LAM Extra for General Practicioners

[Secondary hyperaldosteronism resulting from a feeding disorder]

TÓTH Géza, RÁCZ Károly, FŰTŐ László

JUNE 20, 2010

LAM Extra for General Practicioners - 2010;2(03)

[INTRODUCTION - A number of diseases can cause hyperreninaemia and secondary hyperaldosteronism due to the stimulation of the renin-angiotensin system (RAS). The authors present a case of a patient suffering from a feeding disorder, whose secondary hyperaldosteronism verified by hormone examinations recovered after resolution of the feeding disorder. CASE REPORT - The authors found that the patient, who had been on an extreme vegetarian diet and avioded all forms of common salt as well as natural sodium intake for 8 years, had consistently normal electrolite levels, normal blood pressure, elevated plasma renin activity (PRA) and plasma aldosterone levels. Salt loading and postural tests verified secondary hyperaldosteronism. All known diseases that might lead to elevated RAS activity were excluded. After cessation of the salt-restricted diet, the patient’s PRA and plasma aldosteron levels returned to the normal range, which confirmed the possibility that the secondary hyperaldosteronism developed because of the feeding disorder. CONCLUSION - The authors have not found similar hormon alterations due to alimentary causes in humans in the literature. According to their hypothesis, the feeding disorder might lead to secondary hyperaldosteronism via affecting the system or systems that regulate RAS activity.]

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[Secondary hyperaldosteronism resulting from a feeding disorder]

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[INTRODUCTION - A number of diseases can cause hyperreninaemia and secondary hyperaldosteronism due to the stimulation of the renin-angiotensin system (RAS). The authors present a case of a patient suffering from a feeding disorder, whose secondary hyperaldosteronism verified by hormone examinations recovered after resolution of the feeding disorder. CASE REPORT - The authors found that the patient, who had been on an extreme vegetarian diet and avioded all forms of common salt as well as natural sodium intake for 8 years, had consistently normal electrolite levels, normal blood pressure, elevated plasma renin activity (PRA) and plasma aldosterone levels. Salt loading and postural tests verified secondary hyperaldosteronism. All known diseases that might lead to elevated RAS activity were excluded. After cessation of the salt-restricted diet, the patient’s PRA and plasma aldosteron levels returned to the normal range, which confirmed the possibility that the secondary hyperaldosteronism developed because of the feeding disorder. CONCLUSION - The authors have not found similar hormon alterations due to alimentary causes in humans in the literature. According to their hypothesis, the feeding disorder might lead to secondary hyperaldosteronism via affecting the system or systems that regulate RAS activity.]

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