Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
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Postural stimulation tests (PST) from 146 patients with primary aldosteronism were reviewed: 83 had an aldosterone-producing adenoma (APA), 48 idiopathic hyperaldosteronism (IHA), nine primary adrenal hyperplasia (PAH), and six aldosterone-producing renin-responsive adenoma (AP-RA). Plasma aldosterone and cortisol levels were measured after overnight recumbency and in response to upright posture for 2 to 4 h. The test was considered invalid in 32% of the patients because cortisol levels increased during the maneuver. As both cortisol and aldosterone are responsive to ACTH in subjects with primary aldosteronism, as well as in normal subjects, we examined their percent variation instead of the absolute values. In order to validate those tests in which cortisol increased, we subtracted the percent cortisol change from the percent aldosterone response. An aldosterone increase of less than 30% (considered a positive response for the presence of an adenoma) identified 76 of the 89 patients with an adenoma (APA and AP-RA) (sensitivity of 85%). Among the 13 false-negative tests, six were proven cases of AP-RA. In each and every case an adenoma was detected by CT/MRI scanning (or bilateral adrenal vein catheterization). Hypertension was ameliorated or cured by surgery. A postural response of less than 30% was also present in 11 of the 57 patients who did not have a discrete adenoma confirmed by imaging techniques (specificity of 81%). Among these false-positive results there were the nine cases of PAH where the hypertension could be ameliorated or cured by partial removal of hyperplastic adrenal tissue.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reassessment of the predictive value of the postural stimulation test in primary aldosteronism. 193 Aug 62

We report a rare case of primary hyperaldosteronism due to a unilateral adrenal cortical adenoma in an 11-year-old female patient. The patient presented with hypertension, hypokalaemia and metabolic alkalosis, associated with inappropriate kaliuresis. The diagnosis was supported by the following laboratory findings: elevated plasma aldosterone, suppressed plasma renin activity, nonsuppressible aldosterone secretion following saline infusion and absent plasma aldosterone response to ambulation. MRI revealed a 1 cm-diameter adrenal tumour on the left side. Even though the NP-59 scintigraphy showed the negative result, laparotomy with left adrenalectomy was performed. Pathological examination confirmed an adenoma in the adrenal cortex. The patient's blood pressure and biochemical laboratory data normalized postoperatively within 2 days. We recommend that in hypertensive children with hypokalaemia and metabolic alkalosis, primary aldosteronism should be considered.
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PMID:Aldosterone-secreting adrenal cortical adenoma in an 11-year-old child and collective review of the literature. 781 26

We report a rare case of primary hyperaldosteronism in an 11-year-old female patient due to a unilateral adrenal cortical adenoma. The patient presented with hypertension, hypokalaemia and metabolic alkalosis associated with inappropriate kaliuresis. The diagnosis was supported by the following laboratory findings: elevated plasma aldosterone, suppressed plasma renin activity, nonsuppressible aldosterone secretion following saline infusion and absent plasma aldosterone response to ambulation. MRI revealed a 1 cm diameter adrenal tumour on the left side. Even though the NP-59 scintigraphy gave a negative result, laparotomy with left adrenalectomy was performed. Pathological examination confirmed an adenoma in the adrenal cortex. The patient's blood pressure and biochemical laboratory data normalized postoperatively within 2 days. We recommended that in hypertensive children with hypokalaemia and metabolic alkalosis, primary aldosteronism should be considered.
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PMID:Aldosterone-secreting adrenal cortical adenoma in an 11-year-old child and collective review of the literature. 775 31

A 38 year old woman and her first cousin, a 41 year old man, presented both with hypertension, hypokalemia, hyperaldosteronism, and low plasma renin activity in our Hospital. In both patients, plasma and urine aldosterone were constantly above the normal range, even on a high NaCl diet (250 mEq/day), while the plasma aldosterone response to postural changes was normal. In the female patient abdominal ultrasonic scan, CT scan, MRI, and adrenal gland phlebography were normal, but blood from the left adrenal vein contained 1002 pg/ml of aldosterone, versus 91 pg/ml in the contralateral one. Interestingly, the secretion of cortisol was also lateralized (plasma cortisol levels being of 28.8 mcg% in the left, 2.3 mcg% in the right adrenal gland), although neither clinical nor laboratory signs of hypercortisolism were present. Spironolactone treatment (100 mg/daily) completely reversed the syndrome of mineralocorticoid excess. After 2 years, patient has normal blood pressure and serum K+ levels.
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PMID:Unilateral adrenal hypersecretion of both aldosterone and cortisol in two first cousins with a syndrome of mineralocorticoid excess but without signs of hypercortisolism. 805 32

A 43-year-old man was admitted to our hospital in January, 1991 for further examination of polydipsia, polyuria and hypertension. He had had a personal history of hypertension since 1976 and of diabetes mellitus since 1982. Physical examination and routine laboratory studies showed that the patient was characterized by asymptomatic hypertension in the presence of hypokalemia and increased urinary potassium excretion. Plasma aldosterone concentrations (PAC) were elevated and plasma renin activity (PRA) was suppressed, resulting in a considerable increase in the ratio of PAC to PRA. PAC was not normally suppressed by saline infusion (2 1/2h, iv). PRA remained suppressed and PAC did not rise after stimulation with iv injection of furosemide (40 mg) in combination with walking for 60 min. PAC was increased in response to ACTH injection (0.25 mg, iv) but not suppressed by dexamethasone administration (2 and 8 mg/day, po). PAC did not rise after iv infusion of angiotensin II (20 ng/kg/min for 30 min). Venous sampling showed that PAC was considerably elevated in the bilateral adrenal vein. CT and MRI demonstrated tumor mass in the bilateral adrenal gland and the remaining normal portion in the left adrenal gland. Scintigraphic imaging with 133I-aldosterol during dexamethasone suppression provided bilateral uptake in the adrenals. Oral administration of spironolactone (375 mg/day) suppressed blood pressure and elevated PRA and serum potassium. Elevated PCA and PRA levels as well as hypertension were corrected by right-total and left-subtotal adrenalectomy performed in March, 1991. However, impaired glucose tolerance was not changed after surgery, and plasma glucose levels were well controlled with a small dose of insulin (9U/day). Pathological studies revealed adrenocortical adenoma cells of clear cell type with spironolactone bodies in the bilateral adrenal tumors. These findings indicate that this is a very rare case of primary aldosteronism due to bilateral functioning adrenocortical adenomas, which is accompanied by diabetes mellitus.
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PMID:[A rare case of primary aldosteronism due to bilateral functioning adrenocortical adenomas]. 846 28

The physicochemical properties of water enable it to act as a solvent for electrolytes, and to influence the molecular configuration and hence the function--enzymatic in particular--of polypeptide chains in biological systems. The association of water with electrolytes determines the osmotic regulation of cell volume and allows the establishment of the transmembrane ion concentration gradients that underlie nerve excitation and impulse conduction. Fluid in the central nervous system is distributed in the intracellular and extracellular spaces (ICS, ECS) of the brain parenchyma, the cerebrospinal fluid, and the vascular compartment--the brain capillaries and small arteries and veins. Regulated exchange of fluid between these various compartments occurs at the blood-brain barrier (BBB), and at the ventricular ependyma and choroid plexus, and, on the brain surface, at the pia mater. The normal BBB is relatively permeable to water, but considerably less so to ions, including the principal electrolytes Brain fluid regulation takes place within the context of systemic fluid volume control, which depends on the mutual interaction of osmo-, volume-, and pressure-receptors in the hypothalamus, heart and kidney, hormones such as vasopressin, renin-angiotensin, aldosterone, atriopeptins, and digitalis-like immunoreactive substance, and their respective sites of action. Evidence for specific transport capabilities of the cerebral capillary endothelium, for example high Na+K(+)-ATPase activity and the presence at the abluminal surface of a Na(+)--H+ antiporter, suggests that cerebral microvessels play a more active part in brain volume regulation and ion homoeostasis than do capillaries in other vascular beds. The normal brain ECS amounts to 12-19% of brain volume, and is markedly reduced in anoxia, ischaemia, metabolic poisoning, spreading depression, and conventional procedures for histological fixation. The asymmetrical distributions of Na+ K+ and Ca2+ between ICS and ECS underlie the roles of these cations in nerve excitation and conduction, and in signal transduction. The relatively large volume of the CSF, and extensive diffusional exchange of many substances between brain ECS and CSF, augment the ion-homeostasing capacity of the ECS. The choroid plexus, in addition to secreting CSF principally by biochemical mechanisms (there is an additional small component from the extracellular fluid), actively transports some substances from the blood (e.g. nucleotides and ascorbic acid), and actively removes others from the CSF. In contrast with CSF secretion, CSF reabsorption is principally a biomechanical process, passively dependent on the CSF-dural sinus pressure gradient. Pathological increases in intracranial water content imply development of an intracranial mass lesion. The additional water may be distributed diffusely within the brain parenchyma as brain oedema, as a cyst, or as increase in ventricular volume due to hydrocephalus. Brain oedema is classified on the basis of pathophysiology into four categories, vasogenic, cytotoxic, osmotic and hydrostatic. The clinical conditions in which brain oedema presents the greatest problems are tumour, ischaemia, and head injury. Peritumoural oedema is predominantly vasogenic and related to BBB dysfunction. Ischaemic oedema is initially cytotoxic, with a shift of Na+ and CI- ions from ECS to ICS, followed by osmotically obliged water, this shift can be detected by diffusion-weighted MRI. Later in the evolution of an ischaemic lesion the oedema becomes vasogenic, with disruption of the BBB. Recent imaging studies in patients with head injury suggest that the development of traumatic brain oedema may follow a biphasic time course similar to that of ischaemic oedema. Hydrocephalus is associated in the great majority of cases with an obstruction to the circulation or drainage of CSF, or, occasionally, with overproduction of CSF by a choroid plexus papilloma. In either case, the consequence is a ris
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PMID:The normal and pathological physiology of brain water. 907 71

We report an uncommon case of small renin secreting tumor of the kidney located in the medulla. The tumor was primarily detected by MRI and subsequently studied by spiral CT. The results and limitations of both techniques are discussed.
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PMID:[Renin-secreting tumor detected by MRI]. 975 7

On November, 1997, a 15-year-old boy visited our hospital because of headache, fever and arthralgia. He was treated with 5 mg/day of prednisolone thereafter. On October 21, 1998, he was admitted because of remittent fever and multiple arthralgia and diagnosis of juvenile rheumatoid arthritis (JRA) was made. He was also found to have hypertension of 210/110 mmHg, and soon developed ptosis of the eye, facial paresis and perceptive deafness of the right side. Cerebrospinal fluid showed protein of 98 mg/dl and mildly elevated IgG, IgA and IgM levels with normal cell count. Brain MRI examination revealed multiple cerebral lesions in the frontal, parietal and cerebellar areas on the right, whose cause was thought to be vasculitis. Renal angiography demonstrated a right renal artery stenosis, compatible with renovascular hypertension. He was treated with 60 mg of prednisolone per day, which brought about a satisfactory improvement of the above rheumatic and neurologic signs. On November 17, 1998, he received a follow-up study of MRI, which failed to show any cerebral lesions, supporting the effectiveness of prednisolone. An angiotensin converting enzyme inhibitor successfully normalized hypertension and renin activity in serum, although renal blood flow did not increase.
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PMID:[A case with juvenile rheumatoid arthritis who developed cerebral vasculitis and venovascular hypertension]. 1121 60

We report a 14 year-old peripubertal girl who presented at our clinic with the primary complaint of delayed puberty. She was asymptomatic except for vague complaints of fatigue. Physical examination was significant for mucosal hyperpigmentation and lack of secondary sexual characteristics. Laboratory evaluation revealed a morning cortisol concentration of <0.1 microg/dl (normal range [n.r.]: 4.3-22.4 microg/dl) and a simultaneous ACTH concentration of 2 pg/ml (n.r. 25-62 pg/ml); FSH 66.8 IU/l (n.r. for age: 1-12.8 IU/l); LH 41.1 IU/l (n.r. for age: 1-12 IU/l); E2 38 pg/ml (n.r. for age: 7-60 pg/ml). She had a flat cortisol response to an ACTH stimulation test. MRI of the pituitary gland failed to reveal a lesion. Plasma renin activity, thyroid function tests, parathyroid hormone, prolactin, IGF-I, IGFBP-3 concentrations and serum electrolytes were normal. However, her urinary sodium concentration was high. She was diagnosed with autoimmune polyglandular endocrinopathy including ovarian failure, adrenal failure and autoimmune anterior hypophysitis presenting as isolated ACTH deficiency. We emphasize that autoimmune etiology should be considered in the differential diagnosis of delayed puberty and ovarian failure and that the presence of other endocrinopathies should be searched for even in asymptomatic patients.
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PMID:Autoimmune polyglandular endocrinopathy and anterior hypophysitis in a 14 year-old girl presenting with delayed puberty. 1151 33

Primary aldosteronism (PA) is a disorder typically characterized by resistant hypertension, hypokalemia, alkalosis and suppressed plasma renin activity, and excessive aldosterone production. A true estimate of the prevalence of the disorder is difficult to estimate because its detection is dependent on the awareness of the healthcare provider to the disorder, but it has generally been felt to be a rare occurrence. Its frequency of detection began to change when Hiramatsu suggested calculating the ratio of plasma aldosterone/plasma renin activity as a screening tool for the disorder. He found a ratio greater than 75 as a sensitive indicator for aldosterone-producing adenomas. Using the ratio, several investigators have found prevalence ranging from 3 to 9%. Two major classifications of PA exist: aldosterone-producing adrenal adenoma (APA) and zona glomerulosa hyperplasia (IHA). Distinguishing between these 2 entities is important clinically, because removal of a unilateral aldosterone-producing adenoma may result in correction of elevated blood pressure and hypokalemia. Thus, when evaluating hypertensive patients, PA should be suspected in those with moderate to severe hypertension or with hypertension refractory to standard treatment or in hypertensive patients with disease onset at an early age. The aldosterone-to-renin ratio is an easy, inexpensive, and rapid means of screening for the disorder. The ratio is the screening test of choice, but further confirmatory testing is required to clinch the diagnosis. Frequently employed confirmatory tests include urinary aldosterone excretion on a high-salt diet, aldosterone suppression after a saline infusion, and the fludrocortisone suppression test, which is considered the most sensitive confirmatory maneuver. Both high-resolution CT and MRI scans appear to have similar ability to differentiate between APA and IHA. As with essential hypertension, the goal of treatment is to prevent the long-term sequela of hypertension. The underlying pathology resulting in PA dictates the treatment strategy. The drug of choice is spironolactone. Surgical intervention should be entertained in those patients with PA in whom imaging studies suggest an adenoma.
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PMID:Hyperaldosteronism: the internist's hypertensive disease. 1238 96


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