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

Criteria for the screening, diagnosis and therapy of primary aldosteronism (PA) were defined on the basis of its symptoms analysis in 40 PA patients. A diagnosis of PA was proved in 4.12% of 970 patients admitted for arterial hypertension. The presence of polyuria, nocturia, neuromuscular disorders, hypertension, hypopotassaemia, alkalosis, elevated urinary potassium excretion, improving after Spironolactone, was most valuable for the purposes of screening. High plasma aldosterone concentration (PAC) and suppressed renin activity (PRA) provided evidence of the presence of PA. The most successful technique to differentiate aldosterone producing adenoma (APA) from idiopathic hyperaldosteronism (IHA) proved to be adrenal phlebography combined with determination of PAC in the adrenal veins. APA was associated with a 5.9 fold higher PAC in the vein of the adenoma - affected adrenal in contrast with a symmetric PAC rise in both adrenal veins in IHA. A paradoxical decrease of PAC occurred in the peripheral blood of most patients with APA after standing up, but 23.8% exhibited the same orthostatic increase as IHA patients. In all APA patients, unilateral adrenalectomy eliminated the symptoms of hyperaldosteronism and improved or cured hypertension. Spironolactone was indicated preoperatively for all surgical candidates, for non-operated APA patients, and for all IHA patients.
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PMID:Primary aldosteronism -- screening, diagnosis and therapy. 702 94

Four cases of BARDET-Biedl syndrome (BBS) are described which all suffer from renal abnormalities. Polyuria or polydipsia with impairment of renal concentration capacity were the earliest signs of renal dysfunction. Renal insufficiency developed in 3 cases and hypertension in two. Urographic abnormalities were demonstrated in all patients. The most remarkable features were cystic spaces communicating with the calices and lobulation of kidney. Caliceal clubbing and caliectasis surrounded by narrowed, unscarred parenchyma were frequent findings. Previous investigators reported various renal histological pictures in BBS. We found tubulo- interstitial lesions in all cases. Features of dysplasia and cystic formations were less frequent. Mesangial proliferation was not noted. Ultra-structural changes in the glomerular basement membrane were not observed in this study. Thirty-one of 32 recently reported cases of BBS included renal lesions which are the major cause of death. It is therefore suggested that renal abnormalities are accepted as the cardinal feature of this syndrome.
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PMID:Renal abnormalities in the Bardet-Biedl syndrome. 714 91

The history of a newborn developing severe renin-induced hypertension is reported. A thrombotic occlusion of the lower a.abdominalis with an ascending thrombus into the left a.renalis caused hypertension according to the two-kidney-one-clip hypertension. High pressure diuresis induced weight loss by polyuria, hyponatremia and hypokalemia by severe renal salt losses. The vicious circle of malignant hypertension was initiated by sodium losses, not sufficiently recompleted by therapy. The full picture of an acute hypertensive renal damage was seen at autopsy in the unclamped kidney.
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PMID:Sodium loss as leading symptom of renovascular hypertension in the newborn. 720 91

High dosages of nephrotoxic drugs in elderly patients might be correlated with an increase in the number of patients with tubulo-interstitial nephritis (TIN). In patients with acute TIN, marked fever, back or flank pain, CVA tenderness, skin rash, arthralgia, eosinophilia, and eosinouria are observed. Clinical symptoms might be induced by glomerular, proximal tubular or distal tubular dysfunction in chronic TIN. Mild to moderate proteinuria, edema, hypertension, azotemia, glucosuria, aminoaciduria, polyuria and polydipsia are characteristic findings in patients with chronic TIN. These findings are slowly progressive in such patients. It appears that the marked fibrosis with lymphocyte infiltration in the interstitium is a poor clinical marker in patients with TIN. Furthermore, it is important to differentiate TIN from glomerulonephritis.
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PMID:[Symptoms in patients with tubulo-interstitial nephritis]. 756 29

We report a 2-year-old boy with renovascular hypertension caused by stenosis of the left renal artery that was successfully treated by percutaneous transluminal angioplasty (PTA). He initially presented with severe hyponatremia, hypokalemia, polyuria, transient proteinuria and weight loss. This phenomenon is known to occur in patients with renovascular and malignant hypertension, called hyponatremia hypertensive syndrome, but was thought to be rare in children. Renovascular hypertension should be considered as a cause of hyponatremia in children. In addition, PTA is an appropriate treatment even in very young children with renovascular hypertension.
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PMID:Severe hyponatremia in a patient with renovascular hypertension: case report. 783 Aug 65

Twenty-four cats with spontaneous systemic hypertension were retrospectively studied. Blood pressure (BP) was measured indirectly by the Doppler technique in 17 cats (mean systolic 219.4 +/- 43.2 mm Hg) and directly by femoral arterial puncture in 15 cats (mean systolic/diastolic 233.2 +/- 40.9/148.1 +/- 28.7 mm Hg). All cats had bilateral retinal hemorrhages and/or detachments. Twenty cats presented because of blindness. Other presenting signs included polyuria/polydipsia, weight loss, neurological signs, and/or epistaxis. Diagnostic tests were performed to determine the presence and the cause of any secondary organ damage. Common findings included retinal hemorrhages/detachments, low-grade systolic murmurs, cardiomegaly with left ventricular hypertrophy (LVH), small kidneys, mild azotemia, and urine specific gravity < or = 1.020. Only 3 cats had hyperthyroidism. One cat was transiently diabetic. Necropsies on 2 cats with neurological signs showed nephrosclerosis, arteriosclerosis, and multifocal cerebral hemorrhages. Twenty cats were treated with diuretics, beta-adrenergic antagonists, and/or an angiotensin converting enzyme (ACE) inhibitor. One cat was treated with methimazole only, and 1 was treated with insulin transiently. The median survival of the 24 cats was 18 months. Response to therapy did not appear to have an impact on survival time.
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PMID:Spontaneous systemic hypertension in 24 cats. 804 80

We report a case of hyponatremia, polyuria-polydipsia, hypokalemia, nephrotic syndrome, and hypertension caused by unilateral renal ischemia, and the resolution after nephrectomy of the ischemic kidney. The renin-angiotensin-aldosterone axis seems to play an essential role in the pathogenesis of these features. Mechanisms by which angiotensin II, hypokalemia, and proteinuria can affect salt and water balances, and the role of angiotensin II as a cause of heavy proteinuria are discussed. Renovascular hypertension should be considered in the differential diagnosis of hyponatremia, hypokalemia, and polyuria-polydipsia.
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PMID:Multiple manifestations of renovascular hypertension. 820 70

The effects of MRX-III, a new amino acid solution for renal failure, on survival, progression of renal insufficiency, metabolism of calcium and phosphorous, and nutritional status were studied in rats with chronic renal failure induced by 7/8 renal ablation. These rats were injected intraperitoneally with MRX-III, an essential amino acid solution for renal failure (Amiyu; Sol. A) or a general amino acid solution (Moripron-F; Sol. M) for 12 weeks under the condition of a 3.5% protein diet, and these effects were compared with those in control rats infused with Sol. M under a 22% protein diet.1) Infusion of MRX-III or the other solutions under a low protein diet prolonged survival time and improved the uremic status indicated by azotemia, polyuria, albuminuria, hypocalcemia and hypertension. 2) Increase in body weight and tissue weight of rats treated with MRX-III or Sol. A was better than those in rats treated with Sol. M. MRX-III as well as Sol. A showed a tendency to provide a better nutritional effect in comparison with Sol. M.
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PMID:[Effects of MRX-III on chronic renal failure in rats]. 826 4

1. The present study was undertaken to test whether insulin acts as a pressor agent and causes hypertension in rats. 2. Insulin at doses of 10 or 100 units day-1 kg-1 was administered daily by subcutaneous injection to normal rats for 6 weeks. As it has been suggested that sodium retention plays a major role in the putative hypertensive activity of this hormone, insulin was also administered to saline- (1% NaCl) drinking rats according to the same protocol. Water- and saline-drinking rats served as controls. 3. After 6 weeks of insulin treatment, the mean arterial blood pressure did not increase in any of the insulin-treated or the insulin-salt-treated groups. However, in both insulin-salt-treated groups, absolute and relative ventricular and renal hypertrophy with increased ventricular water content as well as increased urine output with reduced osmolality were observed. 4. All insulin-treated groups showed increased plasma levels of glucose, insulin and antidiuretic hormone when compared with their respective controls. 5. These results demonstrate that chronic insulin treatment did not increase blood pressure in rats, even when drinking water was supplemented with NaCl, and suggest that a polyuria-polydipsia syndrome was present in both insulin-salt-treated groups. Moreover, increased plasma levels of antidiuretic hormone were observed in all insulin-treated groups.
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PMID:Chronic insulin treatment in rats: evidence against a role for insulin as a pressor agent. 838 50

A 62-year-old male with small cell lung cancer (SCLC) associated with Cushing's syndrome and diabetes insipidus (DI) is reported. The patient was referred to our hospital for treatment of SCLC. A diagnosis of paraneoplastic Cushing's syndrome was made on the basis of an elevated serum ACTH (623.5 pg/ml) level, elevated excretion of urinary 17-OHCS (18.01 mg/day), obesity, hypertension, hyperglycemia, persistent hypokalemia, alkalosis, and no history of diabetes mellitus. He was also diagnosed as having DI based on polyuria and polydipsia, low specific gravity of the urine (1.007-1.010), low serum ADH (1.4 pg/ml) level, normal plasma osmolarity (29 mOsm/kg H2O), and the results of water deprivation test. DI and a left visual field defect was suggestive of metastasis to the pituitary region, but no lesion was detected by either CT scan or MRI scan. The patient failed to show a good response to intensive chemotherapy, and died of the tumor five months after commencing chemotherapy. Post-mortem examination revealed metastases to the hypothalamic-neurohypophyseal region, lungs, liver, adrenal glands, bone, bone marrow, and hilar and mediastinal lymph nodes.
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PMID:[A case of small cell lung cancer associated with diabetes insipidus and Cushing's syndrome]. 839 May 89


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