathy. Diabetes-associated Na+ retention, vasculopathy, and a presumably inherited predisposition for both diabetes and essential hypertension may represent important complementary factors favoring the frequent occurrence of hypertension in the diabetic population.
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PMID:Central role of sodium in hypertension in diabetic subjects. 204 37

The frequent concurrence of other cardiovascular risk factors in hypertensive patients, such as obesity and diabetes mellitus, suggests that overlapping genetic and environmental factors may contribute to the common metabolic and cardiovascular derangements observed in these populations. Hypertension and hyperglycemia accelerate atherosclerosis in diabetics, and play an important role in associated morbidity and mortality. Several abnormalities in blood pressure regulatory systems such as the renin-angiotensin system, the sympathetic nervous system, and sodium/volume control have been described in diabetes mellitus. Sodium retention and cardiovascular hyperreactivity appear to occur early in the course of diabetes mellitus, even at normal blood pressure levels and before onset of renal failure, and could set the stage for the development of hypertension. The relationship between obesity and hypertension is also well-established, and may reflect metabolic and cardiovascular adaptations in obese subjects which predispose to blood pressure elevations. Obese subjects display changes in sympathetic nervous system activity, sodium metabolism, and vascular hemodynamics. Sodium-sensitive blood pressure responses in the obese may be secondary to increased cardiac output or fluid volume, and are directly related to circulating insulin levels. Certain metabolic and vascular characteristics of obesity and diabetes mellitus are found in patients with essential hypertension. It has been suggested that insulin and insulin resistance may be the common link between these risk factors. Improved understanding of metabolic considerations in the treatment of obese and diabetic hypertensives should lead to more careful selection of medications that avoid metabolic complications. Although diuretics and beta-blockers may be useful in some patients, there are several reasons not to recommend their use as initial therapy in obese and diabetic hypertensives. On the other hand, calcium channel blockers and angiotensin converting enzyme inhibitors are highly effective, with minimal effects on metabolic parameters, and are well-suited as first-line therapy in the treatment of obese and diabetic hypertensives.
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PMID:Metabolic considerations in hypertension. 207 23

Clinically apparent proteinuria in essential hypertension is associated with increased cardiovascular and total mortality and is an independent risk factor for cardiovascular and cerebrovascular disease. Subclinical elevation of urinary albumin excretion is seen more frequently than clinical proteinuria in essential hypertension and the levels of microalbuminuria (excretions of 30 to 300 mg/24 h) correlate with blood pressure. The increased urinary albumin excretion in hypertension may be explained by several factors such as renal hemodynamic changes, permselectivity changes of the glomerular filter, and structural arteriolar and glomerular changes due to nephrosclerosis. It has been clearly demonstrated that microalbuminuria is a risk factor for the development of clinical proteinuria, renal failure and increased cardiovascular mortality in insulin-dependent diabetes mellitus. It is still not known whether microalbuminuria also predicts development of proteinuria and decline in renal function in hypertension but there is some evidence indicating that microalbuminuria may be a marker of increased cardiovascular risk in hypertensives.
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PMID:Microalbuminuria in essential hypertension. 208 Oct 17

The extended use of ambulatory monitoring has permitted the identification of many conditions in which the circadian rhythm of blood pressure is altered. The common denominator seems to be an impairment of the autonomic nervous system function. We examined whether the circadian blood pressure rhythm is altered in chronic renal failure (where autonomic dysfunction is usually present) by using a standardized chronobiological inferential statistical method in hospitalized subjects. For this purpose, a group of 30 non-hemodialysis hypertensive patients with chronic renal failure was compared with a second group of 30 patients affected by uncomplicated mild-to-moderate essential hypertension. The two groups were matched by age, sex and circadian mesors of blood pressure. Diet, meal times, sleep, and activity logs were standardized. Blood pressure and heart rate recordings were obtained by using an automatic oscillometric recorder and subsequently analyzed according to the cosinor method. A mean circadian rhythm of blood pressure was documented in both groups, but while the mean acrophases occurred between 2 and 3 p.m. in essential hypertension, in renal failure they were between 11 p.m. and midnight for blood pressure and around 7 p.m. for heart rate. In addition, the mean circadian amplitudes were significantly lower in renal failure, while the mean circadian mesor of heart rate was significantly higher. Our data demonstrate that the circadian rhythms of blood pressure and heart rate are altered also in hypertension due to chronic renal failure.
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PMID:Altered circadian rhythms of blood pressure and heart rate in non-hemodialysis chronic renal failure. 208 73


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