Hyperkalemia, 고칼륨혈증 유발 약제, 평가 공식, 관리 & 치료

고칼륨혈증 유발 메커니즘

• 신장의 칼륨 배설 장애
• 칼륨의 세포 이동 메커니즘 손상

 

고칼륨혈증 치료 방향 ⇛ Laboratory test 평가 

• Urine potassium, creatinine, and osmolarity 
• Serum potassium, creatinine, and osmolarity

 

고칼륨혈증 치료

• IV calcium : in reversing ECG changes and reducing the risk of arrhythmias (serum K에는 영향 X)
• IV insulin & glucose
• nebulized β-2 agonist
• sodium polystyrene therapy
• IV furosemide & saline

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Clinical recommendation

Patients with hyperkalemia who have electrocardiographic (ECG) changes, a rapid rate of rise of serum potassium, decreased renal function, or significant acidosis should be urgently treated.

Patients with hyperkalemia and characteristic ECG changes should be given intravenous calcium gluconate.

Acutely lower potassium by giving intravenous insulin with glucose, a beta2 agonist by nebulizer, or both.

Total body potassium should usually be lowered with sodium polystyrene sulfonate

Disorders causing hyperkalemia

칼륨의 신배설 장애로 인한 고칼륨혈증	세포외공간(extracellular space)로의 칼륨 이동(shift) 장애로 인한 고칼륨혈증
Acquired hyporeninemic hypoaldosteronism Addison’s disease Congenital adrenal hyperplasia (recesssive or autosomal dominant) Mineralocorticoid deficiency Primary hypoaldosteronism or hyporeninemia Pseudohypoaldosteronism Renal insufficiency or failure Systemic lupus erythematosus Type IV renal tubular acidosis	Acidosis Damage to tissue from rhabdomyolysis, burns, or trauma Familial hyperkalemic periodic paralysis Hyperosmolar states, (e.g., uncontrolled diabetes, glucose infusions) Insulin deficiency or resistance Tumor lysis syndrome

Hyporeninemic hypoaldosteronism

• 고칼륨혈증이 나타난 DM 환자에게서 판별 진단 고려(대체적으로 당뇨 환자의 serum aldosterone 낮음)
• oral fludrocortisone[플로리네프 정] 투여 → hyporeninemic hypoaldosteronism 환자라면 serum K 약제 시작 후 1-2 이내 정상치

Agents that may cause hyperkalemia

성분명	메커니즘 & 참고
Amiloride[아미로 정]	Diminishes potassium secretion by reducing the electrical gradient between the intracellular space and the renal tubule, causing potassium to leave the cells
Amino acids*	Lysine, arginine, or epsilon-aminocaproic acid enters cells in exchange for potassium, causing hyperkalemia
ARBs and ACE inhibitors	Decreases aldosterone synthesis; hyperkalemia often can be reduced by concomitant diuretic use; ARBs less likely to cause hyperkalemia than ACE inhibitors
Azole antifungals	Inhibits adrenal steroid synthesis, which can lead to aldosterone deficiency
Beta blockers	Decreases sodium-potassium adenosine triphosphatase (ATPase) activity; beta2 agonists decrease potassium levels
Cyclosporine [사이폴 엔 연질캡슐]	Suppresses renin release, leading to decreased aldosterone synthesis, decreased potassium secretion in collecting duct
Digoxin at toxic levels	Decreases sodium-potassium ATPase activity
Glucose infusions or insulin deficiency	Hypertonicity caused by hyperglycemia from glucose infusions can drive potassium out of the intracellular space, leading to hyperkalemia. Hyperkalemia may occur with continuous infusions or with boluses of hypertonic glucose. May be present with hypertonicity caused by other agents such as mannitol (Osmitrol) as well.
Heparins	Can cause hyperkalemia in patients with decreased renal function; inhibits adrenal aldosterone synthesis
NSAIDs	Decreased prostaglandin production leads to decreased afferent arteriolar flow, suppressing renin and aldosterone secretion. Typical of NSAIDs as well as cyclooxygenase-2 selective inhibitor drugs.
Packed red blood cells	Stored cells can partially hemolyze and release potassium when infused.
Potassium supplements or salt substitutes	Ingestion of potassium can lead to hyperkalemia, particularly if renal function is impaired; dietary sources include bananas, melon, and orange juice.
Spironolactone [알닥톤 정]	Inhibits binding of aldosterone to receptors in the renal tubule
Succinylcholine [석시콜린 주]	Increases nicotinic acetylcholine receptors in damaged skeletal muscle (e.g., trauma or burn patients)
Tacrolimus [아드바그랍 서방캡슐, 프로그랍 캡슐]	Suppresses renin release, leading to decreased aldosterone synthesis and decreased potassium secretion in collecting duct
Trimethoprim [셉트린 정, 세바트림 주]	Diminishes potassium secretion by reducing the electrical gradient between the intracellular space and the renal tubule, causing potassium to leave the cells.

* Hyperkalemia can occur in the setting of amino acids administered intravenously as part of total parenteral nutrition. It is unknown whether oral dietary amino acid supplements cause hyperkalemia

Treatment of hyperkalemia

성분명	용법/용량	onset	length of effect	주의
Calcium gluconate*	10% 용액 10-20 mL IV over 2-3 min	immediate	30 min	- digoxin toxicity 악화
Insulin	RI 10 IU + 50% DW 50 mL	15-30 min	2-6 hr	- 지속적인 insulin 투여 시 생길 수 있는 저혈당 예방을 위해 5DW 100 cc/hr add - BST 250 mg/dL 시 glucose add 불필요
Albuterol	10-20 mg by 네뷸 over 10 min (농도 : 5 mg/mL)	15-30 min	2-3 hr	- brief initial rise in serum potassium 발생할 수 있음
Furosemide	20-40 mg IV (volume delpetion 예방 위해 saline)	15-60 min	4 hr	- loop계 이뇨제에 반응성 남아있을 때 효과적임
Sodium polystyrene sulfonate	PO : 50 g Rectal : 50 g	1-2 hr (rectal route is faster)	4-6 hr	- sodium retention 유발 가능성 있음

* An alternative is to consider using magnesium instead of calcium to stabilize the myocardium.

* Some experts suggest using a slower calcium infusion for 20 to 30 minutes in patients with hyperkalemia who are on digitalis therapy.

** Sodium bicarbonate is no longer recommended to lower potassium, although it may be appropriate in patients with severe metabolic acidosis.

⇛ Hyperkalemia caused by the use of ACE inhibitors or angiotensin receptor blockers in patients with chronic renal failure and metabolic acidosis may respond to sodium bicarbonate supplementation. The dosage is 25 to 50 mEq daily (two tablets twice a day at 8 mEq each,) or baking soda (1/2 to 1 tsp daily). Concomitant diuretic use limits the risk of volume overload.

 

성분명	상품명	함량
Sodium bicarbonate	타스나 정 500 MG	≒ 6 mEq/1정 (as bicarbonate)

* sodium bicarbonate 몰질량 84g/mol

 

 

reference:

1) Hollander-Rodriguez, Joyce C., and James F. Calvert. "Hyperkalemia." American family physician 73.2 (2006): 283-290.