
Health Dictionary
Reliable, easy-to-read patient information on common medical conditions β written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.
Hypoaldosteronism history and symptoms
Introduction
Overview
Overview
Hypoaldosteronism often has a gradual onset. Patients of hypoaldosteronism should be enquired about the use of drugs that can alter aldosterone production or function. These drugs include ACE inhibitors, angiotensin receptor blockers and NSAIDs. The most common symptoms of hypoaldosteronism include fatigue, muscle weakness, and low blood pressure. Other less common symptoms of hypoaldosteronism include hyperpigmentation, gastrointestinal disturbances, and abdominal pain.
History and Symptoms
History and Symptoms
History
Obtaining a history gives important information in making a diagnosis of hypoaldosteronism. It provides an insight into the cause, precipitating factors, and associated comorbid conditions. A complete history will help determine the correct therapy and helps in determining the prognosis. Hypoaldosteronism patients are usually asymptomatic. Patients with hypoaldosteronism may have a positive history of:[1][2][3]
- Renal disease
- Diabetes mellitus
- History of fatigue
- Episodes of lightheadedness and palpitations
- Drug use such as ACE inhibitors, angiotensin receptor blockers and NSAIDs
- Craving for salty food
Common Symptoms
Common symptoms of hypoaldosteronism include:[4][5][6][7]
- Chronic fatigue
- Low blood pressure
- Lightheadedness
- Palpitations
- Muscle weakness
- Anorexia
- Weight loss
- Salt craving
- Dizziness
Less Common Symptoms
Less common symptoms of hypoaldosteronism include:[8]
- Hyperpigmentation
- Gastrointestinal disturbances
- Abdominal pain
- Depression
References
References
- β Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:14-15
- β Raebel MA (2012). “Hyperkalemia associated with use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers”. Cardiovasc Ther. 30 (3): e156β66. doi:10.1111/j.1755-5922.2010.00258.x. PMIDΒ 21883995.
- β Mann JF, Yi QL, Sleight P, Dagenais GR, Gerstein HC, Lonn EM, Bosch J (2005). “Serum potassium, cardiovascular risk, and effects of an ACE inhibitor: results of the HOPE study”. Clin. Nephrol. 63 (3): 181β7. PMIDΒ 15786818.
- β RodrΓguez Soriano J (2002). “Renal tubular acidosis: the clinical entity”. J. Am. Soc. Nephrol. 13 (8): 2160β70. PMIDΒ 12138150.
- β Tan SY, Burton M (1981). “Hyporeninemic hypoaldosteronism. An overlooked cause of hyperkalemia”. Arch. Intern. Med. 141 (1): 30β3. PMIDΒ 7004370.
- β Sarkar SB, Sarkar S, Ghosh S, Bandyopadhyay S (2012). “Addison’s disease”. Contemp Clin Dent. 3 (4): 484β6. doi:10.4103/0976-237X.107450. PMCΒ 3636818. PMIDΒ 23633816.
- β Arlt W, Allolio B (2003). “Adrenal insufficiency”. Lancet. 361 (9372): 1881β93. doi:10.1016/S0140-6736(03)13492-7. PMIDΒ 12788587.
- β Torpy DJ, Stratakis CA, Chrousos GP (1999). “Hyper- and hypoaldosteronism”. Vitam. Horm. 57: 177β216. PMIDΒ 10232050.
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Akshun Kalia M.B.B.S.[2]
