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.

Severe cases require hemodialysis or hemofiltration, which are the most rapid methods of removing potassium from the body. These are typically used if the underlying cause cannot be corrected swiftly while temporizing measures are instituted or there is no response to these measures.

Potassium can bind to agents in the gastrointestinal tract. Sodium polystyrene sulfonate with sorbitol (Kayexalate) has been approved for this use and can be given by mouth or rectally. However, careful clinical trials to demonstrate the effectiveness of sodium polystyrene are lacking, and use of sodium polystyrene sulfonate, particularly if with high sorbitol content, is uncommonly but convincingly associated with colonic necrosis. There are no systematic studies (>6 months) looking at the long-term safety of this medication. Another medication by the name of patiromer was approved in 2015.

Loop diuretics (furosemide, bumetanide, torasemide) and thiazide diuretics (e.g., chlorthalidone, hydrochlorothiazide, or chlorothiazide) can increase kidney potassium excretion in people with intact kidney function.

Fludrocortisone, a synthetic mineralocorticoid, can also increase potassium excretion by the kidney in patients with functioning kidneys. Trials of fludrocortisone in patients on dialysis have shown it to be ineffective.

Patiromer is a selective sorbent that is taken by mouth and works by binding free potassium ions in the gastrointestinal tract and releasing calcium ions for exchange, thus lowering the amount of potassium available for absorption into the bloodstream and increasing the amount that is excreted via the feces. The net effect is a reduction of potassium levels in the blood serum.

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

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:

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.