Hypoaldosteronism overview: Difference between revisions
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===Primary Prevention=== | ===Primary Prevention=== | ||
There are no established measures for the [[primary prevention]] of hypoaldosteronism. | |||
===Secondary Prevention=== | ===Secondary Prevention=== | ||
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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
Common risk factors in the development of hypoaldosteronism include diabetes mellitus, sickle cell anemia, HIV, graves' disease, hypoparathyroidism, hypopituitarism myasthenia gravis, and pernicious anemia. Other less common risk factors include multiple myeloma, SLE-associated renal disease and Wolmans disease.
Screening
There is insufficient evidence to recommend routine screening for hypoaldosteronism.
Natural History, Complications, and Prognosis
If left untreated, hypoaldosteronism leads to hyperkalemia which can alter the function of cardiac conduction pathways. Depending upon the severity of hypoaldosteronism, hyperkalemia can be a life threatening condition. When serum potassium rises above ≥ 9 mEq/L, hyperkalemia may lead to ventricular fibrillation, PEA and even cardiac arrest. Common complications of hypoaldosteronism include hyperkalemia, metabolic acidosis, hypotension, hypovolemia and hyponatremia. Depending on the extent of the hyperkalemia and underlying renal or adrenal condition at the time of diagnosis, the prognosis of hypoaldosteronism may vary. Prognosis of hypoaldosteronism is generally good for patients who receive treatment.
Diagnosis
Diagnostic Criteria
There is no established criteria for the diagnosis of hypoaldosteronism. However, a positive history of hypotension, muscle weakness and fatigue should raise suspicion for hypoaldosteronism. These patients should first be tested for serum potassium levels, plasma renin activity (PRA), serum aldosterone, and serum cortisol. Asymptomatic hypoaldosteronism can also be discovered on routine laboratory evaluations.
History and Symptoms
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 ACEi, ARB and NSAID. 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.
Physical Examination
Patients with hypoaldosteronism usually appear fatigued. Physical examination of patients with hypoaldosteronism is usually unremarkable, unless there is severe hyperkalemia. Increased level of serum potassium level may present with muscle tenderness, hyporeflexia/areflexia and cardiac arrhythmias. The physical exam may also represent findings of underlying condition such as chronic kidney disease or diabetic nephropathy.
Laboratory Findings
Laboratory findings consistent with the diagnosis of hypoaldosteronism include hyperkalemia and mild non-anion gap metabolic acidosis. Other lab findings include hyponatremia, decreased aldosterone level, and variable amounts of plasma renin activity (depends upon the underlying condition).
Electrocardiogram
In hypoaldosteronism there are no specific ECG findings. However, hypoaldosteronism predisposes to hyperkalemia (decreased renal excretion) and occasional hyponatremia (from decreased renal absorption). Hyperkalemia leads to depression of SA node and conduction pathways such as AV node and His-Purkinje system causing bradycardia and conduction blocks. On the other hand, severe hyponatremia may present with ST segment elevation mimicking acute myocardial infarction.
X-ray
There are no x-ray findings associated with hypoaldosteronism.
Ultrasound
The best initial test to diagnose hypoaldosteronism include measuring plasma renin activity and aldosterone levels. However, ultrasound may be helpful in the diagnosis of hypoaldosteronism from disorders of renal or adrenal glands. Chronic kidney disease is an important cause of hypoaldosteronism and on ultrasound presents with reduced renal length, reduced renal cortical thickness, poor visibility of the renal pyramids and the renal sinus. Hypoaldosteronism from adrenal insufficiency may present with irregularly shrunken adrenal glands, adrenal nodules, and signs of calcium deposits.
CT scan
There are no CT scan findings associated with hypoaldosteronism. A CT scan is not routinely done for the diagnosis of hypoaldosteronism.
MRI
There are no specific MRI findings associated with hypoaldosteronism.
Other Imaging Findings
There are no other imaging findings associated with hypoaldosteronism.
Other Diagnostic Studies
There are no other diagnostic studies associated with hypoaldosteronism.
Treatment
Medical Therapy
Surgery
Primary Prevention
There are no established measures for the primary prevention of hypoaldosteronism.
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.