Cases reported "Hyperaldosteronism"

Filter by keywords:



Filtering documents. Please wait...

21/31. Hyperreninemia, lysozymuria, and erythrocytosis in fanconi syndrome with medullary cystic kidney.

    adult onset fanconi syndrome with medullary cystic kidney was diagnosed in a 30-year-old male with muscular weakness, hypokalemia, normal BP, hyperreninemia, and secondary aldosteronism. He also had non-specific aminoaciduria, lysozymuria, and beta 2-microglobulinuria. Urinary concentrating and acidifying capacity was impaired, and both sodium and potassium were lost into the urine. I.v. pyelography revealed medullary cystic kidney. Renal biopsy showed juxtaglomerular hyperplasia, heavy subintimal deposits and C3 and IgG in preglomerular arteriolar walls, and degenerative changes in the tubules, including loss of brush border and "macula densa-like" lesions. polycythemia with elevated serum erythropoietin levels, and raised blood ACTH values with features of cortisolism were also present. indomethacin therapy decreased plasma renin activity (PRA), plasma aldosterone, and urinary loss of potassium and sodium, while serum potassium approached normal levels. metoprolol, a beta-adrenergic blocking agent, caused similar effects. Insensitivity to the pressor effect of angiotensin ii was reversed by indomethacin treatment. somatostatin infusion lowered PRA and aldosterone without affecting BP. Several biochemical aberrations of this patient resemble Bartter's syndrome, including the effect of indomethacin.
- - - - - - - - - -
ranking = 1
keywords = kidney
(Clic here for more details about this article)

22/31. Surreptitious habitual vomiting simulating Bartter's syndrome.

    A patient with hypokalemic alkalosis, normotensive hyperreninism, hyperaldosteronism, increased levels of urinary and plasma prostaglandin E, and vascular hyporesponsivity to angiotensin ii was thought to have Bartter's syndrome. Results of a kidney biopsy showed hyperplasia of the juxtaglomerular apparatus but no renomedullary cell hyperplasia. A 24-hour urine collection showed a low chloride level and no increase in the fractional chloride clearance, thus excluding Bartter's syndrome. Subsequent disclosure of surreptitious, habitual vomiting explained the hypokalemia.
- - - - - - - - - -
ranking = 0.16666666666667
keywords = kidney
(Clic here for more details about this article)

23/31. hyperaldosteronism, hyperparathyroidism, medullary sponge kidneys, and hypertension.

    hyperparathyroidism and hyperaldosteronism coexisted in association with medullary sponge kidneys in a 27-year-old woman with severe hypertension. A modest fall in systolic and diastolic pressure followed removal of a parathyroid adenoma. blood pressure was controlled with spironolactone therapy and restored to normal after removal of an aldosterone-secreting adrenal tumor. Elevated levels of aldosterone may have been responsible for the severe hypertension, while hypercalcemia may have had a synergistic effect on the arteriolar response to circulating vasoactive peptides.
- - - - - - - - - -
ranking = 0.83333333333333
keywords = kidney
(Clic here for more details about this article)

24/31. hypertension in disguise--a trap for the unwary.

    A 36-year-old asymptomatic Chinese male with polycystic kidney disease (PKD) developed hypertension 1 year after the diagnosis of PKD. The patient was treated initially as for hypertension associated with PKD. However, over a 6-year period his hypertension became progressively difficult to control and he developed severe symptomatic hypokalemia. Subsequent investigations confirmed the presence of primary hyperaldosteronism. The initial computed tomographic scans of the adrenals did not reveal any definite adenomas. The patient subsequently underwent bilateral adrenal venous sampling, which suggested a left-sided source of aldosterone excess. A repeat computed tomography of the adrenals with fine cuts revealed a 6-mm diameter adenoma of the left adrenal gland. He underwent an uncomplicated left adrenalectomy. All antihypertensive and potassium supplements were stopped on the 5th postoperative day. Two and half years after the adrenalectomy he remains normotensive and normokalaemic without any medication. The case illustrates the importance of measuring serum potassium before initiation of any therapy and the need to consider secondary causes even if a primary association is known. It also reinforces the fact that when hypertension becomes difficult to control, a secondary cause has to be searched actively. The association between primary aldosteronism and renal cysts has been highlighted only recently. The association of polycystic kidneys and primary aldosteronism has been reported in the literature only once previously.
- - - - - - - - - -
ranking = 5.201331946039
keywords = kidney disease, kidney
(Clic here for more details about this article)

25/31. Reversible nephrotic syndrome due to high renin state in renovascular hypertension.

    Unilateral renal artery stenosis can lead to a non-functional kidney which secretes large amounts of renin. Four cases are presented in which the high renin state resulted in hypertension, proteinuria from the intact contralateral kidney, and secondary aldosteronism. The proteinuria was in the nephrotic range, which is unusual in renovascular hypertension, but gradually disappeared after correction of the high renin state by removal of the renin-secreting kidney or administration of an ACE inhibitor. Accordingly, when there is marked proteinuria in the presence of new-onset or rapidly progressive hypertension, hypokalaemic alkalosis, and a high peripheral PRA, renal artery stenosis should be considered since the proteinuria may be reversible after nephrectomy, repair of the ischaemic kidney or medical therapy.
- - - - - - - - - -
ranking = 0.66666666666667
keywords = kidney
(Clic here for more details about this article)

26/31. Primary aldosteronism detected after renal transplantation.

    A 44-year old female was admitted to our hospital for evaluation of uncontrolled hypertension. She received renal transplantation 3 months ago and suffered from a tingling sensation and weakness on both hands. Laboratory findings (low serum potassium, low plasma renin activity and elevated plasma aldosterone level) was consistent with primary aldosteronism. Through the postural study for plasma aldosterone and the adrenal CT finding we diagnosed this case as adrenal adenoma, which was confirmed by surgical removal. A retrospective review of medical records showed that characteristic findings in primary aldosteronism (hypokalemia and low plasma renin activity) were masked by renal failure and became evident after successful renal transplantation. It was suggested that impaired urinary potassium excretion and excess release of renin from the ischemic kidney masked the characteristic findings of primary aldosteronism. To our knowledge, this is the first report documenting the change of renin-angiotensin-aldosterone system after renal transplantation in a case of coexistence of primary aldosteronism and chronic renal failure.
- - - - - - - - - -
ranking = 0.16666666666667
keywords = kidney
(Clic here for more details about this article)

27/31. Autosomal dominant polycystic kidney disease complicated by primary aldosteronism. Case report and review of the literature.

    We report the case of a 42-year-old woman with autosomal dominant polycystic kidney disease complicated by primary aldosteronism. She had a history of hypertension for 12 years and was found to have hypokalemia and polycystic renal and hepatic disease. Endocrinological tests revealed hyporeninemia and hyperaldosteronemia. Adrenal scintigraphy and venography demonstrated a left adrenal adenoma. Blood sampled from the adrenal veins confirmed hyperaldosteronemia originating from the left adrenal gland. Left adrenalectomy was performed. After surgery, plasma renin activity, plasma aldosterone titer, and serum potassium level normalized. The mechanism for the development of primary aldosteronism with autosomal dominant polycystic kidney disease may be related to the activation of the renin-angiotensin system. Four years after left adrenalectomy, hepatic but not renal cysts showed a remarkable increase; the improvement in hypokalemia may have delayed the progression of kidney cysts.
- - - - - - - - - -
ranking = 30.374658342901
keywords = kidney disease, kidney
(Clic here for more details about this article)

28/31. prevalence of adrenal and extra-adrenal Conn syndrome in hypertensive patients.

    BACKGROUND: Primary aldosteronism (PA) is caused by an adrenal aldosterone-producing tumor (A-APT) or adrenal hyperplasia. An extra-adrenal APT (E-APT) as a cause of PA has been reported in 5 cases. autopsy studies show a high incidence of ectopic adrenocortical tissue. We did a prospective study of the prevalence of A-APTs and E-APTs and the biochemical features of E-APTs in patients with PA. methods: Hypertensive patients (N = 3900) referred to our unit were screened for PA by measuring renin activity, urinary aldosterone-18-glucuronide, tetrahydroaldosterone, and 18-hydroxycorticosterone (18-OH-B). Primary aldosteronism was found in 257 cases. The differentiation between A-APTs and adrenal hyperplasia was based on the results of postural response of renin, plasma aldosterone, 18-OH-B, computed tomography, isotope scanning, or adrenal venous aldosterone. Ultrasound examination of the abdomen was used to screen for E-APT. RESULTS: The cause of PA was bilateral adrenal hyperplasia in 101 cases, unilateral adrenal hyperplasia in 2, an A-APT in 146, and an E-APT in 1. The site of aldosterone production was uncertain in 7 patients who had normal adrenal glands on computed tomography but refused to undergo isotopic scanning and adrenal venous catheterization. Ultrasound examination disclosed normal retroperitoneum in 4 of the 7 cases but could not rule out E-APT in 3 cases. The biochemical features of the patient with the E-APT were similar to classic A-APT, with low renin, high aldosterone, and high 18-OH-B values without appropriate response to posture or to short-term volume expansion. The excision of the E-APT in the right kidney resulted in normalization of blood pressure and renin, aldosterone, and 18-OH-B levels. CONCLUSION: Although E-APT is rare, it should be considered in the interests of specific therapy for PA because aldosterone-secreting malignant ovarian tumors also have been reported.
- - - - - - - - - -
ranking = 0.16666666666667
keywords = kidney
(Clic here for more details about this article)

29/31. cystic fibrosis presenting with hypokalemia and metabolic alkalosis in a previously healthy adolescent.

    cystic fibrosis (CF) is an exocrine disease affecting multiple organ systems. patients with CF usually present with respiratory or gastrointestinal abnormalities. This study presents a case of a previously healthy 17-yr-old man who was diagnosed with CF after presenting with metabolic alkalosis and hypokalemia. The defect associated with CF is in the cystic fibrosis transmembrane regulator (CFTR), which acts primarily as a chloride channel. Partially functional CFTR may be associated with less severe pulmonary and gastrointestinal manifestations, as in the case presented. Dysfunctional CFTR in the sweat ducts of CF patients are responsible for excessive chloride and sodium losses, especially in warm weather. hypokalemia seen with heat stress is secondary to sweat as well as renal potassium wasting. Metabolic alkalosis is maintained by the excessive sweat sodium chloride losses which leads to extracellular fluid (ECF) volume contraction and chloride depletion. Generation of alkalosis may be related to dysfunctional CFTR in the kidney, but is most likely secondary to hypokalemia with ECF volume contraction. Finally, one must consider CF when confronted with hypokalemia and alkalosis in a previously healthy patient.
- - - - - - - - - -
ranking = 0.16666666666667
keywords = kidney
(Clic here for more details about this article)

30/31. indomethacin in Bartter's syndrome: does the syndrome represent a state of hyperprostaglandinism?

    In three patients with Bartter's syndrome, indomethacin administration resulted in the disappearance of the hypokalemic alkalosis and in a normalization of the elevated plasma renin activity. Changes in calcium and phosphate metabolism during indomethacin medication seemed to indicate an increase in reabsorption activity of the renal proximal tubulus. A kidney biopsy performed in one of the patients showed, besides hyperplasia of juxtaglomerular cells, hyperplasia of interstitial medullary cells which are presumed to produce prostaglandins. As indomethacin is a well-known inhibitor of prostaglandin synthesis, the observations suggest that an overproduction of renal prostaglandins could well be of pathogenetic significance in Bartter's syndrome.
- - - - - - - - - -
ranking = 0.16666666666667
keywords = kidney
(Clic here for more details about this article)
<- Previous || Next ->


Leave a message about 'Hyperaldosteronism'


We do not evaluate or guarantee the accuracy of any content in this site. Click here for the full disclaimer.