Cases reported "Hyperaldosteronism"

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1/31. Primary hyperaldosteronism without suppressed renin due to secondary hypertensive kidney damage.

    Primary hyperaldosteronism is characterized by high plasma and urinary aldosterone and suppressed PRA. renin suppression is due to aldosterone-dependent sodium retention and mild extracellular volume expansion. We observed three patients with primary hyperaldosteronism, severe refractory hypertension, and normal to high normal PRA levels whose aldosterone/renin ratios were still elevated because of disproportionately high aldosterone levels. All available medical data on the patients as well as publications on the aldosterone/renin relationship in primary hyperaldosteronism were reviewed to explain the unusual findings. In one patient, histologically proven renal arteriolosclerosis was the probable cause of the escape of PRA from suppression by an aldosterone-producing adenoma. In the other two patients, hypertensive kidney damage due to primary hyperaldosteronism was the most likely explanation for the inappropriately high PRA, as in patient 1. All patients had high normal or slightly elevated serum creatinine levels and responded to 200 mg spironolactone/day with increased serum creatinine and hyperkalemia. hyperkalemia was probably due to a decreased filtered load of sodium and a spironolactone-induced decrease in mineralocorticoid function. Two patients were cured of hyperaldosteronism by unilateral adrenalectomy but still need some antihypertensive therapy, whereas one patient has probable bilateral adrenal disease, with normal blood pressure on a low dose of spironolactone. In patients with severe hypertension due to primary hyperaldosteronism, PRA can escape suppression if hypertensive kidney damage supervenes. An increased aldosterone/PRA ratio is still useful in screening for primary hyperaldosteronism. These patients may respond to spironolactone therapy with a strong increase in serum creatinine and potassium. Early specific treatment of primary hyperaldosteronism is therefore indicated, and even a patient with advanced hypertension will profit from adrenalectomy or cautious spironolactone treatment.
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2/31. hypertension in an adolescent boy.

    We report the case of an adolescent boy who presented with hypertension and hypokalemia. A systematic work-up revealed hyperreninemic hyperaldosteronism. Further study revealed Page kidney caused by trauma-associated renal hematoma. The evaluation and management of hyperaldosteronism and Page kidney are discussed.
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3/31. Autosomal dominant polycystic kidney disease with primary hyperaldosteronism.

    We report three cases of primary aldosteronism associated with autosomal dominant polycystic kidney disease. The diagnosis of primary hyperaldosteronism was based on the presence of hypokalaemia with excessive urinary potassium excretion and/or the characteristic hormonal changes. Renal function impairment due to autosomal dominant polycystic kidney disease could mask hypokalaemia. The interpretation of adrenal imagery may be hindered by adjacent renal cysts. In one case an adrenal adenoma was detected and surgically removed, with only partial correction of the blood pressure. This could be explained by the persisting underlying autosomal dominant polycystic kidney disease. We conclude that in a hypertensive patient with polycystic kidney disease, extrarenal causes of hypertension may be present.
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4/31. Cardiomyopathy in an adult with Bartter's syndrome and hypokalemia. Hemodynamic, angiographic and metabolic studies.

    A case of an adult with Bartter's syndrome (hyperplasia of the juxtaglomerular complex with hyperaldosteronism and hypokalemic alkalosis) is described; the patient had the unusual manifestation of cardiomyopathy, probably secondary to severe hypokalemia. Results of metabolic studies and kidney biopsy were consistent with Bartter's syndrome; angiographic and hemodynamic findings were abnormal. The cardiomyopathy was confirmed at autopsy after the patient's sudden death. Conclusions from this case are that severe hypokalemia can pose a serious threat both immediately in the form of dangerous arrhythmias and in the long term in the form of cardiomyopathy.
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5/31. A case of pseudoaldosteronism, accompanied with hypocalcemia and exaggerated ACTH response.

    glycyrrhizic acid (GA) inhibits the activity of 11beta-hydroxysteroid dehydrogenase type 2 in the kidney, with the resulting increase in intrarenal cortisol concentration leading to hypertension and suppression of the renin-aldosterone system. In this paper we describe an interesting case of pseudoaldosteronism, associated with hypocalcemia and an exaggerated ACTH response. A 72-year-old woman was referred to our department for further evaluation of hypokalemia and hypocalcemia. The patient had been taking GA (150 mg/day) for the previous year for treatment of liver damage. plasma renin activity and aldosterone concentration were both within lower normal limits. Urinary excretion of potassium and calcium was within the upper limit of the normal range and increased with administration of supplements. plasma ACTH levels increased markedly in response to an intravenous injection of CRH. Cessation of GA and the potassium and calcium supplements on admission, led to a gradual normalization of serum potassium and calcium levels and blood pressure. The hypocalcaemia in our patient was related to decreased tubular reabsorption of calcium as a consequence of renal corticoid excess. It is possible that an increase in the number of CRH receptors in the pituitary following GA treatment caused the exaggerated ACTH response in association with pseudoaldosteronism. The existence of hypocalcemia and an exaggerated ACTH response should be observed carefully when managing pseudoaldosteronism.
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6/31. Renal transplantation unveils Conn's syndrome: a case report.

    Primary hyperaldosteronism or Conn's syndrome is rare after renal transplantation. We present a case of a 34-year-old woman with end-stage renal disease, who had received a living renal transplant and showed persistent hypertension and hypokalemia. The common causes of hypertension after kidney transplantation were excluded and hypokalemia persisted despite potassium supplementation and angiotensin converting enzyme inhibitors. Biochemical findings revealed extremely elevated plasma aldosteron levels, suppressed plasma renin activity, and massive urinary potassium wasting. Abdominal computerized tomography scan showed a left 25-mm adrenal nodule. Her hypertension and hypokalemia was cured by the removal of the adenoma.
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7/31. Mast cell chymase in the ischemic kidney of severe unilateral renovascular hypertension.

    Chymase degrades angiotensin I (AI) to form angiotensin ii (AII), probably constituting a bypass of the renin-angiotensin cascade. Chymase activity increases in some vascular diseases. In the kidney, an increase in chymase activity was reported in an animal model of ischemic kidney of renovascular hypertension (RVH); however, no such evidence has been provided in humans. We treated a 64-year-old patient with severe unilateral RVH and atherosclerosis, for whom removal of the ischemic kidney was the only option. Using immunohistochemical staining, we investigated chymase activity in the removed kidney and associated artery and vein. An increase in chymase activity, together with mast cells infiltrating the interstitium, was observed where interstitial fibrosis was seen. In the renal artery, where severe atherosclerosis was seen, and also in the vein, mast cell infiltration in the adventitia was accompanied by chymase. The captopril test showed an increase in serum aldosterone level, with a concomitant increase in plasma renin activity and decrease in blood pressure. Because the decrease in blood pressure implies a decrease in circulatory AII levels, it is plausible that in this patient, chymase had a role in AII formation in the adrenal gland to stimulate aldosterone secretion. Thus, by means of captopril, AI levels increased, and chymase may have produced AII in loci tissues, which, in turn, stimulated aldosterone secretion. This is the first report of an increase in chymase activity in the interstitium of an ischemic kidney and renal artery and vein in a patient with RVH and atherosclerosis.
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8/31. Laparoscopic adrenalectomy for Conn's syndrome complicated by ipsilateral congenital pelvic kidney.

    A patient presented with hypertension, hypokalemia, and a 1.2-cm left adrenal tumor. Conn's syndrome was diagnosed, for which laparoscopic adrenalectomy is now the therapy of choice. This case was complicated by an ipsilateral ectopic pelvic kidney. A laparoscopic left adrenalectomy was performed via a lateral transabdominal approach. Without the usual anatomic landmark of the ipsilateral kidney, the left adrenal gland was difficult to identify, so intraoperative ultrasound was used to locate the lesion. Postoperatively, the patient's blood pressure and potassium normalized. This is the first documented report of a laparoscopic adrenalectomy performed for adrenal adenoma with the anatomic disruption of an ipsilateral pelvic kidney.
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9/31. Long-term follow-up of a girl with primary aldosteronism: effect of potassium supplement.

    We followed up a girl with primary aldosteronism for 8 y, which was diagnosed at 6 y of age when she was referred to us for evaluation of heart murmur and growth failure. The diagnosis of bilateral adrenal hyperplasia was made by selective adrenal venous sampling. Following potassium supplement, her retarded growth was corrected dramatically, and she attained a normal adult height. puberty developed normally and menarche occurred at 12 y of age. blood pressure was also controlled adequately. Myocardial hypertrophy associated with aortic damage was noted at 13 y of age. Chronic renal failure developed with proteinuria and enlarged renal cysts. CONCLUSION: serum electrolytes should be included in the evaluation of children with impaired growth. Although primary aldosteronism is a rare occurrence in children, the condition appears to deserve special attention not only from the viewpoint of growth failure and hypokalaemia but from the occurrence of late organ damage to the kidney and heart.
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10/31. Functional interpretation of the kidney juxtaglomerular apparatus using renin immunohistochemistry in Bartter's, pseudo-Bartter's and Conn's syndromes.

    A comparative study of renin immunoreactivity in the juxtaglomerular apparatus of the human kidney was performed using the indirect immunoperoxidase method on a random microscopic sections. In renal biopsies taken from a case of Bartter's syndrome and a case of pseudo-Bartter's syndrome, the number of renin-positive juxtaglomerular apparatus (JGA) and the number of renin-positive cells in each JGA were significantly greater than in five renal specimens from control autopsy cases. In Conn's syndrome, none of the glomeruli contained renin-immunoreactive JGA. The number of renin-positive cells/mm2 in the renal cortex in cases of Bartter's and pseudo-Bartter's syndromes were 17.5 and 20.3, respectively, while in the control group, the range was 0.78-1.77 (mean 1.08). Together with other histochemical findings routinely examined in renal specimens, renin immunohistochemistry on random sections may be helpful in diagnostic renal pathology.
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