Hypoaldosteronism overview: Difference between revisions
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==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
In hospitalized [[patients]] the [[incidence rate]] of hypoaldosteronism is 3000 per 100,000 individuals. The [[prevalence]] rate of hypoaldosteronism in United states is estimated to be 200,000 cases. Hypoaldosteronism is most commonly seen in middle-aged and older individuals. Both men and women are affected equally. Hypoaldosteronism is more prevalent in African-American, Native Americans, and Hispanics. | |||
==Risk Factors== | ==Risk Factors== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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Overview
Hypoaldosteronism refers to decreased levels of the hormone aldosterone.
There are several causes for this condition, including primary adrenal insufficiency, congenital adrenal hyperplasia, and medications (certain diuretics, NSAIDs, and ACE inhibitors).
This condition may result in hyperkalemia, which can be serious medical condition. It can also cause hyponatremia.
Historical Perspective
Hypoaldosteronism was first described by an American physician Hudson JB in the year 1956. Later on, in the year 1964, physicians Viser and Ulick gave a description on isolated and congenital hypoaldosteronism respectively.
Classification
Hypoaldosteronism may be classified into two categories depending on the level of plasma renin and depending on the level of aldosterone into hyporeninemic hypoaldosteronism or hyperreninemic hypoaldosteronism, and aldosterone deficiency or aldosterone resistance.
Pathophysiology
Hypoaldosteronism is defined as decreased levels of the hormone aldosterone or a resistance of the target tissue to the actions of aldosterone. Hypoaldosteronism from decreased production is seen in conditions such as congenital isolated hypoaldosteronism, primary adrenal insufficiency, diabetic nephropathy, critical illness, and drugs such as ACE inhibitors, NSAIDs and calcineurin inhibitors. Resistance of the target tissue to the actions of aldosterone is seen with mineralocorticoid receptor defects (seen in pseudohypoaldosteronism) and with drugs such as potassium-sparing diuretics and trimethoprim. Hypoaldosteronism results in reduced reabsorption of sodium in the principal cells of cortical collecting tubules (CCT). This leads to decreased excretion of potassium (hyperkalemia) and mild non-anion gap metabolic acidosis. On gross pathology, adrenal glands may be irregularly shrunken or hyperplastic.
Causes
The most common cause of hypoaldosteronism is diabetic nephropathy, acute glomerulonephritis, tuberculosis, hemorrhage, infarction, sarcoidosis, AIDS, CMV, and Addison's disease. Less common causes of hypoaldosteronism include sarcoidosis, amyloidosis, fungal infections, AIDS complications, and hemochromatosis.
Differentiating Hypoaldosteronism from Other Diseases
Hypoaldosteronism must be differentiated from other diseases that cause hypotension and muscle weakness such as Addison's disease, myopathies, celiac disease, Peutz-Jeghers syndrome, anorexia nervosa, syndrome of inappropriate anti-diuretic hormone (SIADH), neurofibromatosis, porphyria cutanea tarda, salt-depletion nephritis and bronchogenic carcinoma. In addition, measurement of plasma renin activity (PRA), serum aldosterone, and serum cortisol is used to differentiate among various subtypes of hypoaldosteronism.
Epidemiology and Demographics
In hospitalized patients the incidence rate of hypoaldosteronism is 3000 per 100,000 individuals. The prevalence rate of hypoaldosteronism in United states is estimated to be 200,000 cases. Hypoaldosteronism is most commonly seen in middle-aged and older individuals. Both men and women are affected equally. Hypoaldosteronism is more prevalent in African-American, Native Americans, and Hispanics.
Risk Factors
Screening
Natural History, Complications, and Prognosis
Diagnosis
Diagnostic Criteria
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
In hypoaldosteronism there are no specific ECG findings. However, hypoaldosteronism predisposes to hyponatremia (decreased renal absorption) and hyperkalemia (decreased renal excretion). Severe hyponatremia may present with ST segment elevation mimicking acute myocardial infarction. On the other hand, hyperkalemia leads to depression of SA node and conduction pathways such as AV node and His-Purkinje system causing bradycardia and conduction blocks.
X-ray
Ultrasound
CT scan
MRI
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Effective measures for the secondary prevention of hypoaldosteronism include liberal salt intake of 4gm/day (to increase plasma sodium concentration), decreasing potassium intake and avoidance of drugs that affects renin angiotensin aldosterone system (RAAS) such as ACE inhibitors, ARBs, potassium sparing diuretics and β-Adrenergic receptor blockers.