vitamin-b-12 and Hyperaldosteronism

Primary aldosteronism is one of the most frequent causes of secondary arterial hypertension, and whether primary aldosteronism is associated with masked hypertension is unknown.. We describe a 64-year-old man with a history of hypothyroidism, recurring hypokalaemia, and normal home and office blood pressure values. Ambulatory blood pressure monitoring revealed masked hypertension with strikingly high systolic blood pressure variability and typical hypertension-mediated organ damage.. The patient required gradual escalation of antihypertensive medication to four drugs. During the diagnostic process we identified primary aldosteronism, cobalamin deficiency, severe obstructive sleep apnoea, and low baroreflex sensitivity (1.63 ms/mmHg). Following unilateral adrenalectomy, cobalamin supplementation and continuous positive airway pressure, we observed a spectacular improvement in the patient's blood pressure control, baroreflex sensitivity (4.82 ms/mmHg) and quality of life.. We report an unusual case of both masked arterial hypertension and primary aldosteronism. Elevated blood pressure values were masked in home and office measurements by coexisting hypotension which resulted most probably from deteriorated baroreflex sensitivity. Baroreflex sensitivity increased following treatment, including unilateral adrenalectomy. Hypertension can be masked by coexisting baroreceptor dysfunction which may derive from structural but also functional reversible changes.

Topics: Blood Pressure; Blood Pressure Monitoring, Ambulatory; Humans; Hyperaldosteronism; Hypertension; Male; Masked Hypertension; Middle Aged; Quality of Life; Vitamin B 12

Persistent hyperkalaemia was found in a patient with vitamin B12 unresponsive methylmalonic acidaemia associated with hyperuricaemia. At 3 years and 8 months of age, a serum potassium level of 6.8 mmol L-1 was found when blood gas measurement was normal. One year later azotaemia was noted. At the age of 5 years, renal function studies disclosed hyperaldosteronism, decreased creatinine clearance, reduction of the reabsorption of sodium at distal diluting segments and inadequate concentration of urine at the collecting ducts. The reduction of the reabsorption of sodium, which may have resulted in decreased potassium excretion, and the decrease in glomerular filtration rate, together with the superimposed excess intake of potassium, appeared to be responsible for the hyperkalaemia. Dietary potassium restriction was effective in suppressing the hyperkalaemia.

Topics: Child; Female; Glomerular Filtration Rate; Humans; Hyperaldosteronism; Hyperkalemia; Malonates; Metabolism, Inborn Errors; Methylmalonic Acid; Uremia; Uric Acid; Vitamin B 12