Optimal recovery of cytomegalovirus from urine as a function of specimen preparation

BACKGROUND/AIMS: Early liver transplantation is crucial in children with liver disease and pulmonary artery hypertension. Some severe pulmonary vascular anomalies associated with portal hypertension disappear after isolated liver transplantation. Evolution of pulmonary artery hypertension due to plexogenic arteriopathy is controversial, as this association is still considered a contraindication to isolated liver transplantation. Outcome of pulmonary hypertension after isolated liver transplantation is reported in three patients with portal hypertension. METHODS: After echocardiographic diagnosis, the patients had a complete hemodynamic exploration, and two had a lung biopsy. After liver transplantation, the survivors had echocardiographic follow up and a second hemodynamic exploration. RESULTS: In two children, pulmonary pressures and resistances returned to near-normal values 1 and 6 years after successful isolated liver transplantation. The third patient, with the most severe arteriopathy, had to wait 1 year for a donor, and the attempted transplantation was complicated by ventricular tachycardia; death occurred 2 days after surgery. CONCLUSIONS: Liver transplantation can reverse pulmonary artery hypertension due to high pulmonary resistances complicating liver disease with portal hypertension, provided it is carried out at an early stage. Early detection of pulmonary hypertension by systematic echocardiography may thus be crucial in these children with portal hypertension.     

Pulmonary vascular disorders in portal hypertension

The wide spectrum of pulmonary vascular disorders in liver disease and portal hypertension ranges from the hepatopulmonary syndrome characterized by intrapulmonary vascular dilatations, to pulmonary hypertension (portopulmonary hypertension), in which pulmonary vascular resistance is elevated. Since hepatopulmonary syndrome and portopulmonary hypertension have been reported in patients with nonhepatic portal hypertension, the common factor that determines their development must be portal hypertension. The clinical presentations are very different, with gas exchange impairment in the hepatopulmonary syndrome and haemodynamic failure in portopulmonary hypertension. The severity of hepatopulmonary syndrome seems to parallel the severity of liver failure, whereas no simple relationship has been identified between hepatic impairment and the severity of portopulmonary hypertension. Resolution of hepatopulmonary syndrome is common after liver transplantation, which has an uncertain effect in portopulmonary hypertension. The pathophysiology of both syndromes may involve vasoactive mediators and angiogenic factors.     

Hypertension in diseases of the kidney. Pathogenesis and therapy

Renal disease is the cause of hypertension in about 5% of all hypertonics. Patients with renal hypertension are threatened by cardiovascular complications of hypertension even more frequently than patients with essential hypertension. Hypertension is moreover an important factor in the progression of renal insufficiency. In the pathogenesis of renal hypertension an important role is played by sodium and fluid retention and activation of the renin-angiotensin system. Progression of rental insufficiency can be retarded only by more strict control of hypertension than in patients with normal renal function. Optimal treatment is administration of angiotensin converting enzyme inhibitor which moreover in the majority of patients retards the progression of renal insufficiency more markedly than other antihypertensive drugs.     

Pulmonary hypertension associated with portal hypertension. Apropos of 2 cases

The authors report the cases of two patients with pulmonary hypertension associated with portal hypertension. This is a rare association with a reported prevalence ranging from 0.25 to 0.73%. The diagnosis of portal hypertension preceded that of pulmonary hypertension by several years. The physiopathological mechanism of the latter is not well known although several hypotheses have been proposed. Treatment is only symptomatic. The prognosis is usually poor, the causes of death being related to complications of liver failure and/or portal hypertension or to those of pulmonary hypertension.     

Diabetes and hypertension: the bad companions

DIABETES AND HYPERTENSION: Diabetes mellitus and hypertension are interrelated diseases that strongly predispose people to atherosclerotic cardiovascular disease. Hypertension is about twice as frequent in individuals with diabetes as in those without. The prevalence of coexisting hypertension and diabetes appears to be increasing in industrialized nations because populations are aging, and both hypertension and non-insulin-dependent diabetes mellitus (NIDDM) increase with age. An estimated 35-75% of diabetic cardiovascular and renal complications can be attributed to hypertension. ESSENTIAL HYPERTENSION: Essential hypertension accounts for the majority of hypertension in individuals with diabetes, particularly those with NIDDM, who constitute over 90% of those with a dual diagnosis of diabetes and hypertension. Diabetic nephropathy, which occurs after 15 years of diabetes in one-third of those with insulin-dependent diabetes and 20% of those with NIDDM, is an important contributing factor to the development of hypertension in the diabetic. New investigations should focus increasingly on identifying appropriate antihypertensive agents that not only lower blood pressure but also reduce cardiovascular risk and retard the rate of progression of diabetic renal disease.     

Clinical profile of arterial hypertension in patients with cerebrovascular diseases

The aim this work was to assess retrospectively the history of hypertension in patients admitted for cerebrovascular diseases. Two hundred and forty eight patients were studied (69% with ischemic strokes, 24% with hemorrhagic strokes and 7% with transient ischemic attacks. 76% of cases had a history hypertension with an evolution of ten years or more in 81% of cases. No differences in the prevalence of hypertension was observed among the different types of strokes. Of the 139 patients in whom the severity of hypertension was registered, 37% had mild, 45% moderate, 15% severe and 3% systolic hypertension. Those with severe hypertension had a higher incidence of hemorrhagic stroke. Fundoscopic examination was abnormal in 81% of the 64 patients in whom it was performed, left ventricular hypertrophy was found in 62% of the 146 patients in whom it was investigated. 51% of patients were receiving anti hypertensive treatment and it was effective in 26% of them. Thirty one percent of subjects had old lesions in the CAT scan; these subjects had a similar prevalence of hypertension and effectiveness of treatment than patients without old lesions. It is concluded that a history of more than ten years of hypertension is a risk factor for cerebrovascular disease, that severe hypertension is mostly associated to hemorrhagic strokes and that only 26% of patients with stroke had and adequate anti hypertensive treatment.     

Does essential hypertension cause progressive renal disease?

In the distant past, terminal renal failure occurred mainly as a result of malignant hypertension. The introduction of effective antihypertensive therapy has made malignant hypertension rare, and researchers have stopped focusing on the kidney's role in their hypertension research. However, recent long-term observational studies have documented an impressive relationship between hypertension and impaired renal function in patients without primary chronic renal disease; elderly and African American individuals with hypertension have the worst prognoses. The hallmark of hypertensive renal injury is thought to be a progressive increase in intrarenal vascular resistance, which may precede changes in renal structure. Because we lack evidence from renal biopsy studies, it is unclear whether an increase in albumin (protein) excretion correlates with these disturbances of renal function and structure. Nevertheless, because urinary excretion of albumin in patients with essential hypertension is related to the risk of cardiovascular complications, its measurement provides important clinical information.     

Who contributes to the public health function?

OBJECTIVES: To describe patterns of hypertension history in patients with various types of end-stage renal disease (ESRD) and in persons with normal kidney function; and to identify risk factors for the diagnosis 'hypertensive ESRD'. DESIGN: A case-control study. SETTING: Population-based. PARTICIPANTS: Patients with ESRD due to hypertension (n = 214), diabetes (n = 239), other specified causes (n = 181), unknown causes (n = 82) and control subjects drawn from the general population (n = 361). MAIN OUTCOME MEASURES: Participants' history of hypertension. RESULTS: The prevalence of hypertension was 90% in ESRD patients and 27% in controls. Only 6% of patients with hypertensive ESRD had a history of malignant hypertension. Patients with hypertensive ESRD were more likely to have been hospitalized because of hypertension (36%) than were other ESRD patients (18%) or controls (5%). ESRD of any cause was more strongly associated with hypertension of > or = 25 years duration (odds ratio 51.0, compared with normal blood pressure) than it was with hypertension of shorter duration (15-25 years: odds ratio 31.8, 5-15 years: odds ratio 16.0, < 5 years: odds ratio 21.2). Among patients who had both hypertension and ESRD, the diagnosis of 'hypertensive ESRD' was associated independently with a long duration of hypertension, greater severity of hypertension, the absence of diabetes, black race, and limited education. CONCLUSIONS: Hypertension is common among patients with ESRD. The risk of ESRD from any cause increases progressively with the duration of hypertension, and with indicators of severe hypertension. This result supports the hypothesis that nonmalignant hypertension of long duration may cause renal insufficiency. The criteria used to diagnose hypertensive ESRD are consistent with pathophysiologic and epidemiologic evidence.     

Management of the patient with renovascular hypertension

Renal artery stenosis, either fibromuscular or atheromatous, is probably the most common cause of secondary hypertension in man. Both of these diseases are active, ongoing processes that may be ameliorated but not cured by medical or surgical treatment. The clinical history and examination of the patient with hypertension may help differentiate renovascular hypertension from essential hypertension. The presence of a systolic-diastolic or continuous bruit is often an indicator of severe renal artery stenosis. Systemic hypertension is the physiologic consequence of significant renal artery stenosis. Knowledge of the basic concepts of the renin-angiotensin-aldosterone system, as has evolved from experimental models of renovascular hypertension, forms the basis for understanding the process of evaluation and treatment of such patients. The treatment of choice for the patient with severe hypertension and a functionally significant renovascular lesion is surgical--both in terms of successful treatment of hypertension and improved long-term prognosis. Diligent periodic reevaluation of these patients as well as those with less severe hypertension who are receiving medical treatment enables the physician to select the proper management that offers optimal control of patient blood pressure and avoids target-organ damage to the kidneys, central nervous system, or cardiovascular system.     

Nephrosclerosis: current status

Nephrosclerosis is the most typical and widespread renal manifestation of hypertension and can be judged as the pathological hallmark of essential hypertension. Nephrosclerosis is an important and frequent cause of progressive renal disease, however, information in the literature on the risk of developing renal failure in the course of essential hypertension is sparse. Traditionally, nephrosclerosis was thought to result from glomerular ischemia. Alternatively, glomerular sclerosis in hypertension may result from glomerular hyperperfusion or hypertension. Studies in experimental models of renal disease have identified a promising intervention with either Ca antagonists or angiotensin-converting enzyme inhibitors. Application of these therapies to patients with nephrosclerosis should await the results of careful clinical trials.     

Mutations and variants of the epithelial sodium channel gene in Liddle's syndrome and primary hypertension

Liddle's syndrome is a rare monogenic form of hypertension caused by truncating or missense mutations in the C termini of the epithelial sodium channel beta- or gamma-subunits. These mutations delete or alter a conserved proline-rich amino acid sequence referred to as the PY-motif. We report here a Liddle's syndrome family with a betaArg564X mutation with a premature stop codon deleting the PY-motif of the beta-subunit. This family shows marked phenotypic variation in blood pressure, serum potassium levels, and age of onset of hypertension. Given the similarity with primary hypertension, changes in the C termini of the beta- or gamma-subunits may contribute to the development of primary hypertension or to hypertension associated with diabetic nephropathy. Accordingly, the coding sequences for the cytoplasmic C termini of the beta- and gamma-subunits were screened for mutations with the use of polymerase chain reaction, single-strand conformation polymorphism, and direct DNA sequencing in 105 subjects with primary hypertension and 70 subjects with diabetic nephropathy. One frequent polymorphism was identified, but its frequency did not differ among subjects with primary hypertension, subjects with diabetic nephropathy, or control subjects. Two of the 175 subjects with primary hypertension or diabetic nephropathy showed variants that were not present in 186 control subjects. None of the variants changed the PY-motif sequence. In conclusion, a betaArg564X mutation is the likely cause of Liddle's syndrome in this Swedish family, but it is unlikely that mutations in the beta- and gamma-subunit genes of the epithelial sodium channel play a significant role in the pathogenesis of primary hypertension or diabetic nephropathy.     

Familial benign intracranial hypertension

Three sisters with benign intracranial hypertension are reported. This is the first documentation of benign intracranial hypertension in three family members. Obesity is a striking feature in these patients as well as five of the six previously reported patients with familial benign intracranial hypertension. Pregnancy and chronic dysfunctional uterine bleeding, well known predisposing factors in this syndrome when it occurs sporadically, were present in two of the sisters. A familial metabolic defect may be responsible for the intracranial hypertension in these patients.     

Sex differences in the pharmacological treatment of hypertension: a review of population-based studies

OBJECTIVE: To summarize all available literature on sex differences in the pharmacological treatment of hypertension with respect to the percentage of hypertensive patients treated pharmacologically and the selection of antihypertensive drugs. The influences of the calendar period, age, definition of hypertension, prevalence of hypertension and country on these sex differences were examined. DATA IDENTIFICATION: A secondary analysis of data from 46 population-based studies in 22 countries on the prevalence of pharmacologically treated hypertension was conducted to estimate sex ratios for the prevalence of drug treatment for hypertension. RESULT: Overall, women with hypertension were 1.33-fold [95% confidence interval (CI) 1.32-1.34] more likely to be treated pharmacologically for hypertension than were hypertensive men. With increasing age, the female: male ratio for pharmacological treatment of hypertension decreased from 2.26 (95% CI 1.56-3.27) at ages 20-29 years to 1.22 (95% CI 1.11-1.34) at ages 60-69 years. In all countries more women than men were treated for hypertension, with the biggest difference observed in the USSR (1983-1986), where about twice as many women as men were treated for hypertension. Women more frequently used diuretics, whereas men more often used beta-blockers, angiotensin converting enzyme inhibitors and calcium antagonists. CONCLUSIONS: Hypertensive women are more often treated for hypertension than hypertensive men and their pattern of use of antihypertensive drugs differs from that of men. Further research is required in order to explain sex differences in the treatment of hypertension with respect to the prevalence of pharmacological treatment of hypertension and choice of antihypertensive drugs, and to investigate the consequences of this difference for long-term outcomes.     

Hypertension in insulin-dependent diabetes

Hypertension is seen in approximately 85% of IDDM patients with diabetic nephropathy and blood pressure elevation is an early event in the development of this complication. In IDDM patients with clinical nephropathy, a positive correlation has been demonstrated between the blood pressure and the urinary albumin excretion and reduction of blood pressure reduces albuminuria as well as the rate of decline in glomerular filtration rate. Also extrarenal abnormalities such as retinopathy, cardiovascular diseases and signs of endothelial dysfunction, sometimes seen in non-diabetics with severe and/or prolonged hypertension, are frequently demonstrated in IDDM patients with clinical nephropathy. The aim of the present study was to provide circumstantial evidence for the thesis that hypertension in IDDM patients with nephropathy is secondary to the kidney involvement and not the cause of the kidney disease. Furthermore, by familial and physiological studies the review also aimed to contribute to the understanding of the pathogenesis of hypertension in patients with clinical nephropathy. Finally the question of optimal pharmacological antihypertensive treatment was discussed. It was demonstrated that in IDDM patients with elevated urinary albumin excretion above normal level the prevalence of hypertension is 60%, whereas in patients without signs of renal impairment hypertension is not more prevalent as in the age and sex-matched background population (about 4% in both groups). Based upon the observation, that some of these IDDM patients with hypertension but normal UAE were hypertensive for many years, we designated this group as IDDM patients with essential hypertension for further studies. In this group, we had the opportunity to study the association between blood pressure and the development of extrarenal complications in patients with IDDM. The group with essential hypertension and IDDM showed to have less retinopathy compared with diabetics with similar blood pressure but elevated UAE. In contrast to the hypertensive patients with nephropathy, a normal transcapillary escape rate of albumin and normal plasma levels of von Willebrand factor, of angiotensin-converting-enzyme and of inactive renin were demonstrated in the former group of patients. Thus, the extrarenal abnormalities found in IDDM patients with hypertension are more closely associated to the presence of albuminuria than to the elevation of blood pressure, indirectly supporting the hypothesis that hypertension per se is not the cause of these abnormalities in the IDDM patients with nephropathy. Furthermore, the present study does not disclose a genetic disposition to hypertension in IDDM patients with elevated UAE.     

Genetics in hypertension research. What can we learn from it regarding common essential hypertension?

Essential hypertension is a polygenic disease. Various genes responsible for rare monogenic forms of hypertension have been identified in the recent years. These are glucocorticoid remediable aldosteronism (GRA), Liddle's syndrome and apparent mineralocorticoid excess (AME). A fourth form, the Bilginturan syndrome is associated with brachydactyly and resembles essential hypertension. The investigations of the pathomechanisms in these rare diseases can help us to understand common hypertension.     

Treatment of hypertension in the presence of coexisting medical conditions

Treating hypertension reduces morbidity and mortality. Unfortunately, hypertension often exists in patients with other medical conditions. In these patients, the selection of an antihypertensive agent is often influenced by the presence of the coexisting condition. Conversely, the treatment of the coexisting medical condition may be influenced by the presence of hypertension. Given the vast array of antihypertensive medications available today, appropriate treatment of both hypertension and coexisting conditions can be achieved with careful selection of medications. This review discusses factors to consider when treating elderly patients with hypertension with the following coexisting conditions: dyslipidaemia, glucose intolerance, sexual dysfunction, cardiovascular disease, pulmonary disease, renal disease and neuropsychiatric disorders. Hypothyroidism, hyperthyroidism and various states of high cardiac output may cause hypertension. These conditions should be identified, since they are often treatable with subsequent resolution of the hypertension.     

The effect of different factors on cardiac rhythm variability in patients with arterial hypertension

The purpose of this study was to evaluate the influence of different factors, among them left ventricular hypertrophy (LVH) on long-term heart rate variability (HRV) in patients with hypertension. 38 patients with arterial hypertension of different genesis were included in the study. Ischemia was excluded in all the patients by the data of clinical and instrumental methods of investigation. LVH data obtained from HRV of 20 healthy subjects was used as control. HRV was evaluated by estimating variations for short intervals of a rhythmogram (VSI). A HRV decrease did not depend on sex, but essentially depended on patients'a age, disease duration and the form of hypertension. A marked tendency leading to the rate variability decrease was observed only in moderate LVH. In cases of original LVH variability data did not differ from those in patients without signs of LVH. Low or marginal HRV was more often observed in patients with essential hypertension and in those with hypertension of endocrine genesis. As far as renal hypertension is concerned low variability was less frequent. There were a lot of factors which affect the change of HRV. The more significant of them were the patients' age, hypertension genesis and form of hypertension. Factors leading to the rate variability decrease were the following age above 40, endocrine or essential hypertension and moderate form of hypertension.     

Arterial hypertension: its impact on perioperative morbidity and mortality

Chronic hypertension is associated with structural as well as functional changes of the vasculature, in particular of the coronary, cerebral and renal circulation. It is important to realise that [1] functional changes are often the result of structural changes, [2] the longer lasting the hypertension, the slower and less complete the regression of structural changes, and [3] acute "normalisation" of arterial pressure in long-standing hypertension may initially induce functionally subnormal smooth muscle and/or cardiac activity because the structure of the cardiovascular system is adapted to function at elevated pressures. Despite a multitude of studies, the impact of hypertension on peri-operative morbidity and mortality remains controversial. There are as many studies seeming to suggest that preoperative hypertension correlates with adverse outcome as there are studies that fail to establish such a relationship. When looking at the combined evidence, one is inclined to conclude that hypertension is a predictor of "soft" outcomes (e.g. peri-operative myocardial ischaemia and transient post-operative neurologic deficit) rather than an independent predictor of "hard" outcomes (e.g. unstable angina, myocardial infarction and cardiac death). In view of lack of convincing outcome data, it is impossible to recommend a generally acceptable management strategy for the hypertensive patient. Although, in general, a gradual reduction of blood pressure over a period of weeks to months is the optimal therapeutic approach, we will be hard-pressed delaying surgery for the sole purpose of "better blood pressure control". With full appreciation and detailed knowledge of the pathophysiology of hypertension, combined with sophisticated haemodynamic monitoring and interventions in the peri-operative period, acutely anaesthetising an inadequately treated hypertensive patient will probably not adversely affect his outcome. Delaying surgery for additional work-up may possibly improve outcome in patients with target organ disease, evidence of secondary hypertension, in the most severe forms of hypertension or sudden-onset hypertension.     

Arterial hypertension in patients with primary glomerulonephritis

Arterial hypertension is a state of blood pressure permanently higher than 160/90 mm Hg (21.3/12.6 kPa). The renal cause of hypertension occurs in about 10% of all cases. The aim of this article was to establish the frequency, the level, and the connection of the hypertension in different types of primary glomerulonephritis. In this study 90 patients with primary glomerulonephritis were observed. Hypertension was present in 45 patients (50%) and different frequency were noticed in different types of glomerulonephritis. The smallest frequency was recorded in the group with minimal changes and IgA nephritis. In the group with mesangioproliferative glomerulonephritis 52% of patients had hypertension and in the group with focal segmental sclerosis 78%. The most frequent hypertension was observed in the group with rapidly progressive glomerulonephritis. Renal failure was more frequent in patients with hypertension. Different frequencies of hypertension was established in different types of glomerulonephritis. It was not severe and was well controlled by remedies. In most cases it suggest a severe glomerular lesions and fast progression of the disease.     

Expression of endothelin-1 in the lungs of patients with pulmonary hypertension

BACKGROUND: Pulmonary hypertension is characterized by an increase in vascular tone or an abnormal proliferation of muscle cells in the walls of small pulmonary arteries. Endothelin-1 is a potent endothelium-derived vasoconstrictor peptide with important mitogenic properties. It has therefore been suggested that endothelin-1 may contribute to increases in pulmonary arterial tone or smooth-muscle proliferation in patients with pulmonary hypertension. We studied the sites and magnitude of endothelin-1 production in the lungs of patients with various causes of pulmonary hypertension. METHODS: We studied the distribution of endothelin-1-like immunoreactivity (by immunocytochemical analysis) and endothelin-1 messenger RNA (by in situ hybridization) in lung specimens from 15 control subjects, 11 patients with plexogenic pulmonary arteriopathy (grades 4 through 6), and 17 patients with secondary pulmonary hypertension and pulmonary arteriopathy of grades 1 through 3. RESULTS: In the controls, endothelin-1-like immunoreactivity was rarely seen in vascular endothelial cells. In the patients with pulmonary hypertension, endothelin-1-like immunoreactivity was abundant, predominantly in endothelial cells of pulmonary arteries with medial thickening and intimal fibrosis. Likewise, endothelin-1 messenger RNA was increased in the patients with pulmonary hypertension and was expressed primarily at sites of endothelin-1-like immunoreactivity. There was a strong correlation between the intensity of endothelin-1-like immunoreactivity and pulmonary vascular resistance in the patients with plexogenic pulmonary arteriopathy, but not in those with secondary pulmonary hypertension. CONCLUSIONS: Pulmonary hypertension is associated with the increased expression of endothelin-1 in vascular endothelial cells, suggesting that the local production of endothelin-1 may contribute to the vascular abnormalities associated with this disorder.