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

Aldosterone deficiency is caused by various defects of aldosterone biosynthesis in the adrenal gland or hyporeninism. The most important symptoms are hyponatremia and hyperkalemia. These electrolyte disturbances are also found in pseudohypoaldosteronism. Pseudohypoaldosteronism type I is characterized by insensitivity of the distal nephron for aldosterone. Hyperabsorption of chloride in the distal nephron leads to pseudohypoaldosteronism type II, which is linked with hypertension, whereas blood pressure in the other mentioned disorders is decreased. Renal tubular acidosis, mainly type 4, with impaired production of ammonia due to hyperkalemia, is frequently observed in hypoaldosteronism and both types of pseudohypoaldosteronism as well. The therapeutic regimen is different: low doses of fludrocortisone in hypoaldosteronism, potassium restriction, sodium bicarbonate and loop diuretics in type I of pseudohypoaldosteronism, and sodium restriction and chloruretic diuretics (thiazide) in type II of pseudohypoaldosteronism. In some cases hyperkalemia requires the use of potassium-binding resins.
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PMID:[Primary hypoaldosteronism, pseudo-hypoaldosteronism and distal tubular acidosis]. 638 50

Selective hypoaldosteronism is defined as diminished production of aldosterone, and sometimes also of 18-hydroxycorticosterone, with otherwise intact adrenal function. A decrease in the secretion of potassium and H+-ions and in the reabsorption of sodium in the distal nephron may result and lead to hyperkalemia, hyperchloremic acidosis, and impaired renal sodium conservation. The form of hypoaldosteronism which occurs in the adult is characterized by the following additional features: the aldosterone deficiency is due in the majority of cases to a decrease in enzymatically active plasma renin ("hyporeninemic hypoaldosteronism"), while various endogenous mechanisms as well as certain drugs (prostaglandin inhibitors, beta-blockers) may contribute. Other disturbances of the renin-angiotensin system (e.g. during treatment with converting-enzyme inhibitors) may rarely be responsible. Abnormalities in adrenal cortical synthesis may sometimes coexist, but proof that adrenal enzymatic defects play a primary pathogenic role in selective hyperaldosteronism in the adult is lacking. Such patients are frequently older (greater than 50 years), and often have diabetes mellitus and/or nephropathy (diabetic, interstitial, or hydronephrosis). Hyperkalemia and acidosis tend particularly to develop in association with mild to moderate impairment of renal function. The differential diagnosis should include other causes of impaired renal potassium secretion (Addison's disease, renal resistance to mineralocorticoids, potassium-sparing diuretics). Moreover, possible extrarenal factors contributing to hyperkalemia (oral potassium intake and redistribution of intracellular/extracellular space, particularly with associated insulin deficiency) should also be considered. For treatment, dietary potassium restriction is recommended as a general step. Replacement with the mineralocorticoid fludrocortisone acetate usually reverses the hyperkalemia and acidosis, but may sometimes induce sodium retention and hypertension. Loop diuretics, potassium-exchanging preparations and/or bicarbonate may also be useful as alternatives or additives.
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PMID:[Hyporeninemic hypoaldosteronism and the differential diagnosis of hyperkalemia]. 675 13

Neoplasia-induced hypercalcemia in the Fischer rat results in hypertension 1 wk after Leydig cell tumor transplantation. Systolic blood pressure, plasma catecholamine, prolactin, plasma renin activity (PRA), and aldosterone responses to immobilization stress were evaluated in Fischer rats 10 days after tumor transplantation and in age-matched nontransplanted controls. Basal systolic blood pressure, norepinephrine, and PRA levels at 10 days after tumor transplantation were higher in association with elevated calcium levels in tumor-transplanted rats than in controls. Systolic pressure, norepinephrine, and epinephrine responses to immobilization stress were greater in the hypercalcemia 10-day transplanted rats. Although basal levels of prolactin and aldosterone were similar in the two groups. These observations suggest that elevated levels of the vasoactive hormones norepinephrine and angiotensin may play a pivotal role in development of hypertension in association with neoplasia-induced hypercalcemia. Further, neoplasia-induced hypercalcemia in the Fischer rat is associated with a relative hyperreninemic hypoaldosteronism state.
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PMID:Hormonal changes associated with hypertension in neoplasia-induced hypercalcemia. 704 41

A 13-year-old girl with severe hypertension (240/140 mm Hg), short stature, marked hyperkalemia (8.6 mEq/liter), and renal tubular acidosis was studied. Renal parenchymal and renovascular diseases as well as endocrinologic causes of hypertension were ruled out by appropriate studies. The hypertension was associated with sodium retention, increased plasma volume, suppressed plasma renin activity, and decreased urinary excretion of aldosterone. Impaired renal excretion of potassium was demonstrated by sodium sulfate infusion when the patient was fed a high-sodium diet but a significant kaliuresis occurred when the test was performed on a low-sodium diet suggesting that renal sodium retention may play a role in the defect in potassium excretion. The renal tubular acidosis was associated with normal distal acidification but a low bicarbonate threshold (19 mmoles/liter) and marked suppression of urinary ammonium excretion. The hypertension, hyporeninemia, and hypoaldosteronism as well as the hyperkalemia and acid-base abnormalities were completely reversed by dietary sodium restriction or the administration of thiazides or furosemide. It is concluded that an unusual avidity for sodium chloride reabsorption by the renal tubules leading to extracellular volume expansion and renin-aldosterone suppression plays a significant pathogenic role in this syndrome and may explain the hypertension and biochemical abnormalities discussed.
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PMID:Severe hypertension, hyperkalemia, and renal tubular acidosis responding to dietary sodium restriction. 706 87

The concentrations of angiotensin II and aldosterone in plasma were measured in 101 consecutive unselected out-patient diabetic patients and in fifty-three normal controls. The concentration of angiotensin II was similar in diabetics without complications and controls, but was significantly lower in patients with hypertension or peripheral neuropathy. In contrast, plasma aldosterone was not reduced in any sub-group. The concentrations of angiotensin II and aldosterone were positively correlated in controls, in diabetes without complications and in hypertensive diabetics, but this relationship was not found in patients with peripheral neuropathy, retinopathy or nephropathy. There was no evidence of overt hypoaldosteronism in any of the diabetic patients. No individual aldosterone concentration was below the range found in controls and no plasma angiotensin II concentration is reduced in patients with specific diabetic complications such as neuropathy, plasma aldosterone may be maintained by factors other than the renin-angiotensin system. This would explain why hypoaldosteronism is rare among unselected diabetics.
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PMID:Plasma angiotensin II and aldosterone in unselected diabetic patients. 716 68

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

During long-term treatment of arterial hypertension with calcium antagonists of the dihydropyridine type activation of the sympathetic nervous system and subsequently also of the renin-angiotensin-aldosterone system persists, while the haemodynamic reaction to vasodilatation, manifested by an elevated pulse rate and minute volume from the initial stage of therapy, recedes. In type II diabetics the basal and stimulated response of the renin-angiotensin-aldosterone system is reduced. The administration of calcium antagonists of the dihydropyridine type does not stimulate significantly the renin-angiotensin-aldosterone system as the starting function of the sympathetic nervous system is impaired within the framework of vegetative neuropathy. In almost 20% NIDDM plasma renin activity and aldosterone do not respond to furosemide administration and the vertical posture. In others the response is found but takes place at reduced levels. Hyporeninaemic hypoaldosteronism is thus manifested not so much by a drop of plasma renin and aldosterone beneath the lower range of reference values as by a reduced response to stimulation. Functional hyporeninaemic hypoaldosteronism is another, frequent late complication of diabetes. In advanced forms a further block of the renin-angiotensin-aldosterone system by ACE inhibitors can then produce, even in the absence of diabetic nephropathy, in the stage of chronic renal failure dangerous hyperkaliaemia which may threaten the patient. Dynamic examination of the sympathetic nerve and the renin-angiotensin-aldosterone system makes it possible to predict this condition. In practice it is necessary in diabetics with arterial hypertension after starting with ACE inhibitors during the first days to monitor repeatedly plasma potassium and creatinine. ACE inhibitors and calcium antagonists are otherwise for diabetics drugs of first choice which can arrest the progression of nephropathy, effectively reduced the blood pressure without causing deterioration of insulin resistance and hyperlipoproteinaemia and lead even to regression of hypertrophy of the vascular wall and left ventricle.
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PMID:[The effect of long-term treatment of arterial hypertension with Ca antagonists on the renin-angiotensin-aldosterone system in diabetics. Hyporeninemic hypoaldosteronism]. 857 95

We report the case of a 16-month-old boy who presented with chronic vomiting, failure to thrive, arterial hypertension and medullary nephrocalcinosis. Laboratory results revealed hypokalaemia, metabolic alkalosis, increased urinary potassium excretion and a hyporeninaemic hypoaldosteronism. Chromatographic determination of urinary steroid metabolites showed an abnormal elevation of tetrahydrocortisol and allo-tetrahydrocortisol compared to tetrahydrocortisone; this pattern of urinary steroid excretion is essential for the diagnosis of the syndrome of apparent mineralocorticoid excess type 1 and believed to be a result of the underlying metabolic defect, a decreased activity of the 11 beta-hydroxysteroid dehydrogenase. A second variant, called syndrome of apparent mineralocorticoid excess type 2, has similar clinical features but lacks the typical urinary steroid profile. Therapy with spironolactone resulted in growth, weight gain and blood pressure control.
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PMID:Diagnosis and treatment of a child with the syndrome of apparent mineralocorticoid excess type 1. 883 92

Isolated hypoaldosteronism is found in 75% diabetics where the disease has persisted for 10 or more years. Sporadically it is found in congenital autonomous neuropathy, in acute glomerulonephritis, in gouty kidney, tubulointerstitial nephritis, after transplantation of the kidney, on mytomycin etc. During dynamic testing of the response of plasma renin activity and aldosterone to the administration of furosemide and a vertical position in diabetics a significantly reduced response was recorded as compared with non-diabetic hypertonic subjects. In 18.3% no response was observed (decompensated form of IHH). Diabetic hypertonics behaved like control hypertonics on long-term beta-blocker treatment. In the decompensated form of IHH after administration of drugs interfering with the activity of SNS-RAAS activity (ACEI, spirolactone etc.) a hyperkalaemic crisis may develop which threatens the patient with acidosis, dehydration, myoplegia, muscular spasms, however, in particular with fatal disorders of the cardiac rhythm. A similar effect may be exerted also by blockers of prostaglandin synthetase (non-steroid antirheumatics) and other drugs. The cause of IHH in diabetics is the coincidence of several pathogenic factors: 1. hypersecretion of ANF with hyperosmolar hyperglycaemic hypervolaemia and hyperfiltration already at the onset of DN, 2. early development of autonomous neuropathy of the sympathetic nerve, 3. reduced renin and prostaglandin formation already in the early stages of DN, 4. reduced extrarenal isorenin formation, 5. reduced conversion of prorenin into active renin, 6. reduced reactivity of the zona glomerulosa to AII, hyperkalaemia and ACTH for its functional reconstruction as a result of periodic activation of contraregulative hormones by fluctuations of the blood sugar level in diabetic patients, 7. reduced response of the distal renal tubule to aldosterone because of tubulointerstitial changes. IHH is thus another serious but rarely diagnosed late complication of diabetes which depends only partly on the stage of DN. It must be, however, diagnosed and respected with regard to the selection of drugs for the treatment of arterial hypertension and the syndrome of insulin resistance and the 5H syndrome resp., i.e. the association of hyperinsulinism which compensates insulin resistance with hyperglycaemia (NIDDM), hypertension, hyperlipoproteinaemia and hirsutism in women (so-called Stein-Leventhal syndrome).
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PMID:[Diabetic nephropathy and isolated hyporeninemic hypoaldosteronism]. 892 9

Aldosterone participates in blood volume and serum potassium homeostasis, which in turn regulate aldosterone secretion by the zona glomerulosa of the adrenal cortex. Autonomous aldosterone hypersecretion leads to hypertension and hypokalemia. Improved screening techniques have led to a re-evaluation of the frequency of primary aldosteronism among adults with hypertension, recognizing that normokalemic cases are more frequent than was previously appreciated. The genetic basis of glucocorticoid remediable aldosteronism has been elucidated and adequately explains most of the pathophysiologic features of this disorder. A new form of familial aldosteronism has been described, familial hyperaldosteronism type II; linkage analysis and direct mutation screening has shown that this disorder is unrelated to mutations in the genes for aldosterone synthase or the angiotensin II receptor. The features of aldosterone hypersecretion may be due to non-aldosterone-mediated mineralocorticoid excess. These include two causes of congenital adrenal hyperplasia (11 beta-hydroxylase deficiency and 17 alpha-hydroxylase deficiency), the syndrome of apparent mineralocorticoid excess (AME) due to 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) deficiency, primary glucocorticoid resistance, Liddle's syndrome due to activating mutations of the renal epithelial sodium channel, and exogenous sources of mineralocorticoid, such as licorice, or drugs, such as carbenoxolone. The features of mineralocorticoid excess are also often seen in Cushing's syndrome. Hypoaldosteronism may lead to hypotension and hyperkalemia. Hypoaldosteronism may be due to inadequate stimulation of aldosterone secretion (hyporeninemic hypoaldosteronism), defects in adrenal synthesis of aldosterone, or resistance to the ion transport effects of aldosterone, such as are seen in pseudohypoaldosteronism type I (PHA I). PHA I is frequently due to mutations involving the amiloride sensitive epithelial sodium channel. Gordon's syndrome (PHA type II) is due to resistance to the kaliuretic but not sodium reabsorptive effects of aldosterone for which the genetic basis is still unknown. This review aims to provide a survey of the clinical disorders of aldosterone excess and deficiency and their clinical management, with a focus on primary aldosteronism and isolated aldosterone deficiency.
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PMID:Hyper- and hypoaldosteronism. 1023 50


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