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)

The healthy term, and particularly the premature infant, is born with a very low glomerular filtration rate (GFR), controlled by a delicate balance of intrarenal vasoconstrictor and vasodilator forces. Vasoactive disturbances can easily further reduce the already low GFR. The newborn infant is thus prone to develop vasomotor nephropathy (VMNP) or acute renal failure (ARF). The main causes for ARF at this young age are prerenal mechanisms, and include hypotension, hypovolemia, hypoxemia perinatal asphyxia, and neonatal septicemia. Other causes include the administration of angiotensin converting enzyme inhibitors, indomethacin and tolazoline. The most-important factors governing the ultimate renal prognosis are the severity of the underlying disorder, the rapidity of an accurate diagnosis, prompt treatment, and avoidance of severe iatrogenic complications. The immediate treatment is of particular importance in VMNP, i.e., prerenal ischemic ARF, and consists of correcting abnormalities in fluid homeostasis and reduction of the complications of the acute azotemic state (uremia, hyperkalemia, acidosis, and hypertension). In severe and prolonged (established) ARF, temporary dialysis therapy may be indicated. Prerenal ARF with oliguria or anuria warrants immediate volume resuscitation. Special attention should be given to infants with congestive heart failure (CHF). The sick neonate with persistent oliguria and CHF should be treated with intravenous dopamine. Furosemide (FM) is the second line of therapy for babies with indomethacin-induced ARF. In most other conditions, the therapeutic effect of FM is limited to a transient increase in urine flow, without improving basic renal function. The special conditions of the maturing kidney have to be appreciated in order to protect babies from undue renal injury. With the increasing knowledge of the mechanisms governing the development of ARF, progress has been made in the development of new treatment modalities. For example theophylline, calcium antagonists, ATP-MgCl2, thyroxine, and a variety of cytokines may in the near future be used to prevent or ameliorate VMNP and/or recently established ARF. With a combination of time-honored and new therapeutic strategies, there may well be a brighter future for neonates with vasomotor, prerenal, ischemic ARF.
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PMID:The stressed neonatal kidney: from pathophysiology to clinical management of neonatal vasomotor nephropathy. 1075 64

Haemolytic uraemic syndrome (HUS) associated with Escherichia coli O157:H7 is the commonest cause of acute renal failure (ARF) in childhood. Production of verotoxin by the organism is pivotal in the pathogenesis of the disease. Verotoxin binds to a receptor on blood and endothelial cells, expressed as the P1 blood group antigen on red blood cells. A protective effect of the P1 phenotype has been proposed in this disease. This study investigates prognostic factors and the relationship between outcome and P1 phenotype in 27 cases of diarrhoea-associated HUS. A poor outcome as defined by the presence of chronic renal failure (CRF), hypertension or proteinuria on 6 month follow-up was associated with the age of the patient at presentation and with the following clinical markers: maximum WBC and duration of raised WBC, duration of anuria and duration of need for dialysis. None of these outcome measures or prognostic factors, and no extra-renal manifestations of the disease were associated with P1 phenotype.
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PMID:Haemolytic uraemic syndrome: prognostic factors. 1081 11

Nitric oxide (NO) has some relevance to the pathophysiology of hypertension. We examined the distribution of endothelial nitric oxide synthase (ecNOS4) gene polymorphism in patients with essential hypertension (n = 107) in comparison with healthy subjects (n = 362), and then studied the possibility that ecNOS4 gene polymorphism affects changes in blood pressure (BP) due to water load in hemodialysis patients. Though the NO metabolite (NOx) level in subjects with the a allele (31.2 +/- 1.76 micromol/l) was significantly lower than in those without the a allele (35.6 +/- 0.90 micromol/l) (p = 0.0263), we found no association between this gene polymorphism and essential hypertension. However, there still remains the possibility that the NO response to elevation of BP might be suppressed in patients with hypertension. In order to examine the association between ecNOS4 gene polymorphism and volume-dependent hypertension, 181 hemodialysis patients with complete anuria were recruited. Depending on the increase in mean BP (mm Hg) divided by percent increase in body weight (deltaBP/deltaBW), patients were divided into high responders (High-R: deltaBP/deltaBW >2.0 mm Hg; n = 90) and low responders (Low-R: deltaBP/deltaBW <2.0 mm Hg; n = 91). In the High-R group, the frequencies of a/a, b/a and b/b genotypes were 1.1, 32.1 and 66.8%, respectively, and in the Low-R group, these frequencies were 1.1, 9.4 and 89.5%, respectively. The relative risk for those in the High-R group conferred by the ecNOS4 a allele (b/a + a/a) was 3.64 (95% confidence intervals: 1.60-8.24, p = 0.0089). This study did not show a strong involvement of ecNOS4 gene polymorphism, at least in the basal NO production in patients with essential hypertension, however, it indicated that ecNOS4 gene polymorphism might modulate changes in BP due to water load in patients on hemodialysis, thus indicating that these polymorphisms may be involved in the pathophysiology of volume-dependent hypertension.
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PMID:An intron 4 gene polymorphism in endothelial cell nitric oxide synthase might modulate volume-dependent hypertension in patients on hemodialysis. 1086 38

Thirty-six patients on peritoneal dialysis (PD) for more than ten years in six North American centers were analyzed retrospectively. In the six centers, the percentage of patients surviving for more than ten years varied between 0.8% and 7.3%. The study group included 27 females and 9 males aged 38.6 +/- 14.2 years [mean +/- standard deviation (SD)] at the start of treatment. Of the 36 patients, 28 were Caucasian. The most common cause of end-stage renal disease (ESRD), present in 12 patients, was chronic glomerulonephritis. Only 4 patients had diabetes. At the beginning of the study, 19 patients had hypertension (the most common comorbid condition); 11 had no comorbid conditions at the start. Creatinine clearance at the start was 4.12 +/- 3.5 mL per minute, and the mean duration to anuria was 51 +/- 25 months. Mean initial body weight was 55 +/- 9 kg, and mean body surface area was 1.5 +/- 0.2 m2. Serum albumin levels showed an increase from 33.8 +/- 3.6 g/L at the start of the study to 38.2 +/- 3.9 g/L at the end. Hospitalization rate was low at 0.5 +/- 0.3 admissions per patient-year, and duration of hospitalization was 4.8 +/- 3.7 days per patient-year. Peritonitis was the most common cause of hospitalization. The mean peritonitis rate was 1 episode every 52 +/- 48 patient-months. There were 36 catheter changes in 18 patients; 16 patients had a single PD catheter throughout the period of study. Autonomous hyperparathyroidism was the most common long-term complication. At the end of the study period, 11 patients were still on PD, 9 had died, 5 had been transferred to hemodialysis (HD), 1 was alive with a functioning allograft, and 1 was lost to follow-up. We conclude that patients who survive longer than ten years on PD are most likely to be young Caucasian females, small in body size, who are non diabetic, with few comorbid conditions. These long-term survivors have few hospitalizations, and their peritonitis rate is low. In this group of patients, severe autonomous hyperparathyroidism is the most common long-term complication.
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PMID:Patients on chronic peritoneal dialysis for ten years or more in North America. 1091 58

Every year in France, about 100 children, most of them less than 3 years old, have typical diarrhea-associated HUS (D + HUS). Evidence of exposure to verotoxin producing E. coli (VTEC), mostly the O157: H7 serotype, is demonstrated in about 85% of cases. A prodromal illness of acute gastroenteritis with diarrhea, often bloody, precedes the HUS by 1 to 15 days. HUS onset is sudden, with the typical association of hemolytic anemia with fragmented red blood cells, thrombocytopenia and acute renal insufficiency. Involvement of other organs than the kidneys may occur, such as severe hemorrhagic colitis with rectal prolapse, bowel wall necrosis or secondary stenosis, acute pancreatitis, central nervous system involvement which determines the vital outcome. Early accurate supportive treatment allows a current mortality rate below 5%, with most deaths due to central nervous system involvement. Five to 10% of children develop end stage renal disease, rarely directly, more often after having recovered some renal function with chronic renal insufficiency during a few years. After 15 or more years follow-up, at least one third of patients have some degree of proteinuria and/or hypertension, and eventually chronic or end stage renal failure. Predictive features of poor renal outcome at the acute phase are severe gastrointestinal involvement, severe CNS involvement, polyncleosis over 20,000/mm3, and duration of initial anuria longer than one week. The role of VTEC in D + HUS makes the disease a public health problem. Preventive measures are essential.
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PMID:[Post-diarrhea hemolytic-uremic syndrome: clinical aspects]. 1158 27

ABSTRACT. Licorice-associated hypertension is thought to be due to increased renal sodium retention. The active compound of licorice, glycyrrhetinic acid (GA), inhibits renal 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) and by that mechanism increases access of cortisol to the mineralocorticoid receptor that causes renal sodium retention and potassium loss. In addition, a direct vascular effect of 11beta-HSD activity has recently been incriminated to promote hypertension, a contention based on in vitro observations. This investigation was designed to establish whether this extrarenal effect of 11beta-HSD is relevant for BP regulation and potassium concentrations in plasma. In a prospective, double-blind, cross-over study, seven patients with anuria on chronic hemodialysis were randomly assigned after a baseline period of 2 wk to placebo or GA (1 g/d) for 2 wk, separated by a washout phase of 3 wk. The ratio of plasma cortisol/cortisone, determined by gas chromatography-mass spectrometry, increased in all patients after GA intake (F = 9.705; P < 0.004), which indicates inhibition of 11beta-HSD. Twenty-four-hour BP values did not change throughout the study. The increase of the plasma cortisol/cortisone ratio was paralleled by a decline in the plasma potassium concentration in every patient. The mean +/- SD plasma potassium concentration decreased from 5.5 +/- 0.6 mM/L at baseline to 4.9 +/- 0.7 and 4.5 +/- 0.8 mM/L after 1 and 2 wk on GA, respectively (F = 9.934, P < 0.003). Extrarenal 11beta-HSD activity influences serum potassium concentrations but does not regulate BP independently of renal sodium retention.
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PMID:Glycyrrhetinic acid decreases plasma potassium concentrations in patients with anuria. 1175 37

We studied the features of acute renal failure (ARF) in elderly patients treated in a hospital, without an intensive care unit, to identify etiological factors and establish adequate preventive measures and treatment. During twelve consecutive months we studied prospectively 99 patients with ARF diagnosed by conventional criteria, an incidence of 1,238 cases per million per year. ARF affected 1.78% of patients admitted to hospital. We analyzed age, sex, serum creatinine, diuresis, etiology, type of ARF, preexisting chronic diseases, treatment, complications and outcome. Preexisting chronic diseases were common, the most frequent being hypertension (54%) and diabetes (39%). Previous treatments for cardiovascular diseases were frequent (angiotensin-renin system blockade 35.4%, diuretics 50.5%). 79% of ARF arose in hospital, 21% outside hospital. ARF was pre-renal in 60%, renal in 31% and post-renal in 9%. 34.7% were caused by volume depletion, 23.4% by low cardiac output and 23.4% by infection. 44.4% of ARF patients had oliguria or anuria latrogenic factors contributed to the ethiology of ARF in 35.3% of patients. Hospital stay was doubled by ARF the presence of ARF and the mortality was 36.4%. The rate was higher in ARF arising in hospital than in ARF acquired before admission. Factors that had a significant influence on the mortality rate were comorbid conditions, oliguroanuria, ARF of renal origin and serum albumin. We conclude that ARF has a high incidence, morbidity and mortality in this elderly population. Volume depletion, associated cardiovascular pathology and pharmacological treatment are important etiological factors in those with ARF outside hospital. Adequate treatment of ARF and avoidance of nephrotoxic medications are necessary in hospital.
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PMID:[Characteristics of acute renal failure in elderly patients admitted to a small town hospital]. 1251 88

OBJECTIVE: To describe an unusual case with clinical features of the antiphospholipid syndrome. DESCRIPTION: White child, two years and six months old, with renal failure, renal arterial thrombosis, and diagnosis of antiphospholipid syndrome was hospitalized with a history of abdominal pain, pallor, lethargy, and anuria for 36 hours. On physical examination, the patient showed malnutrition, high blood pressure, moderate edema, and hypochondrial pain. Laboratory findings included: urea=112mg/dl, serum creatinine= 4.5 mg/dl, blood pH= 7.47, blood bicarbonate= 12.8 mmol/L, K=7.2 mEq/L. Peritoneal dialysis was started and maintained for 11 days. After 7 weeks, the patient still needed anti-hypertensive drugs and the renal function was still abnormal. Renal biopsy was performed and revealed renal infarction. The result of Doppler ultrasonography revealed absent renal blood flow on the right side. Renal arteriography showed total occlusion of the right renal artery. Results for collagen diseases were negative. A right nephrectomy was performed and the blood pressure was controlled. The child was hospitalized again at 5 years and 8 months old with episodes of absence seizures and abdominal and precordial pain. Anticardiolipin antibody test was positive. The child is now 7 years old, asymptomatic, with negative anticardiolipin antibody, and has been under regular follow-up. COMMENTS: Children with arterial thrombosis should be investigated for a possible association with the antiphospholipid antibody syndrome even in the absence of collagen disease.
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PMID:[Renal arterial thrombosis and the antiphospholipid antibody syndrome: a case report] 1464 33

Atherosclerotic renal artery stenosis (RAS) is an increasingly important cause of end-stage kidney disease, and may cause hypertension, progressive renal failure, and recurrent pulmonary edema. Herein, we report two episodes of anuria and acute pulmonary edema associated with losartan treatment in a hypertensive patient with preexisting severe renal artery stenosis in a solitary kidney. After successful percutaneous renal balloon angioplasty procedure, urine flow was started immediately, despite 10 days of anuria. Blood pressure measurements were still at acceptable levels with a low dose Beta blocker, and serum creatinine levels were normal even after eight months. PTRA should be done in such patients, even with prolonged anuria. Physicians who recommend angiotensin receptor blockers in patients with RAS, especially in patients wih hypovolemia or a solitary kidney, should be careful about this complication.
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PMID:Two episodes of anuria and acute pulmonary edema in a losartan-treated patient with solitary kidney. 1468 57

Severe mid-trimester twin-twin transfusion syndrome (TTS) complicates about 15% of monochorionic twin pregnancies. If left untreated, the mortality is 80-100%. The pathophysiological prerequisite for the onset of TTS is unequal blood flow via arteriovenous placental anastomoses from the so-called donor to the recipient twin. This can result in hypovolemia, hypotension and oligo- or anuria in the donor, and hypervolemia, hypertension, polyuria and finally heart failure in the recipient. Leading sonographic signs of TTS include severe oligo- or anhydramnios and a small or absent bladder filling in the donor in contrast to polyhydramnios with increased bladder filling in the recipient. Patients might present with clinical symptoms due to massive polyhydramnios. In severe mid-trimester TTS, fetoscopic laser occlusion of the anastomosing vessels on the placental surface under local anaesthesia plus subsequent amniodrainage is the most promising therapeutic option at present. In acute TTS after 26 weeks of gestation, amniodrainage is the therapy of choice. All patients suspected of this high-risk condition should be referred to a specialized fetal medicine centre.
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PMID:How can we diagnose and manage twin-twin transfusion syndrome? 1527 16


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