Archives of Clinical and Biomedical Research. Citation: Mohammad Tinawi. Archives of Clinical and Biomedical Research 4 : It is essential to the function of all living cells. Careful history and basic laboratory tests are usually adequate to diagnose most cases of hypokalemia.

Hypokalemia; Electrolyte disorder; Potassium disorders. Potassium is the most abundant intracellular cation. The amount excreted in the stool increases in advanced kidney disease as in patients on dialysis. The major segments of the nephron are the proximal tubule, the loop of Henle with its thin and thick limbs, the distal tubule, and the collecting duct which consists of the connecting tubule, the cortical collecting duct and the medullary collecting duct, see Figure 1.

The number of intercalated cells decline as the collecting duct slopes toward the medulla. Potassium filtered through the glomerulus is almost completely absorbed before reaching the collecting duct. Figure 1: The Nephron.

Figure 2.

renal manifestations of hypokalemia

In case of low effective circulatory volume, the renin-angiotensin-aldosterone system RAAS is activated with subsequent increase in angiotensin II and aldosterone levels. In case of hyperkalemia, aldosterone secretion is increased but angiotensin II is not activated. Recently, the complex molecular mechanism of these phenomena has been elucidated [10]. In a steady state potassium intake equals potassium excretion. See Table 1.

Hypokalemia is common in hospitalized and community dwelling subjects. A study in about community subjects aged 55 years or older the Rotterdam Study found hypokalemia in about 2. The prevalence in women was twice as in men. Hypokalemia was most prevalent in patients on thiazide diuretics, odds ratio OR : 7.

Inadequate intake is seen in starvation, dementia, and anorexia. See Table 2. This is seen in acute myelogenous leukemia AML.

renal manifestations of hypokalemia

Redistribution is seen in hypokalemic periodic paralysis.The most common cause is excess loss from the kidneys or gastrointestinal tract. Clinical features include muscle weakness and polyuria; cardiac hyperexcitability may occur with severe hypokalemia.

Diagnosis is by serum measurement. Treatment is giving potassium and managing the cause. See also Overview of Disorders of Potassium Concentration. Hypokalemia can be caused by decreased intake of potassium but is usually caused by excessive losses of potassium in the urine or from the gastrointestinal GI tract. Protracted vomiting or gastric suction which removes volume and hydrochloric acid causes renal potassium losses due to metabolic alkalosis and stimulation of aldosterone due to volume depletion; aldosterone and metabolic alkalosis both cause the kidneys to excrete potassium.

The transcellular shift of potassium into cells may also cause hypokalemia. This shift can occur in any of the following:.

renal manifestations of hypokalemia

Glycogenesis during total parenteral nutrition or enteral hyperalimentation stimulating insulin release. Stimulation of the sympathetic nervous system, particularly with beta 2-agonists eg, albuterolterbutalinewhich may increase cellular potassium uptake.

Thyrotoxicosis occasionally due to excessive beta-sympathetic stimulation hypokalemic thyrotoxic periodic paralysis. Familial periodic paralysis is a rare autosomal dominant disorder characterized by transient episodes of profound hypokalemia thought to be due to sudden abnormal shifts of potassium into cells.

Episodes frequently involve varying degrees of paralysis. They are typically precipitated by a large carbohydrate meal or strenuous exercise. Excess mineralocorticoid ie, aldosterone effect can directly increase potassium secretion by the distal nephrons and occurs in any of the following:. Adrenal steroid excess that is due to Cushing syndromeprimary hyperaldosteronismrare renin-secreting tumors, glucocorticoid-remediable aldosteronism a rare inherited disorder involving abnormal aldosterone metabolismand congenital adrenal hyperplasia.

Bartter syndromean uncommon genetic disorder that is characterized by renal potassium and sodium wasting, excessive production of renin and aldosterone, and normotension. Bartter syndrome is caused by mutations in a loop diuretic—sensitive ion transport mechanism in the loop of Henle. Gitelman syndrome is an uncommon genetic disorder characterized by renal potassium and sodium wasting, excessive production of renin and aldosterone, and normotension.

Gitelman syndrome is caused by loss of function mutations in a thiazide-sensitive ion transport mechanism in the distal nephron.

Liddle syndrome is a rare autosomal dominant disorder characterized by severe hypertension and hypokalemia. Liddle syndrome is caused by unrestrained sodium reabsorption in the distal nephron due to one of several mutations found in genes encoding for epithelial sodium channel subunits. Inappropriately high reabsorption of sodium results in both hypertension and renal potassium wasting.

Renal potassium wasting can also be caused by numerous congenital and acquired renal tubular diseases, such as the renal tubular acidoses and Fanconi syndromean unusual syndrome resulting in renal wasting of potassium, glucose, phosphate, uric acid, and amino acids.

Hypomagnesemia is a common correlate of hypokalemia. Much of this correlation is attributable to common causes ie, diuretics, diarrheabut hypomagnesemia itself may also result in increased renal potassium losses.

Diuretics are by far the most commonly used drugs that cause hypokalemia. Potassium-wasting diuretics that block sodium reabsorption proximal to the distal nephron include. By inducing diarrhea, laxatives, especially when abused, can cause hypokalemia. Surreptitious diuretic or laxative use or both is a frequent cause of persistent hypokalemia, particularly among patients preoccupied with weight loss and among health care practitioners with access to prescription drugs.

Mild hypokalemia serum potassium 3 to 3. Other muscular dysfunction includes cramping, fasciculations, paralytic ileus, hypoventilation, hypotension, tetany, and rhabdomyolysis. Persistent hypokalemia can impair renal concentrating ability, causing polyuria with secondary polydipsia.

renal manifestations of hypokalemia

When the mechanism not evident clinically, hour urinary potassium excretion and serum magnesium concentration. It should be suspected in patients with typical changes on an ECG or who have muscular symptoms and risk factors and confirmed by blood testing. ECG should be done on patients with hypokalemia.This material must not be used for commercial purposes, or in any hospital or medical facility.

Failure to comply may result in legal action. Medically reviewed by Drugs. Last updated on Nov 16, Hypokalemia is a low level of potassium in your blood. Potassium helps control how your muscles, heart, and digestive system work. Hypokalemia occurs when your body loses too much potassium or does not absorb enough from food. You may not have any signs or symptoms if you have mild hypokalemia. You may have any of the following if it is more severe:. You will receive potassium to bring your levels back to normal.

This may be given as a pill or IV.

What to know about hypokalemia

The amount of potassium you will be given depends on your potassium level. Foods that are high in potassium include bananas, oranges, tomatoes, potatoes, and avocado. Pinto beans, turkey, salmon, lean beef, yogurt, and milk are also high in potassium. Ask your healthcare provider or dietitian for more information about foods that are high in potassium. Always consult your healthcare provider to ensure the information displayed on this page applies to your personal circumstances.

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Disorders of Potassium Balance: Hypokalemia & Hyperkalemia

Subscribe to Drugs. This material is provided for educational purposes only and is not intended for medical advice, diagnosis or treatment. Skip to Content. CareNotes Hypokalemia Print Share. Hypokalemia Medically reviewed by Drugs. Learn more about Hypokalemia Associated drugs Hypokalemia. More About Hypokalemia Medication Guide 1 related article. Subscribe to our newsletters. FDA Safety Alerts. Daily MedNews. Weekly Drug News Roundup.

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Monthly Newsletter. I accept the Terms and Privacy Policy. Email address. Select one or more newsletters to continue.Low potassium hypokalemia has many causes. The most common cause is excessive potassium loss in urine due to prescription medications that increase urination. Also known as water pills or diuretics, these types of medications are often prescribed for people who have high blood pressure or heart disease. Vomiting, diarrhea or both also can result in excessive potassium loss from the digestive tract.

Occasionally, low potassium is caused by not getting enough potassium in your diet. Causes shown here are commonly associated with this symptom. Work with your doctor or other health care professional for an accurate diagnosis.

Hypokalemia: Treatment

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Request Appointment. Symptoms Low potassium hypokalemia. Definition Causes When to see a doctor. Products and services. Free E-newsletter Subscribe to Housecall Our general interest e-newsletter keeps you up to date on a wide variety of health topics.

Sign up now. Show references Adams JG.Patient information : See related handout on potassiumwritten by the authors of this article. Hypokalemia and hyperkalemia are common electrolyte disorders caused by changes in potassium intake, altered excretion, or transcellular shifts.

Diuretic use and gastrointestinal losses are common causes of hypokalemia, whereas kidney disease, hyperglycemia, and medication use are common causes of hyperkalemia. When severe, potassium disorders can lead to life-threatening cardiac conduction disturbances and neuromuscular dysfunction.

Therefore, a first priority is determining the need for urgent treatment through a combination of history, physical examination, laboratory, and electrocardiography findings.

Indications for urgent treatment include severe or symptomatic hypokalemia or hyperkalemia; abrupt changes in potassium levels; electrocardiography changes; or the presence of certain comorbid conditions.

Hypokalemia is treated with oral or intravenous potassium. To prevent cardiac conduction disturbances, intravenous calcium is administered to patients with hyperkalemic electrocardiography changes. Insulin, usually with concomitant glucose, and albuterol are preferred to lower serum potassium levels in the acute setting; sodium polystyrene sulfonate is reserved for subacute treatment.

For both disorders, it is important to consider potential causes of transcellular shifts because patients are at increased risk of rebound potassium disturbances.

Potassium disorders are common.

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Hypokalemia serum potassium level less than 3. Patients with a history of congestive heart failure or myocardial infarction should maintain a serum potassium concentration of at least 4 mEq per L 4 mmol per L. Intravenous calcium should be administered if hyperkalemic ECG changes are present. Intravenous insulin and glucose, inhaled beta agonists, and dialysis are effective in the acute treatment of hyperkalemia.

Sodium polystyrene sulfonate Kayexalate may be effective in lowering total body potassium in the subacute setting. Hypokalemia results from abnormal losses, transcellular shifts, or insufficient intake Table 1. Laxatives and enemas. Osmotic diuresis. Mineralocorticoid excess.Hypokalemia describes a person having too little potassium in their blood.

If it is severe, it can lead to muscle weakness, which can have many health consequences. Hypokalemia is always a symptom of another illness or a side effect of a medication.

It is not an illness in itself. Therefore, the underlying condition requires treatment to resolve the hypokalemia. A person may not be aware of mild hypokalemia. However, if hypokalemia is moderate or severe, the individual is likely to have other signs of being unwell, for example, vomiting or diarrhea. If a person feels ill for an extended period, they should see a doctor. In this article, we look at the symptoms, causes, diagnosis, and treatment of hypokalemia, as well as the outlook for people with low potassium levels.

However, people who have moderate or severe hypokalemia, are older, or have heart or kidney issues can experience symptoms that relate to severe muscle weakness. According to the National Organization for Rare Disordersthese symptoms can include:. A study in the European Journal of Emergency Medicine looked at the data of 4, people who presented to the emergency department of a hospital with hypokalemia. The researchers found that just 1 percent of these individuals had severe hypokalemia, and only half of the people in this subgroup had any symptoms.

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A person may also not get sufficient potassium if they have a diet that contains very small amounts of it. However, it is unusual for this to be the cause of hypokalemia. Many foods contain potassium, and the kidneys are usually capable of reducing the excretion of potassium if the body is not getting enough.

A person might lose potassium too quickly for several different reasons. According to a clinical updatethese can include:. It can occur as a side effect of various medications. Hypokalemia is not an illness in itself, so when a person receives a diagnosis, the doctor will need to identify what is causing the loss of potassium.

In most cases, this is relatively straightforward. A doctor will check for:. If a doctor suspects that a person is hypokalemic, they may run tests to measure the amount of potassium in their body.

Once a doctor has determined the underlying issue that is causing hypokalemia, they can recommend a suitable treatment.


For example, if a person has hypokalemia as a result of prolonged vomiting, treating the cause of the vomiting will also address the hypokalemia. Alternatively, if a particular medication is making a person hypokalemic, then reducing or replacing that medication may resolve the problem.

The supplement will often be in the form of tablets, but intravenous delivery might be necessary if the hypokalemia is severe. Doctors may also instruct people to eat foods that are rich in potassium, such as bananasavocados, chard, and other plant-based foods. However, the authors of an article in the journal American Family Physician note that, although changing the diet can be beneficial, it is usually far less effective than taking potassium supplements.

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The outlook for a person with hypokalemia will depend on the underlying illness or side effect that is causing them to have low potassium.The extracellular fluid ECF and plasma potassium concentration [K] is much lower—in the 3. The very large transcellular gradient is maintained by active K transport via the Na-K-ATPase pumps present in all cell membranes and the ionic permeability characteristics of these membranes. Normal cell function requires maintenance of the ECF [K] within a relatively narrow range.

This is particularly important for excitable cells such as myocytes and neurons. The pathophysiologic effects of dyskalemia on these cells result in most of the clinical manifestations.

Transcellular ion movement. Most cells contain these pumps, antiporters, and channels. The effects of insulin, catecholamines, and thyroid hormones on K transport are shown. Individual potassium intakes vary widely—a typical Western diet provides between 50 and mEq K per day.

Normally, homeostatic mechanisms maintain plasma [K] precisely between 3. Rapid regulation of potassium concentration is needed to prevent potentially fatal hyperkalemia after every meal and is largely due to transcellular K shifts. Epinephrine and norepinephrine also rapidly regulate transcellular K balance and become especially important during and following vigorous exercise. Metabolic alkalosis stimulates cellular K uptake whereas some forms of hyperchloremic and other inorganic mineral acidoses enhance movement of K out of cells.

However, the common organic metabolic acidoses lactic and ketoacidosis do not directly cause any K shift. Respiratory acid—base abnormalities generally have small effects. Respiratory acidosis increases plasma [K] slightly. Hyperosmotic conditions that shift fluid out of cells are an important cause of K translocation to the ECF. Finally, hypokalemia per se moves K from the intracellular to the extracellular space. Potassium absorption in the small intestine is not specifically controlled.

Although colonic epithelial cells can increase K secretion in response to chronic hyperkalemia patients with chronic kidney diseasethe net effect on K balance is minor. Although the [K] in stool water may be high, the quantity of water in formed stool is small—thus absent diarrhea, total stool K excretion is low and most ingested K is absorbed.

Potassium excretion is principally into the urine and the main regulator of body K balance is the kidney. It is here that major regulation of K excretion occurs. The absorption of large amounts of Na, especially when delivered with an anion not easily absorbed Cl, HCO 3and othersgenerates a negative charge within the lumen and enhances the secretion of K and H Figure 4—2.

Aldosterone regulates the rate of Na absorption through these channels at multiple levels. K handling by the cortical collecting duct.

Aldosterone has multiple effects on electrolyte transport in the cortical collecting duct CCD. The influx of Na causes a negative charge to develop within the lumen. This stimulates K and H secretion into the lumen down electrical and chemical gradients.

Volume-contracted states result in little Na delivery to the CCD due to avid more proximal absorption so that K and H secretion is slight despite high aldosterone levels. Volume-expanded states enhance delivery of Na to the CCD and cause physiologically adequate levels of K and H secretion due to suppressed aldosterone levels. In normal individuals, an inverse relationship exists between aldosterone activity and CCD Na delivery.

A high salt intake will expand ECF volume, inhibit renin and aldosterone levels, and increase distal delivery and excretion of Na. High distal Na delivery counterbalances low aldosterone activity and the net effect is normal CCD K and H secretion and excretion.