1/7. Coexistence of atherosclerotic renal artery stenosis with primary hyperaldosteronism.The discovery of two forms of secondary hypertension in the same patient is unusual and suggests similar pathophysiological mechanisms, a predisposition to one type in the presence of the other or a chance occurrence. We describe two patients with renal artery stenosis who after successful correction of the stenotic lesions were discovered to have primary hyperaldosteronism associated with bilateral adrenal hyperplasia. Initially prior to revascularisation of the renal artery stenosis, the diagnosis of primary hyperaldosteronism was not evident. Both patients were subjected to further diagnostic evaluation after the appearance of hypokalaemia in one patient and continued resistant hypertension in both patients. The addition of spironolactone therapy reduced blood pressure impressively in both patients. Clinicians should be aware of the possibility that these two forms of secondary hypertension may be present in the same patient and that optimal blood pressure control requires diagnostic assessment and intervention for both disorders.- - - - - - - - - - ranking = 1keywords = hyperaldosteronism (Clic here for more details about this article) |
2/7. 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.- - - - - - - - - - ranking = 2keywords = hyperaldosteronism (Clic here for more details about this article) |
3/7. Intermittent hyperaldosteronism in a child due to an adrenal adenoma.aldosterone producing adenoma (APA) is a rare but potentially curable form of paediatric hypertension. We report a case of APA in a 9-year-old boy, suspected due to persistent hypokalaemia. Neither BP nor initial laboratory investigations disclosed the diagnosis and the presence of an APA was suggested by functional tests and radiological findings. Histologically, a cortical tumour was found associated with a marked medullary hyperplasia of both chromaffin and ganglion cells. CONCLUSION: This case reinforces the need for further investigations in patients with misleading clinical and laboratory data.- - - - - - - - - - ranking = 0.66666666666667keywords = hyperaldosteronism (Clic here for more details about this article) |
4/7. Primary hyperaldosteronism associated with hypertensive emergencies.There is growing awareness of primary hyperaldosteronism as a cause of secondary hypertension. Usually, it manifests as hypertension and hypokalemia, or as resistant hypertension. Much less often, primary hyperaldosteronism may be detected after a hypertensive emergency has developed. We highlight this association by reporting on eight patients with a clinical diagnosis of primary hyperaldosteronism whose course was complicated by a hypertensive crisis. In all patients, an elevated serum aldosterone, was accompanied by a suppressed plasma renin activity despite the presence of a hypertensive crisis. A good outcome was obtained either with laparoscopic adrenalectomy (1 patient) or with an antihypertensive drug regimen that included an antialdosterone agent (7 patients). The differential diagnosis of hypertensive emergencies should include primary hyperaldosteronism.- - - - - - - - - - ranking = 1.3333333333333keywords = hyperaldosteronism (Clic here for more details about this article) |
5/7. Angiotensin I level and sporadic hypokalemic periodic paralysis.A patient with secondary (sporadic type) hypokalemic periodic paralysis with relative hypertension had reninism with a high concentration of plasma angiotensin I (ANG-I) but no hyperaldosteronism or high angiotensin ii value. Angiotensin-converting enzyme (ACE) activity was usually normal. Results of other hormonal analyses were also normal. However, the glomerular filtration rate and filtration fraction of the kidneys were greatly elevated. Despite severe hypokalemia, the patient's potassium clearance was high. No evidence of distinct hyperplasia of the juxtaglomerular cells was obtained. These results suggest that decreased affinity of ACE to the substrate ANG-I (so-called ACE dysfunction syndrome) produced the reninism and high concentration of plasma ANG-I, and that the latter induced an increase in the glomerular filtration rate of the kidneys with sequential occurrence of secondary hypokalemic periodic paralysis.- - - - - - - - - - ranking = 0.16666666666667keywords = hyperaldosteronism (Clic here for more details about this article) |
6/7. hypertension, hyperreninemia, and secondary hyperaldosteronism in systemic necrotizing vasculitis.We studied the pathogenesis of hypertension in two patients with hepatitis-B surface antigen-positive systemic necrotizing vasculitis. Both presented with hypertension, hypokalemia, and renal potassium wasting. plasma renin activity and urinary aldosterone levels were markedly elevated. Renal arteriograms showed widespread microaneurysms, and necrotizing vasculitis involving renal arteries was confirmed histologically. hypertension was refractory to conventional treatment in both patients. In one patient, hypertension was easily controlled with the angiotension-converting enzyme inhibitor captopril. Diffuse renal vasculitis with secondary hyperreninemia and hyperaldosteronism appears to be an important cause of hypertension in patients with systemic necrotizing vasculitis.- - - - - - - - - - ranking = 0.83333333333333keywords = hyperaldosteronism (Clic here for more details about this article) |
7/7. Hyperreninemia and secondary hyperaldosteronism in pheochromocytomas.Foremost in the differential diagnosis of hypertension is the identification of surgically correctable lesions. Increased plasma renin activity in a hypertensive patient suggests the presence of a renovascular or renal etiology. We have recently seen two adolescent patients whose hyperreninemia was cuased by a pheochromocytoma. Secondary hyperaldosteronism was an associated finding.- - - - - - - - - - ranking = 0.83333333333333keywords = hyperaldosteronism (Clic here for more details about this article) |