Cases reported "Hyperaldosteronism"

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11/31. Renal tubular involvement mimicking bartter syndrome in a patient with kearns-sayre syndrome.

    A 10-year-old boy had short stature, external ophthalmoplegia, atypical retinal pigmentary degeneration, and sensorineural hearing loss (kearns-sayre syndrome). In addition to ragged-red fibers observed on modified Gomori trichrome staining, there were scattered fibers exhibiting no cytochrome c oxidase activity, indicating a focal deficiency. Cytochrome c oxidase and other respiratory chain enzyme activities were normal biochemically. The patient also had renal tubular dysfunction, including isosthenuria, decreased urine-concentrating ability, and excessive excretion of potassium and magnesium. In addition, he had hyperreninemia and hyperaldosteronism but no hypertension. The renal dysfunction was thought to have resulted from a primary defect in the thick ascending limb of the loop of henle, mimicking bartter syndrome. In contrast to previously described cases of cytochrome c oxidase deficiency with de Toni-Fanconi Debre syndrome, the patient had less intensive muscle abnormalities. A renal biopsy specimen showed ultrastructural changes in mitochondria that were similar to those seen in biopsy specimens of muscle. A large-scale deletion (8.8 kilobases) in mitochondrial dna was found in biopsy specimens of muscle and kidney.
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12/31. Renovascular hypertension presenting with hypokalemic metabolic alkalosis.

    This report describes two adolescents with severe hypertension secondary to renal artery stenosis who had evidence of a hypokalemic metabolic alkalosis in their initial laboratory evaluation. Hypokalemic metabolic alkalosis is known to occur in approximately 16% of adults with renal artery stenosis but has not been well described in the pediatric literature. It is the result of excess aldosterone secretion stimulated by renal artery stenosis-mediated activation of the renin-angiotension system and by an increase in natriuresis from the contralateral, non-stenotic kidney. Although primary hyperaldosteronism must be considered in children with hypertension and hypokalemia, it is a rare disease in children. This report supports current recommendations that the initial focus of medical investigation in the severely hypertensive child should remain on the kidney.
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13/31. A case of normotensive primary aldosteronism with hypopituitarism, epilepsy, and medullary sponge kidney.

    A 55-year-old man with normotensive primary aldosteronism, hypopituitarism, epilepsy, and medullary sponge kidney is reported. Seventeen years before admission, he had been noted to have hypokalemia associated with high potassium clearance, suppressed plasma renin activity, metabolic alkalosis, and normal blood pressure as well as low urinary excretion of 17-hydroxycorticosteroids. He kept normotensive in spite of hyperaldosteronism until nine months after the initiation of replacement therapy with glucocorticoid and thyroxine for hypopituitarism, when he became hypertensive. hypopituitarism seemed to play a role in keeping a normal blood pressure despite long-standing hyperaldosteronism.
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14/31. A case of primary aldosteronism with chronic renal failure undergoing hemodialysis treatment.

    A 56-year-old man with primary aldosteronism and chronic renal failure undergoing hemodialysis is described. He complained of numbness of the extremities and showed persistent hypopotassemia in spite of anuria. In the endocrinological examination, a very high plasma aldosterone concentration was observed, while plasma renin activity was within the normal range. From the abdominal Computed tomography (CT), adrenal scintigraphy, and segmental venous sampling data, he was diagnosed as primary aldosteronism due to left adrenocortical adenoma. In this case, hypopotassemia could not be explained by potassium loss through the kidneys, which suggests potassium excretion in the gastrointestinal tract as the mechanism of hypopotassemia. This was clearly shown from a potassium-balance study and the results of spironolactone administration. Our report is on the first case showing hypopotassemia due to primary aldosteronism in spite of anuria. If a patient treated with maintenance dialysis should have persistent hypopotassemia, as in the present report, it is necessary to consider an association with primary aldosteronism.
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15/31. A renin-secreting tumor.

    A 23-year-old white male was referred for hypertension resistant to triple antihypertensive treatment, with hypokalemia, hyperaldosteronism and elevated levels of circulating plasma renin activity (PRA). Renal angiography and echoscans put in evidence an avascular solid mass at the midlower level of the right kidney. Renal vein catheterization with sampling of blood from the lower branches of the right renal vein showed lateralization of renin secretion from that side. After surgical exeresis, the mass (1.0 cm) was diagnosed as a renal hemangiopericytoma on the basis of light and electron microscopy. Tumor exeresis was followed by a prompt normalization of blood pressure and plasma potassium, with a decrease in PRA and aldosterone. Two months after surgery the patient was still normotensive. Circulating levels of inactive (trypsin-activable) renin were around 60% of the total pool of plasma renin, i.e. much lower than those reported in other cases of renin-secreting tumors. After surgery, inactive and active renin fell in parallel, implying that both were secreted by the tumor. Tumoral PRA responded to postural stimulation, but was unresponsive to acute converting enzyme inhibition, suggesting that sympathetic stimuli were still operative, but the negative feedback inhibition by angiotensin ii on renin secretion was lost. Acute converting enzyme inhibition by captopril dropped blood pressure; however, during long-term treatment, the drug (3 X 50 mg/day) was ineffective in terms of either blood pressure normalization or relief of secondary hyperaldosteronism. Acute calcium entry blockade by nifedipine (10 mg p.o.) caused an evident blood pressure drop.
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16/31. Rapid regression of renal medullary granular change during reversal of potassium depletion nephropathy.

    Structural changes were studied on the kidney of a potassium-depleted man and on rat kidneys during potassium depletion and repletion. light and electron microscopy revealed rapid disappearance of intracytoplasmic granules in the renomedullary cells after potassium repletion in our patient as well as in rats. In potassium-depleted rats a series of ultrastructural changes, which were similar to those observed in the human kidney were seen with potassium repletion. Most of the granules were reduced in size and number, with loss of internal structure, shrinkage and condensation of their contents, and were almost totally eliminated by 72 h of potassium repletion. In some endothelial and interstitial cells, the granules were seen to be in the process of being extruded through an area of gap in the plasma membrane. The results indicate that most of the intracytoplasmic granules in the renal medulla rapidly disappeared by intracytoplasmic digestion and the rest of them were probably eliminated by exocytosis during reversal of potassium depletion nephropathy in man and rats.
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17/31. Intracytoplasmic granules of the inner medulla and papilla of the potassium depleted human kidney.

    Morphological changes were studied in the kidney of a potassium depleted 21-year old Japanese male with Bartter's syndrome. Characteristic features were PAS-positive intracytoplasmic granules in the inner medulla and the papilla. The intracytoplasmic granules were conspicuous towards the papillary tip and ultrastructurally composed of small vesicles, vacuoles, amorphous dense materials, lamellar contents and myelin like figures, and bounded by a single limiting membrane. The granules in this human kidney were, with regard to their distribution and ultrastructural findings, similar to those in the kidney of experimentally potassium depleted rats. The results indicate that the intracytoplasmic granules in the renal inner medulla and the papilla are the characteristic feature of the potassium depleted human kidney and a counterpart to those in the potassium depleted rat.
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18/31. Renovascular hypertension associated with bilateral aldosteronoma.

    The authors present a 35-year-old male patient with renovascular hypertension caused by the stenosis of both renal arteries of the right kidney. Two years after the diagnosis of hypertension was made, an endarterectomy was performed but a successful correction of the upper stenotic artery was not achieved. During the next 2 years the hypertensive disease was uncontrollable with antihypertensive medications and gradually entered into a malignant phase. In addition to the atrophy of the right kidney, an adenoma of the left adrenal gland was revealed (19.75 g) which was operated on. Left adrenalectomy had only a transitory benefit on blood pressure level. Five months later an adenoma of the right adrenal gland was diagnosed and together with the ischaemic right kidney was operated on (right adrenalectomy and nephrectomy) which definitely cured the hypertension. The chronological sequence of events and the course of the disease in the patient point to the possibility that long-standing hyper-reninaemia, due to renal ischaemia, may cause the development of multiple bilateral adrenocortical adenomas and that secondary aldosteronism may transform into primary.
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19/31. nephrocalcinosis in Bartter's syndrome. Demonstration by ultrasonography.

    nephrocalcinosis in Bartter's syndrome has been recognized since 1962, but has not previously been shown in an infant with the syndrome. ultrasonography shows striking echogenicity of the renal pyramids which appears to be a specific finding in medullary nephrocalcinosis. We suspect nephrocalcinosis will be found in many infants with Bartter's syndrome if ultrasonography is used to examine their kidneys.
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20/31. Simultaneous occurrence of hyperkalemia due to aldosterone suppression and hyperfunctioning parathyroid adenoma.

    The change of the pattern of clinical presentation of primary hyperparathyroidism in older patients is illustrated by a case history of a 61-year-old woman with multicystic kidney disease in whom a thiazide antihypertensive drug (clopamide) induced a very severe symptomatic hypercalcemia. Withdrawal of the drug was followed by a prolonged complete clinical remission, normocalcemia, normocalciuria, but consistently elevated parathormone levels. This "normocalcemic biochemical hyperparathyroidism" was complicated with hyperkalemia due to aldosterone suppression, a counterpart of the recently described association with hypokalemia due to primary hyperaldosteronism, necessitating further studies on the occurrence and significance of altered production of aldosterone in geriatric patients with primary hyperparathyroidism.
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ranking = 30.207991676234
keywords = kidney disease, kidney
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