The symptoms of an elevated potassium level are nonspecific, and generally include malaise, palpitations, and muscle weakness. Hyperventilation may indicate a compensatory response to metabolic acidosis, which is one of the possible causes of hyperkalemia. Often, however, the problem is detected during screening blood tests for a medical disorder, or after hospitalization for complications such as cardiac arrhythmia or sudden cardiac death. High levels of potassium (> 5.5 mmol/L) have been associated with cardiovascular events.

Physicians taking a medical history may focus on kidney disease, medication use (e.g. potassium-sparing diuretics), which are common causes.

Mild hypokalemia is often without symptoms, although it may cause elevation of blood pressure, and can provoke the development of an abnormal heart rhythm. Severe hypokalemia, with serum potassium concentrations of 2.5–3 meq/l (Nl: 3.5–5.0 meq/l), may cause muscle weakness, myalgia, tremor, and muscle cramps (owing to disturbed function of skeletal muscle), and constipation (from disturbed function of smooth muscle). With more severe hypokalemia, flaccid paralysis and hyporeflexia may result. Reports exist of rhabdomyolysis occurring with profound hypokalemia with serum potassium levels less than 2 meq/l. Respiratory depression from severe impairment of skeletal muscle function is found in many patients.

Hypokalemia can result from one or more of these medical conditions:

Hyperkalemia, also spelled hyperkalaemia, is an elevated level of potassium (K) in the blood serum. Normal potassium levels are between 3.5 and 5.0 mmol/L (3.5 and 5.0 mEq/L) with levels above 5.5 mmol/L defined as hyperkalemia. Typically this results in no symptoms. Occasionally when severe it results in palpitations, muscle pain, muscle weakness, or numbness. An abnormal heart rate can occur which can result in cardiac arrest and death.

Common causes include kidney failure, hypoaldosteronism, and rhabdomyolysis. A number of medications can also cause high blood potassium including spironolactone, NSAIDs, and angiotensin converting enzyme inhibitors. The severity is divided into mild (5.5-5.9 mmol/L), moderate (6.0-6.4 mmol/L), and severe (>6.5 mmol/L). High levels can also be detected on an electrocardiogram (ECG). Pseudohyperkalemia, due to breakdown of cells during or after taking the blood sample, should be ruled out.

Initial treatment in those with ECG changes is calcium gluconate. Medications that might worsen the condition should be stopped and a low potassium diet should be recommended. Other medications used include dextrose with insulin, salbutamol, and sodium bicarbonate. Measures to remove potassium from the body include furosemide, polystyrene sulfonate, and hemodialysis. Hemodialysis is the most effective method. The use of polystyrene sulfonate, while common, is poorly supported by evidence.

Hyperkalemia is rare among those who are otherwise healthy. Among those who are in hospital, rates are between 1% and 2.5%. It increases the overall risk of death by at least ten times. The word "hyperkalemia" is from "hyper-" meaning high; "kalium" meaning potassium; and "-emia", meaning "in the blood".

Characteristic symptoms are:

- Sudden penetrating pain in the legs, lower back or abdomen

- Confusion, psychosis, slurred speech

- Severe lethargy

- Convulsions

- Fever

- Hyperkalemia (elevated potassium level in the blood)

- Hypercalcemia (elevated calcium level in the blood): the cause of hypercalcemia is a combination of increased calcium input into the extracellular space and reduced calcium removal by the kidney, this last caused by decreased glomerular filtration and increased tubular calcium reabsorption. Both renal factors are secondary to volume depletion and, in fact, improve rapidly during rehydration with saline infusion.

- Hypoglycemia (reduced level of blood glucose)

- Hyponatremia (low sodium level in the blood)

- Hypotension (low blood pressure)

- Hypothyroid (low T4 level)

- Severe vomiting and diarrhea, resulting in dehydration

- Syncope (loss of consciousness and ability to stand)

An overview of types 1, 2, and 4 is presented below (type 3 is usually excluded from modern classifications):

Distal RTA (dRTA) is the classical form of RTA, being the first described. Distal RTA is characterized by a failure of H+ secretion into lumen of nephron by the alpha intercalated cells of the medullary collecting duct of the distal nephron.

This failure of acid secretion may be due to a number of causes, and it leads to an inability to acidify the urine to a pH of less than 5.3. Because renal excretion is the primary means of eliminating from the body, there is consequently a tendency towards acidemia. There is an inability to excrete H while cannot be reclaimed by the cell, leading to acidemia (as builds up in the body) and hypokalemia (as cannot be reabsorbed by the alpha cell).

This leads to the clinical features of dRTA; In other words, the intercalated cells' apical H+/K+ antiporter is non-functional, resulting in proton retention and potassium excretion. Since calcium phosphate stones demonstrate a proclivity for deposition at higher pHs (alkaline), the substance of the kidney develops stones bilaterally; this does not occur in the other RTA types.

- Normal anion gap metabolic acidosis/acidemia

- Hypokalemia, Hypocalcemia, Hyperchloremia

- Urinary stone formation (related to alkaline urine, hypercalciuria, and low urinary citrate).

- Nephrocalcinosis (deposition of calcium in the substance of the kidney)

- Bone demineralisation (causing rickets in children and osteomalacia in adults)

- Sjogren's syndrome

The main causes of hypokalemic acidosis are systemic disorders that can be divided into:

- Carbonic anhydrase inhibitors such as acetazolamide

- Dialysis, in the post-treatment

- Diarrhea

- Renal tubular acidosis

- Treated DKA with insulin therapy

- VIPoma

Adrenal crisis is caused by a deficiency of cortisol resulting from Addison's disease, congenital adrenal hyperplasia (CAH), corticosteroid biosynthetic enzyme defects or pituitary disorders (such as Sheehan's syndrome, pituitary adenoma, hypopituitarism (inactive or underactive pituitary) causing failure to activate the adrenal glands.

Digoxin toxicity is often divided into acute or chronic toxicity. In both of these toxicity, cardiac effects are of the greatest concern. With an acute ingestion, symptoms such as nausea, vertigo, and vomiting are prominent. On the other hand, nonspecific symptoms are more predominate in chronic toxicity. These symptoms include fatigue, malaise, and visual disturbances.

The classic features of digoxin toxicity are nausea, vomiting, abdominal pain, headache, dizziness, confusion, delirium, vision disturbance (blurred or yellow vision). It is also associated with cardiac disturbances including irregular heartbeat, ventricular tachycardia, ventricular fibrillation, sinoatrial block and AV block.

In individuals with suspected digoxin toxicity, a serum digoxin concentration, serum potassium concentration, creatinine, BUN, and serial electrocardiograms is obtained.

Hypokalemic acidosis is a normal anion gap metabolic acidosis that has various direct and associated symptoms. Symptoms are associated with hypokalemia instead of hyperkalemia.

Respiratory acidosis is a medical emergency in which decreased ventilation (hypoventilation) increases the concentration of carbon dioxide in the blood and decreases the blood's pH (a condition generally called acidosis).

Carbon dioxide is produced continuously as the body's cells respire, and this CO will accumulate rapidly if the lungs do not adequately expel it through alveolar ventilation. Alveolar hypoventilation thus leads to an increased "Pa"CO (a condition called hypercapnia). The increase in "Pa"CO in turn decreases the HCO/"Pa"CO ratio and decreases pH.

An attack often begins with muscle pain, cramping, and stiffness. This is followed by weakness or paralysis that tends to develop rapidly, usually in late evening or the early hours of the morning. The weakness is usually symmetrical; the limb muscles closer to the trunk (proximal) are predominantly affected, and weakness tends to start in the legs and spread to the arms. Muscles of the mouth and throat, eyes, and breathing are usually not affected, but occasionally weakness of the respiratory muscles can cause life-threatening respiratory failure. Attacks typically resolve within several hours to several days, even in the absence of treatment. On neurological examination during an attack, flaccid weakness of the limbs is noted; reflexes are usually diminished, but the sensory system is unaffected. Mental status is not affected.

Attacks may be brought on by physical exertion, drinking alcohol, or eating food high in carbohydrates or salt. This may explain why attacks are more common in summer, when more people drink sugary drinks and engage in exercise. Exercise-related attacks tend to occur during a period of rest immediately after exercise; exercise may therefore be recommended to abort an attack.

There may be symptoms of thyroid overactivity, such as weight loss, a fast heart rate, tremor, and perspiration; but such symptoms occur in only half of all cases. The most common type of hyperthyroidism, Graves' disease, may additionally cause eye problems (Graves' ophthalmopathy) and skin changes of the legs (pretibial myxedema). Thyroid disease may also cause muscle weakness in the form of thyrotoxic myopathy, but this is constant rather than episodic.

If hyponatremia (low sodium) and hyperkalemia (high potassium) are severe, the resulting hypovolemia, prerenal azotemia, and cardiac arrhythmias may result in an Addisonian crisis. In severe cases, the patient may be presented in shock and moribund. Addisonian crisis must be differentiated from other life-threatening disorders such as diabetic ketoacidosis, necrotizing pancreatitis, and septic peritonitis.

The most common clinical manifestations are related to mental status and gastrointestinal function; they include lethargy, anorexia, vomiting, weight loss, and weakness. Additional findings may include dehydration, bradycardia, weak femoral pulses, and abdominal pain. Polyuria and polydipsia, diarrhea, and shivering are occasionally reported.

Symptoms of hypoadrenocorticism can include vomiting, diarrhea, lethargy, lack of appetite, tremors or shaking, muscle weakness, low body temperature, collapse, low heart rate, and pain in the hind quarters. Hypoglycemia can also be present, and initially may be confused with seizure disorders, insulin-secreting pancreatic tumor (insulinoma), food poisoning, parvovirus enteritis, gastric volvulus, spinal or joint problems, earning hypoadrenocorticism the nicknames of "the Great Mimic" and "the Great Imitator". It is possible not to see any signs of the disease until 90% of the adrenal cortex is no longer functioning.

Thyrotoxic periodic paralysis (TPP) is a condition featuring attacks of muscle weakness in the presence of hyperthyroidism (overactivity of the thyroid gland). Hypokalemia (a decreased potassium level in the blood) is usually present during attacks. The condition may be life-threatening if weakness of the breathing muscles leads to respiratory failure, or if the low potassium levels lead to cardiac arrhythmias (irregularities in the heart rate). If untreated, it is typically recurrent in nature.

The condition has been linked with genetic mutations in genes that code for certain ion channels that transport electrolytes (sodium and potassium) across cell membranes. The main ones are the L-type calcium channel α1-subunit and potassium inward rectifier 2.6; it is therefore classified as a channelopathy. The abnormality in the channel is thought to lead to shifts of potassium into cells, under conditions of high thyroxine (thyroid hormone) levels, usually with an additional precipitant.

Treatment of the hypokalemia, followed by correction of the hyperthyroidism, leads to complete resolution of the attacks. It occurs predominantly in males of Chinese, Japanese, Vietnamese, Filipino, and Korean descent. TPP is one of several conditions that can cause periodic paralysis.

Respiratory acidosis can be acute or chronic.

- In "acute respiratory acidosis", the "Pa"CO is elevated above the upper limit of the reference range (over 6.3 kPa or 45 mm Hg) with an accompanying acidemia (pH <7.36).

- In "chronic respiratory acidosis", the "Pa"CO is elevated above the upper limit of the reference range, with a normal blood pH (7.35 to 7.45) or near-normal pH secondary to renal compensation and an elevated serum bicarbonate (HCO >30 mm Hg).

The clinical picture is often dominated by the underlying cause.The symptoms of acute kidney injury result from the various disturbances of kidney function that are associated with the disease. Accumulation of urea and other nitrogen-containing substances in the bloodstream lead to a number of symptoms, such as fatigue, loss of appetite, headache, nausea and vomiting. Marked increases in the potassium level can lead to abnormal heart rhythms, which can be severe and life-threatening. Fluid balance is frequently affected, though blood pressure can be high, low or normal.

Pain in the flanks may be encountered in some conditions (such as clotting of the kidneys' blood vessels or inflammation of the kidney); this is the result of stretching of the fibrous tissue capsule surrounding the kidney. If the kidney injury is the result of dehydration, there may be thirst as well as evidence of fluid depletion on physical examination. Physical examination may also provide other clues as to the underlying cause of the kidney problem, such as a rash in interstitial nephritis (or vasculitis) and a palpable bladder in obstructive nephropathy.

In medicine (endocrinology), hypoaldosteronism refers to decreased levels of the hormone aldosterone.

Isolated hypoaldosteronism is the condition of having lowered aldosterone without corresponding changes in cortisol. (The two hormones are both produced by the adrenals.)

Symptoms can vary from person to person. Someone in early stage kidney disease may not feel sick or notice symptoms as they occur. When kidneys fail to filter properly, waste accumulates in the blood and the body, a condition called azotemia. Very low levels of azotaemia may produce few, if any, symptoms. If the disease progresses, symptoms become noticeable (if the failure is of sufficient degree to cause symptoms). Kidney failure accompanied by noticeable symptoms is termed uraemia.

Symptoms of kidney failure include the following:

- High levels of urea in the blood, which can result in:

- Vomiting or diarrhea (or both) which may lead to dehydration

- Nausea

- Weight loss

- Nocturnal urination

- More frequent urination, or in greater amounts than usual, with pale urine

- Less frequent urination, or in smaller amounts than usual, with dark coloured urine

- Blood in the urine

- Pressure, or difficulty urinating

- Unusual amounts of urination, usually in large quantities

- A buildup of phosphates in the blood that diseased kidneys cannot filter out may cause:

- Itching

- Bone damage

- Nonunion in broken bones

- Muscle cramps (caused by low levels of calcium which can be associated with hyperphosphatemia)

- A buildup of potassium in the blood that diseased kidneys cannot filter out (called hyperkalemia) may cause:

- Abnormal heart rhythms

- Muscle paralysis

- Failure of kidneys to remove excess fluid may cause:

- Swelling of the legs, ankles, feet, face, or hands

- Shortness of breath due to extra fluid on the lungs (may also be caused by anemia)

- Polycystic kidney disease, which causes large, fluid-filled cysts on the kidneys and sometimes the liver, can cause:

- Pain in the back or side

- Healthy kidneys produce the hormone erythropoietin that stimulates the bone marrow to make oxygen-carrying red blood cells. As the kidneys fail, they produce less erythropoietin, resulting in decreased production of red blood cells to replace the natural breakdown of old red blood cells. As a result, the blood carries less hemoglobin, a condition known as anemia. This can result in:

- Feeling tired or weak

- Memory problems

- Difficulty concentrating

- Dizziness

- Low blood pressure

- Normally, proteins are too large to pass through the kidneys, however, they are able to pass through when the glomeruli are damaged. This does not cause symptoms until extensive kidney damage has occurred, after which symptoms include:

- Foamy or bubbly urine

- Swelling in the hands, feet, abdomen, or face

- Other symptoms include:

- Appetite loss, a bad taste in the mouth

- Difficulty sleeping

- Darkening of the skin

- Excess protein in the blood

- With high doses of penicillin, people with kidney failure may experience seizures

There are several causes for this condition, including adrenal insufficiency, congenital adrenal hyperplasia, and medications (certain diuretics, NSAIDs, and ACE inhibitors).

- Primary Aldosterone deficiency

1. Primary adrenal insufficiency

2. Congenital adrenal hyperplasia (21 and 11β but not 17)

3. Aldosterone synthase deficiency

- Secondary Aldosterone deficiency

1. Secondary adrenal insufficiency

2. Diseases of the pituitary or hypothalamus

- Hyporeninemic hypoaldosteronism (due to decreased angiotensin 2 production as well as intra-adrenal dysfunction)

1. Renal dysfunction-most commonly diabetic nephropathy

2. NSAIDs

3. Ciclosporin

Crush syndrome (also traumatic rhabdomyolysis or Bywaters' syndrome) is a medical condition characterized by major shock and renal failure after a injury to skeletal muscle. Crush "injury" is compression of extremities or other parts of the body that causes muscle swelling and/or neurological disturbances in the affected areas of the body, while crush "syndrome" is localized crush injury with systemic manifestations. Cases occur commonly in catastrophes such as earthquakes, to victims that have been trapped under fallen or moving masonry.

Victims of crushing damage present some of the greatest challenges in field medicine, and may be among the few situations where a physician is needed in the field. The most drastic response to crushing under massive objects may be field amputation. Even if it is possible to extricate the patient without amputation, appropriate physiological preparation is mandatory: where permissive hypotension is the standard for prehospital care, fluid loading is the requirement in crush syndrome.

Acute kidney injuries can be present on top of chronic kidney disease, a condition called acute-on-chronic kidney failure (AoCRF). The acute part of AoCRF may be reversible, and the goal of treatment, as with AKI, is to return the patient to baseline kidney function, typically measured by serum creatinine. Like AKI, AoCRF can be difficult to distinguish from chronic kidney disease if the patient has not been monitored by a physician and no baseline (i.e., past) blood work is available for comparison.

Acute kidney injury (AKI), previously called acute renal failure (ARF), is an abrupt loss of kidney function that develops within 7 days.

Its causes are numerous. Generally it occurs because of damage to the kidney tissue caused by decreased kidney blood flow (kidney ischemia) from any cause (e.g., low blood pressure), exposure to substances harmful to the kidney, an inflammatory process in the kidney, or an obstruction of the urinary tract that impedes the flow of urine. AKI is diagnosed on the basis of characteristic laboratory findings, such as elevated blood urea nitrogen and creatinine, or inability of the kidneys to produce sufficient amounts of urine.

AKI may lead to a number of complications, including metabolic acidosis, high potassium levels, uremia, changes in body fluid balance, and effects on other organ systems, including death. People who have experienced AKI may have an increased risk of chronic kidney disease in the future. Management includes treatment of the underlying cause and supportive care, such as renal replacement therapy.