In the United States, hyperkalemia is induced by lethal injection in capital punishment cases. Potassium chloride is the last of the three drugs administered and actually causes death. Injecting potassium chloride into the heart muscle disrupts the signal that causes the heart to beat. This same amount of potassium chloride would do no harm if taken orally and not injected directly into the blood.

Several medical treatments shift potassium ions from the bloodstream into the cellular compartment, thereby reducing the risk of complications. The effect of these measures tends to be short-lived, but may temporize the problem until potassium can be removed from the body.

- Insulin (e.g. intravenous injection of 10-15 units of regular insulin along with 50 ml of 50% dextrose to prevent the blood sugar from dropping too low) leads to a shift of potassium ions into cells, secondary to increased activity of the sodium-potassium ATPase. Its effects last a few hours, so it sometimes must be repeated while other measures are taken to suppress potassium levels more permanently. The insulin is usually given with an appropriate amount of glucose to prevent hypoglycemia following the insulin administration.

- Salbutamol (albuterol), a β-selective catecholamine, is administered by nebulizer (e.g. 10–20 mg). This medication also lowers blood levels of K by promoting its movement into cells.

- Sodium bicarbonate may be used with the above measures if it is believed the person has metabolic acidosis.

Pseudohypoaldosteronism (PHA) is a condition that mimics hypoaldosteronism. However, the condition is due to a failure of "response" to aldosterone, and levels of aldosterone are actually elevated, due to a lack of feedback inhibition.

This syndrome was first described by Cheek and Perry in 1958. Later pediatric endocrinologist Aaron Hanukoglu reported that there are two independent forms of PHA with different inheritance patterns: Renal form with autosomal dominant inheritance exhibiting salt loss mainly from the kidneys, and multi-system form with autosomal recessive form exhibiting salt loss from kidney, lung, and sweat and salivary glands.

Treatment of severe forms of PHA requires relatively large amounts of sodium chloride.

These conditions also involve hyperkalemia.

Types include:

Type 4 RTA is not actually a tubular disorder at all nor does it have a clinical syndrome similar to the other types of RTA described above. It was included in the classification of renal tubular acidoses as it is associated with a mild (normal anion gap) metabolic acidosis due to a "physiological" reduction in proximal tubular ammonium excretion (impaired ammoniagenesis), which is secondary to hypoaldosteronism, and results in a decrease in urine buffering capacity. Its cardinal feature is hyperkalemia, and measured urinary acidification is normal, hence it is often called hyperkalemic RTA or tubular hyperkalemia.

Causes include:

- Aldosterone deficiency (hypoaldosteronism): Primary vs. hyporeninemic (including diabetic nephropathy)

- Aldosterone resistance

1. Drugs: NSAIDs, ACE inhibitors and ARBs, Eplerenone, Spironolactone, Trimethoprim, Pentamidine

2. Pseudohypoaldosteronism

Renal tubular acidosis (RTA) is a medical condition that involves an accumulation of acid in the body due to a failure of the kidneys to appropriately the urine. In renal physiology, when blood is filtered by the kidney, the passes through the tubules of the nephron, allowing for exchange of salts, acid equivalents, and other before it drains into the bladder as urine. The metabolic acidosis that results from RTA may be caused either by failure to reabsorb sufficient bicarbonate ions (which are alkaline) from the filtrate in the early portion of the nephron (the proximal tubule) or by insufficient secretion of hydrogen ions (which are acidic) into the latter portions of the nephron (the distal tubule). Although a metabolic acidosis also occurs in those with renal insufficiency, the term RTA is reserved for individuals with poor urinary acidification in otherwise well-functioning kidneys. Several different types of RTA exist, which all have different syndromes and different causes.

The word "acidosis" refers to the tendency for RTA to cause an excess of acid, which lowers the blood's pH. When the blood pH is below normal (7.35), this is called "acidemia". The metabolic acidosis caused by RTA is a normal anion gap acidosis.