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)

In two patients with severe hypertension and moderately severe renal insufficiency, metolazone and furosemide were used in combination with propranolol, methyldopa, and hydralazine to augment control of blood pressure. This combination of diuretics also was used in five patients with refractory congestive heart failure. The patients developed severe electrolyte disturbances with a general pattern of hyponatremia. disproportionate hypochloremia, alkalosis, and phyokalemia. These abnormalities were transient in the patients with severe hypertension and moderately severe renal insufficiency. Effective long-term control of blood pressure was obtained. In the patients with heart failure, edema persisted. Due to the severity of the electrolyte derangements, metolazone and furosemide were discontinued. Because of potential untoward effects, this combination of diuretics should be used with caution.
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PMID:Severe electrolyte disturbances associated with metolazone and furosemide. 63 11

The symptoms and clinical course of chronic hypokalemic nephropathy are described in 21 patients with longstanding potassium deficiency. In 14 patients (group A) the potassium depletion was caused by malnutrition and/or abuse of laxatives and/or diuretics. 7 patients (group B) suffered from primary (6 cases) or secondary (1 case) aldosteronism. The average duration of potassium depletion was 8.8 years in group A and 3.4 years in group B. Depending on the duration of potassium depletion, chronic renal disease develops which may end in terminal renal failure. Urinalysis is non-specific or negative. The clearance of creatinine slowly decreases. Metabolic alkalosis is a constant finding and in group A occurs with a tendency to hyponatremia and hypochloremia, with the development of metabolic acidosis only in advanced renal insufficiency. In contrast to patients of group B, patients of group A have normal or low blood pressures converting to hypertension, if at all only in the late phase. The cases of group A had secondary aldosteronism (and, correspondingly, a hyperplastic juxtaglomerular apparatus). Although urinary tract infection is a regular finding in advanced stages, the clinical, radiological and histological evidence suggests that bacterial pyelonephritis, if occurring at all, is rather a complication than the cause of the disease. In 5 patients 7 instances of acute renal failure of unknown origin were observed which was lethal in one case. Another patient died from terminal renal failure, a third from an intercurrent pneumonia. Renal histology obtained from 13 patients showed the picture of diffuse chronic abacterial interstitial nephritis.
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PMID:Symptoms and course of chronic hypokalemic nephropathy in man. 87 Feb 67

A retrospective analysis of infants with bronchopulmonary dysplasia requiring prolonged hospitalization (greater than 100 days) was carried out to determine those factors associated with fatal outcome. Twenty-three infants made up the study population. Eleven infants died and 12 survived (survivors). No differences were noted between the groups regarding ventilator requirement, radiographic changes, and medication use (digoxin, aldactazide), except for furosemide which was used twice as frequently in the group of infants who died v the group of infants who survived (P less than .001). Differences noted between the groups included moderate hypochloremia (chloride less than 80 mEq/L) in all 11 infants who died v six of 12 survivors, severe hypochloremia (chloride less than 70 mEq/L) in the nine of 11 infants who died v two of 12 survivors, metabolic alkalosis (pH greater than 7.45) in nine of 11 infants who died v three of 12 survivors, hypertension (systolic BP greater than 113 mm Hg) in eight of 11 infants who died v one of 12 survivors, decrease in head growth in ten of the 11 infants who died v one of the 12 survivors; these differences were all significant (P less than .001). The metabolic alkalosis and head growth changes appear to be related to the hypochloremia. The data suggest that chloride deficiency may be an important contributing factor in the genesis of poor outcome in infants with bronchopulmonary dysplasia and that close attention to chloride supplementation might influence outcome.
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PMID:Is chloride depletion an important contributing cause of death in infants with bronchopulmonary dysplasia? 293 79

Acute laminitis-hypertension was produced by carbohydrate overloading of the gastrointestinal tract in 12 adult horses. Obel grade 3 (OG3) lameness developed 40 hours (+/- 3.5, SEM) after overfeeding. At OG3 lameness, mean plasma volume was significantly decreased (P less than 0.005) when compared with base-line values. Before OG3 lameness, transient decreases in serum phosphorus and calcium were recorded. Mild hyponatremia also developed before OG3 lameness and persisted. After establishment of OG3 lameness, persistent hypokalemia and increased plasma aldosterone concentration occurred coincidently. Transient increase in plasma hydrocortisone (cortisol) and renin activity and transient hypochloremia were also recorded during the syndromal phase. Changes in plasma volume and serum electrolytes are discussed and related to the pathogenesis of acute equine laminitis. The alterations in plasma renin activity and aldosterone concentration were interpreted as homeostatic adjustments to fluid and electrolyte imbalances. Differences between the horse and pony during onset of experimental alimentary laminitis are also discussed.
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PMID:Plasma volume, electrolyte, and endocrine changes during onset of laminitis hypertension in horses. 675 27

Hypertension (210 mm Hg), hyponatremia, hypochloremia, and hypokalemia were observed in an 11-day-old infant. After electrolyte repletion, blood pressure rose to 320 mm Hg in spite of administration of antihypertensive drugs. The child died of a massive cerebral hemorrhage on the 17th day of life. At autopsy, the left renal artery was partially thrombosed and the left kidney partially infarcted. The glomeruli in the preserved cortical areas were of normal size; the juxtaglomerular apparatuses markedly enlarged. The blood vessels were inconspicuous. Enlarged glomeruli, multiple ruptures in the mesangium, ectactic glomerular capillaries, and fragile capillary walls were found in the nonconstricted right kidney. Fibrinoid necrosis with occasional fibrin thrombi in the lumina was present in the arterioles. Pronounced intimal edema with fragmented cells and monocytes embedded in the intima were observed in the interlobular and larger arteries. The histologic findings in the blood vessels of the nonconstricted kidney resembled those found in the hemolytic-uremic syndrome (Gasser's syndrome).
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PMID:Morphologic aspects of Goldblatt hypertension in a newborn infant. 719 47

Sodium bicarbonate is an extremely well-known agent that historically has been used for a variety of medical conditions. Despite the widespread use of oral bicarbonate, little documented toxicity has occurred, and the emergency medicine literature contains no reports of toxicity caused by the ingestion of baking soda. Risks of acute and chronic oral bicarbonate ingestion include metabolic alkalosis, hypernatremia, hypertension, gastric rupture, hyporeninemia, hypokalemia, hypochloremia, intravascular volume depletion, and urinary alkalinization. Abrupt cessation of chronic excessive bicarbonate ingestion may result in hyperkalemia, hypoaldosteronism, volume contraction, and disruption of calcium and phosphorus metabolism. The case of a patient with three hospital admissions in 4 months, all the result of excessive oral intake of bicarbonate for symptomatic relief of dyspepsia is reported. Evaluation and treatment of patients with acute bicarbonate ingestion is discussed.
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PMID:Acute toxicity from baking soda ingestion. 828 75

We report on a 4-year-old girl with hyponatremic-hypertensive syndrome (HHS), a rare entity in childhood. The girl was referred to us from a local hospital with a history of recurrent fever, vomiting, and seizures. On admission she was markedly dehydrated. Initial investigations revealed severe hyponatremia (serum Na 120 mmol/l), hypochloremia (serum Cl 68 mmol/l), and mild hypokalemia (serum K 3.3 mmol/l), while serum calcium and magnesium were normal. Serum urea was 5 mmol/l and serum creatinine was 62 mumol/l. Despite hyponatremic dehydration, her urine output was high (2050 ml/24 h), as was her urinary sodium (168 mmol/24 h). She had massive transient proteinuria (maximal 1642 mg/24 h) while being severely hypertensive (blood pressure 210/160 mmHg). Further investigations revealed right kidney scarring, hyper-reflexive bladder dysfunction, massive brain infarcts, and myocardial left ventricular hypertrophy. Renal arteries were normal on arteriography. Blood pressure control resulted in normalization of serum and urinary electrolytes and decrease of proteinuria. Hyponatremia and transient massive proteinuria in this patient seem to be caused by high-pressure-forced diuresis due to malignant renoparenchymal hypertension.
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PMID:Hyponatremic hypertensive syndrome. 1114 28

The glucocorticoid metabolising enzymes, 11beta-hydroxysteroid dehydrogenases (11beta-HSD), play a critical role in determining the availability of glucocorticoids to activate their receptors and hence modulate target gene transcription. There are two isozymes, 11beta-HSD-1 and -2, which act in opposing directions. 11beta-HSD-2 acts as a dehydrogenase, converting active corticosterone (cortisol in humans) to its inactive 11-keto derivative (11-dehydrocorticosterone in rodents and cortisone in humans), whereas 11beta-HSD-1 acts as a reductase, regenerating active glucocorticoids in a tissue-specific manner. Owing to the lack of specific inhibitors of these enzymes, it has been difficult to confirm the roles and determine the importance of these enzymes in vivo. Hence, to address this, we produced transgenic mice with null-mutations in the genes encoding the 11beta-HSD-1 or 11beta-HSD-2 enzymes. 11beta-HSD-2 -/- mice show signs of hypertension, hypotonic polyuria, hypokalemia and hypochloremia. These symptoms arise from illicit activation of mineralocorticoid receptors by glucocorticoids, in the absence of the protective action of 11beta-HSD-2. The phenotype is directly comparable to the Syndrome of Apparent Mineralocorticoid Excess, seen in humans with mutations in the 11beta-HSD-2 gene. Mice lacking 11beta-HSD-1, however, show a more subtle phenotype with reduced activation of glucocorticoid-induced processes. They were unable to convert 11-dehydrocorticosterone to corticosterone in vivo, confirming 11beta-HSD-1 as the sole 11-reductase in the mouse. They have elevated circulating levels of plasma corticosterone levels and adrenal hyperplasia, but they also have attenuated glucocorticoid-induced activation of gluconeogenic enzymes in response to fasting, and lower glucose levels in response to obesity or stress. Overall, these transgenic models have proved very useful for elucidating the roles of 11beta-HSDs in vivo and will be a unique resource for investigating the importance of each enzyme in the diverse actions of glucocorticoids.
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PMID:Phenotypic analysis of mice bearing targeted deletions of 11beta-hydroxysteroid dehydrogenases 1 and 2 genes. 1116 6

Eight cases of myxedema with interesting features are presented. Hypertension is common in myxedema and usually persists when the myxedema is treated. Two patients are reported in whom the hypertension improved with the treatment of the myxedema. Other cases presented with ascites, psychosis, recurrent coma with marked hyponatremia and hypochloremia, ataxia, muscular hypertrophy and myotonia. In each patient the abnormalities were corrected by administration of thyroid hormone. In most instances the mechanism whereby symptoms are produced is poorly understood.
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PMID:UNUSUAL MANIFESTATIONS OF MYXEDEMA. 1430 5

An 11-year-old spayed female domestic shorthair cat was evaluated for anorexia, lethargy and weight loss of 6 days' duration. Bilateral mydriasis, absent menace response, slow-to-absent pupillary light reflexes, bilateral retinal detachment, intermittent horizontal nystagmus, intermittent ventral strabismus and systemic hypertension were present. Biochemical analysis revealed severe hyponatremia, severe hypochloremia and mild hypokalemia. Multifocal central nervous system disease was suspected based on optic, trigeminal sensory (ophthalmic branch), vestibulocochlear and possible oculomotor nerve dysfunction. Thoracic radiographs showed mild cardiomegaly without evidence of congestive heart failure. Ultrasound revealed mild pleural and peritoneal effusion. A cause of the severe hyponatremia was not identified, and it persisted despite fluid therapy. Syndrome of inappropriate antidiuretic hormone secretion (SIADH) was suspected as the cause of hyponatremia. Humane euthanasia was elected owing to continued clinical decline. Serum hyposmolality, urine hyperosmolality, natriuresis and lack of confirmed renal, thyroid and pulmonary disease aided in the presumed diagnosis of SIADH. Post-mortem histopathology of the brain revealed degeneration of the hypothalamus and optic tracts, along with a prominent fluid-filled craniopharyngeal duct (putative Rathke's cleft cyst) separating the pars distalis and the pars intermedius. The hypothalamic degeneration, possibly secondary to a Rathke's cleft cyst, was hypothesized to be the cause of presumptive SIADH in the patient. Although rare in occurrence, Rathke's cleft cyst should be included as a differential diagnosis in dogs and cats with signs of pituitary dysfunction.
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PMID:Syndrome of inappropriate antidiuretic hormone secretion in a cat with a putative Rathke's cleft cyst. 2465 77


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