[鈉與鉀]之15: 高血鉀 - 起手式&開始DD


高血鉀的原因幾乎都可以從低血鉀的機制反過來推,所以D/D比較不複雜(小麻居然連圖都沒有,哈哈),但是治療上面因為是Medical emergency所以是重點唷。


開始D/D


1. 先排除pseudohyperkalemia
  • 含鉀的靜脈輸液、抽血時發生溶血、白血球血小板過多

2. 區分出transcellular shift
  • 酸血症、insulin deficiency(DM)、大量細胞壞死(tumor lysis, 橫紋肌溶解, ischemic bowel, 溶血)、 hyperkalemic periodic paralysis、
  • 藥物: β-blockers、毛地黃中毒、succinylcholine(機制:K+ efflux through AChRs-associated cation channels)

3. 腎臟排出K的能力?
接著要評估的是腎臟排出K的能力,這部分可以分為三個層面來想
(忘記了請回頭看入門概述裡的 "正常生理對鉀離子濃度的調控"):
  • Distal Na delivery不夠?
    1. 別忘了ENaC吸收鈉是ROMK排出鉀的原動力
    2. 這裡抓的閾值Urinary Na < 25mmol/L
  • Urinary Flow不夠?
    1. 別忘了Maxi-K/BK channel負責flow-dependent K secretion,就是tubule分泌能力OK(TTKG>8),但是K總共分泌的量仍然不夠
      Urinary K < 40mmol/L),主要有兩個:
    2. ECF不足(Aldosterone高,但尿腔的水也都被吸光了),或是
    3. Advanced kidney failure(eGFR<20,尿很少)
  • Aldosterone不夠或是作用不好?
    1. 我們使用α-fludrocortisone(本院:Florinef)來做鑑別診斷。α-fludrocortisone的Relative mineralocorticoid activity是glucocorticoid activity的十倍,臨床上用來做Aldosterone的replacement

4. 給α-fludrocortisone後TTKG有改善(>8)
代表本來是aldosterone製造不足的狀況,那我們得要看aldosterone的上游renin分泌的情況
  • 高Renin:先天或後天primary hypoaldosteronism
    1. Primary adrenal insufficiency
    2. Isolated aldosterone deficiency:Loss-of-function mutations in aldosterone synthase
    3. Acquired adrenal insufficiency:Critical illness, amyloidosis, metastasis of carcinoma to the adrenal gland或Antiphospholipid syndrome造成bilateral adrenal hemorrhage
    4. Heparin/LMWH:↓adrenal aldosterone response to Angiotensin-II and hyperkalemia
    5. ACEi, ARB
    6. Ketoconazole:inhibit steroidgenesis
    7. Adrenalitis in HIV patients(由CMV or tuberculosis造成)
  • 低Renin:先天或後天secondary hypoaldosteronism
    1. 臨床常見後天因素:DM, old age, renal insufficiency, SLE, multiple myeloma, acute GN
    2. Interstitial nephritis:減少renin分泌
    3. 藥物NSAID、COX-2 inhibitor、Aliskiren、β-blocker

5. 給了α-fludrocortisone後TTKG卻沒改善(<8)
代表是tubule對aldosterone產生了抗性,以下是可能的原因
  • Hyperkalemic distal RTA:SLE, sickle cell anemia, amyloidosis
  • Renal transplant
  • Pseudohypoaldosteronism (PHA)-I
    1. AD:Loss-of-function mutations of mineralocorticoid receptor
    2. AR:Loss-of-function mutations of ENaC
  • Pseudohypoaldosteronism (PHA)-II,又稱Gordon syndrome
  • Calcineurin inhibitors(Cyclosporine, Tacrolimus,背後的機轉有
    1. ↓COX-2 expression in the macula densa → Renin↓→ hyporeninemichypoaldosteronism
    2. Inhibit apical ROMK channels in the distal nephron
    3. Inhibit basolateral Na/K-ATPase
  • 藥物: Amiloride, Spironolactone, Triamterene, Trimethoprim, Epterenone等等

6.整理藥物對RAA system的影響


7. 最後再來看一下完整的流程圖唷!


上一篇:[鈉與鉀]之14: 低血鉀 - 如何治療
下一篇:[鈉與鉀]之16: 高血鉀 - 你聽過Pseudohypoaldosteronism嗎?


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