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

Systemic hypertension was diagnosed in 58 of 188 untreated cats referred for evaluation of suspected hypertension-associated ocular, neurologic. cardiorespiratory, and urinary disease, or diseases frequently associated with hypertension (hyperthyroidism and chronic renal failure). Hypertensive cats were significantly older than normotensive subjects (13.0 +/- 3.5 years versus 9.6 +/- 5.0 years; P < .01), and had a greater prevalence of retinal lesions (48 versus 3%; P < .001), gallop rhythm (16 versus 0%; P < .001), and polyuria-polydipsia (53 versus 29%: P < .01). Blood pressure was significantly higher (P < .001) in cats with retinopathies (262 +/- 34 mm Hg) than in other hypertensive animals (221 +/- 34 mm Hg). Hypertensive cats had a thicker interventricular septum (5.8 +/- 1.7 versus 3.7 +/- 0.64 mm; P < .001) and left ventricular free wall (6.2 +/- 1.6 versus 4.1 +/- 0.51 mm; P < .001) and a reduced diastolic left ventricular internal diameter (13.5 +/- 3.2 versus 15.8 +/- 0.72 mm; P < .001) than control cats. Left ventricular geometry was abnormal in 33 of 39 hypertensive subjects. No significant difference was found in age or blood pressure at the initial visit between cats that died or survived over a 9-month period after initial diagnosis of hypertension. Mean survival times were not significantly different between hypertensive cats with normal and abnormal left ventricular patterns. Further prospective studies are needed to clearly identify the factors involved in survival time in hypertensive cats.
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PMID:Spontaneous feline hypertension: clinical and echocardiographic abnormalities, and survival rate. 1256 32

About 3% of our hypertensive patients have high blood pressure induced by corticosteroids. Muscle weakness, tiredness, polyuria and polydipsia may indicate hypokalaemia. Hypokalaemic hypertension in the presence of a low plasma renin activity is the typical finding of corticosteroid hypertension. The most frequent cause of corticosteroid hypertension is primary aldosteronism (Conn's syndrome) due to an adrenal adenoma or bilateral hyperplasia of the adrenal glands. The plasma concentration of aldosterone and the ratio between plasma aldosterone and renin concentrations are high, and the kaliuresis exceeds 30 mmol/24 h in the presence of hypokalaemia. Adrenal carcinomas are rare and very malignant. The localization of an adrenal tumour is made by computer tomography (CT-scan) or nuclear magnetic resonance imaging and by measurement of the aldosterone/cortisol concentrations in the adrenal venous blood. Adenomas are removed under laparoscopy, and adrenal hyperplasias are treated with spironolactone (50-400 mg daily) or amiloride (5-30 mg daily). In rare cases (<1%), excessive stimulation of the mineralocorticoid receptor is due to cortisol (apparent mineralocorticoid excess, Cushing's disease, liquorice, or hereditary deficiency of 11beta-hydroxysteroid dehydrogenase) or to a chimeric gene coding for 11beta-hydroxylase (CYP11B1/CYP11B2). In these rare cases, the synthesis of aldosterone is under the control of the adrenocorticotrophic hormone, so treatment with glucocorticoids (dexamethasone 0.25-1.0 mg daily) is therefore possible (glucocorticoid-remediable aldosteronism). Excessive deoxycorticosterone (DOC) causes the same symptoms and signs as hyperaldosteronism. Excessive DOC is found in patients with adrenal tumours that secrete DOC, in those with hereditary or acquired disorders with dysfunctioning glucocorticoid receptors, or in those with congenital hyperplasia of the adrenal glands (deficiency of 17alpha-hydroxylase or 11beta-hydroxylase). Liddle's syndrome is a constitutive hyperactivity of the transepithelial transport of sodium, which under normal conditions is controlled by the mineralocorticoid receptor. Plasma renin and aldosterone concentrations are suppressed and the plasma potassium concentration may be normal. In contrast, plasma aldosterone and renin concentrations are increased in patients with hypokalaemic hypertension which represents secondary aldosteronism. The increased aldosterone is the consequence of stimulated renin activity due to renal or renovascular or other disorders, antihypertensive drugs or other medications. In conclusion, a work-up for corticosteroid-induced hypertension is indicated in patients with hypokalaemic hypertension and in those with severe hypertension even in the absence of hypokalaemia, and in hypertensive patients with a family history of cardiovascular diseases.
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PMID:Investigating mineralocorticoid hypertension. 1292 4

The relative contribution of circulating versus tissue renin-angiotensin systems to the tissue expression of angiotensin peptides in the kidney remains unresolved. To address this issue, intrarenal and urinary levels of the peptide products of the renin-angiotensin system were assessed in a tissue angiotensin-converting enzyme knockout (tisACE-/-) mouse model. Systolic blood pressure was significantly lower (64.6+/-3.6 versus 81.4+/-4.5 mm Hg; P<0.02) and urinary volume was increased (7.25+/-0.86 versus 2.86+/-0.48 mL/d; P<0.001) in tisACE-/- mice compared with wild-type mice. Intrarenal angiotensin II was 80% lower in tisACE-/- mice compared with wild-type mice (5.17+/-0.60 versus 25.5+/-2.4 fmol/mg protein; P<0.001). Intrarenal angiotensin I levels also declined by a comparable extent (73%) in the tisACE-/- mice (P<0.01). Intrarenal angiotensin-(1-7) concentrations were similar between the strains, but the ratio of intrarenal angiotensin-(1-7) to angiotensin II and angiotensin I in tisACE-/- mice increased 470% and 355%, respectively, compared with wild-type mice. Urinary excretion of angiotensin II and angiotensin-(1-7) were not different, but the excretion of angiotensin I increased 270% in tisACE-/- mice (P<0.01). These studies suggest 2 potential mechanisms for the reduction of intrarenal angiotensin II in tisACE-/- mice: (1) an attenuated capacity to form angiotensin II by renal angiotensin-converting enzyme and (2) significant depletion of its direct precursor angiotensin I in renal tissue. Sustained intrarenal levels of angiotensin-(1-7) may contribute to chronic hypotension and polyuria in tisACE-/- mice, particularly in the context of depleted angiotensin II in the kidney.
Hypertension 2004 Apr
PMID:Depletion of tissue angiotensin-converting enzyme differentially influences the intrarenal and urinary expression of angiotensin peptides. 1498 Oct 53

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

We present a 54-yr-old woman with ectopic corticotropin syndrome caused by a neuroendocrine tumor of the pancreas. At initial presentation, the patient suffered from diarrhea, heartburn, and nonspecific abdominal pain. There was no evidence of Cushing's syndrome. A neuroendocrine tumor in the head of the pancreas with metastases into peripancreatic lymph nodes was diagnosed and completely resected. Fourteen months later, abdominal computed tomography and scintigraphy with (111)In-labeled octreotide suggested relapse of the tumor. The patient again had no evidence of Cushing's syndrome. A second in toto tumor resection was performed. Another 8 months later, the patient developed forgetfulness, depressive episodes, muscle weakness, new-onset hypertension, hypokalemia, plethora, diabetes mellitus, polyuria, and weight loss. Endocrine testing suggested a source of ectopic ACTH production. An octreotide scan showed an intense uptake ventromedial of the left kidney, an area that showed a mass lateral of the superior mesenteric artery on abdominal magnetic resonance imaging. A complete pancreatectomy with splenectomy and left-sided adrenalectomy were performed. At this second relapse, this neuroendocrine tumor clinically had changed its hormonal profile. Immunohistochemically, in contrast to primary tumor and first relapse, we found strong immunostaining for ACTH in tumor cells of the second relapse and a MIB-1 index greater than 20%. To our knowledge, this is the first report describing a pancreatic neuroendocrine tumor that started to secrete ACTH de novo at the time of the second relapse after two former complete tumor resections. This case underscores the pluripotency of neuroendocrine tumor cells and the importance of keeping in mind a possible shift in hormone production during tumor evolution and progression.
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PMID:Pancreatic neuroendocrine tumor with ectopic adrenocorticotropin production upon second recurrence. 1529 97

We present three cases of primary hyperparathyroidism (PHPT) in pregnancy. The clinical presentation of PHPT is not altered by pregnancy; however, the disease constitutes a serious risk for the foetus and the newborn. Although rare, hypercalcaemia should be suspected in pregnant women presenting with polydipsia, polyuria and fatigue as well as hypertension or preterm labour.
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PMID:[Primary hyperparathyroidism in pregnancy]. 1615 62

Despite advances in treatment, twin-to-twin transfusion syndrome (TTTS) still carries a high risk for perinatal mortality and morbidity. Simple blood transfer from the donor to the recipient twin cannot explain all of the features of this disease, in particular the recipient's hypertensive cardiomyopathy. We report a case in which TTTS resulted in preterm delivery with early neonatal death of both twins, allowing assessment of the renin angiotensin system (RAS) status of each fetus, both by cord blood renin and aldosterone assay and by renal immunohistochemistry. The donor had severe oliguria/oligohydramnios, whereas the recipient, in addition to severe polyuria/polyhydramnios, had cardiomyopathy, atrioventricular regurgitation, and ascites. Although immunohistochemistry demonstrated that renal secretion of renin was up-regulated in the donor and down-regulated in the recipient, cord blood levels of renin and aldosterone were similar, with high renin levels in both twins. This observation supports the hypothesis that despite renal RAS down-regulation, the recipient is exposed to RAS effectors elaborated in the donor and transferred via placental shunts. This may contribute to cardiomyopathy and hypertension in the recipient, which cannot be accounted for by hypervolemia alone. We thus hypothesized that in TTTS, the recipient's hypertensive cardiomyopathy could be due to a mechanism similar to the classical model of hypertension referred to as "2 kidneys-1 clip." Thus the hypovolemic donor twin, comparable to the clipped kidney, produces vasoactive hormones that compromise the recipient, comparable to the normal kidney, causing hypertension and cardiomyopathy.
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PMID:Paradoxic activation of the renin-angiotensin system in twin-twin transfusion syndrome: an explanation for cardiovascular disturbances in the recipient. 1618 93

Non-alcoholic steatohepatitis (NASH) is one of the most common liver disorders. This is highly prevalent in obese and diabetic subjects. Persons with central obesity are at particular risk. Other clinical predictors are age more than 40-50 years and hyperlipidemias, but none of these factors is invariable for causation of NASH. Other reported associations are, celiac disease, Wilson's Disease and few other metabolic diseases. Drugs, particularly amiodarone, tamoxifen, nucleoside analogues and methotrxate have also been linked to NASH. The disease is evenly distributed in both sexes but advanced disease is more common in women. Ethnic variation exists and African Americans are less affected than Hispanic Americans. Specific clinical features of NASH are infrequent. Patients usually come to clinical attention by elevated liver enzymes found on routine evaluation but on history, about two third of patients will admit to have mild fatigue and about half will report right upper quadrant pain. Rarely, patient may present with a complication of cirrhosis. Physical examination may reveal hepatomegaly and splenomegaly. Research in last few years has stressed that development of steatosis, stetohepatitis, fibrosis with subsequent cirrhosis are most probably the result of insulin resistance. Therefore, clinical features may reflect existence of insulin resistance. Obesity, particularly central obesity is most important of these. Patients may have sleep apnea syndrome. Hypertension and manifestations of diabetes mellitus like polyuria, polydypsia, and neurological deficits may occur. Patients may have varying combination of obesity, diabetes, hyperlipidemia, hypertension and impaired fibrinolysis (syndrome X). Children with insulin resistance may show acanthosis nigricance. Patients with polycystic ovary syndrome, which consists of insulin resistance, diabetes, obesity, hirsutism, oligo or polymenorrha and hyperlipidemia may have NASH. Other rare manifestations of insulin resistance, which can be seen in patients of NASH are lipomatosis, lipoatrophy/lipodystrophy and panniculitis. Most other rare conditions known to cause NASH like peroxisomal diseases, mitochondialpathies, Weber-Christian disease, Mauriac syndrome, Madelung's lipomatosis and abetaliopprotenemia also have insulin resistance. This is believed that primary defect underlying insulin resistance is impairment in postreceptor pathways (through tyrosine kinase activity) of insulin action. Primary defect in insulin receptors appear uncommon. This results in down regulation of insulin receptor substance 1 (IRS-1) signaling by excess free fatty acids. In muscle, activated IRS-1 promotes translocation of glucose transporter protein 4 (GLUT4) to cell membrane. As a result, monocyte glucose uptake by GLUT4 increases glucose disposal from blood and reduced need for insulin. PKC-0 is a likely candidate as serine kinase in muscle regulated by fatty acids that can impair the activation of IRS-1. Insulin resistance is usually evaluated by fasting insulin levels, Quantitative Insulin Check Index (QUICKI) and Homeostasis Model Assessment of Insulin Resistance (HOMA), C-peptid/insulin ratio oral glucose tolerance test and hyper insulinemic euglycemic clamp. The clamp technique is considered the gold standard.
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PMID:Insulin resistance and clinical aspects of non-alcoholic steatohepatitis (NASH). 1619 20

Polycystic kidney disease, an inherited systemic disorder, is characterized by the development of multiple cysts in the kidneys and other organs. Patients can present at any age, but more often come to clinical attention (unless there is a family history) after age 30. Patients who are diagnosed before age 30 have a worse renal survival. Although palpation of the abdomen occasionally provides a clue to the presence of polycystic kidney disease, radiographic procedures most often suggest the diagnosis. Mutations in the PKD1 or PKD2 genes give rise to cyst formation. Flank pain, hematuria, polyuria, nephrolithiasis, urinary tract infections, and hypertension may be part of the syndrome of polycystic kidney disease. It is the fourth most common cause of end-stage renal disease. Blood pressure treatment goals are less than 130/80 mm Hg. Treatment should include the use of angiotensin-converting enzyme inhibitors.
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PMID:Polycystic kidney disease. 1622 65

Studies using a model of non-infectious diarrhea, have shown that increasing fecal mass by using laxatives resulted in greater fecal losses of nutrients and lower intestinal absorption. In the present study we used a diuretic to determine if increasing urine volume could result in greater urinary losses of essential nutrients. This is a relevant question because diuretics are widely and successfully used in the treatment of diseases associated with water retention and hypertension. They are known to increase potassium losses. However, there is less information on the effect of diuretics on the urinary losses of essential nutrients. Accordingly, urinary nitrogen, phosphorous, sodium, potassium, magnesium, zinc and retinol were measured in young rats consuming increasing concentrations of furosemide (0, 0.5, 1.0, 1.5 mg/g diet) in the diet over 15 days. The results showed that dietary furosemide caused a dose-dependent polyuria. In addition it reduced food intake and feed efficiency and leaded to poor growth and greater urinary losses of all the measured nutrients and electrolytes. These losses were proportional to urine volume and represented an important fraction of the rats daily intake. The losses were negatively associated with the body and liver content of the same electrolytes and nutrients. In general, this study showed that the diuretic furosemide caused malnutrition in a short period of time by reducing food intake as well as the capacity of retaining macro and micronutrients including the liposoluble vitamin A in a relatively short period of time. This study, together with our previous studies on diarrhea, indicate that proper nutrient utilization requires both an adequate intestinal and renal function.
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PMID:Effect of the diuretic furosemide on urinary essential nutrient loss and on body stores in growing rats. 1633 25


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