POTASSIUM-HYPERKALEMIA CAUSES

SUMMARY

1. Decreased renin: dysfunctional kidneys that do not release renin ("hyporeninemic hypoaldosteronism"); chronic interstitial nephritis; diabetes; exacerbated by NSAIDs

2. Decreased aldosterone:
- Potassium-sparing diuretics (Spironolactone blocks the aldosterone receptor; amiloride blocks the channel its action depends on)
- ACE inhibitors, angiotensin receptor antagonists, and renin inhibition
- Primary adrenal disease (Addison's), because it affects both the zona glomerulosa (site of aldosterone production) and fasciculata (site of cortisol production): but not secondary adrenal insufficiency because lack of ACTH affects only the zona fasciculata

-
Heparins (Both unfractionated and low molecular weight are directly toxic to the zona glomerulosa)

3. Cellular shift: metabolic acidosis (K⁺/H⁺ exchange), increased cell turnover (tumor lysis syndrome, rhabdomyolysis, acute leukemia)

4. Renal accumulation: Type 4 RTA

5. Drugs: Trimethoprim in TMP/SMX interferes with K⁺ secretion in the late distal tubule and cortical collecting duct

Reference(s)

Wilkinson, I., Furmedge, D. and Sinharay, R. (2017). Oxford handbook of clinical medicine. Oxford: Oxford University Press. Get it on Amazon.
Feather, A., Randall, D. and Waterhouse, M. (2020). Kumar And Clark’s Clinical Medicine. 10th ed. S.L.: Elsevier Health Sciences. Get it on Amazon.
Hannaman, R. A., Bullock, L., Hatchell, C. A., & Yoffe, M. (2016). Internal medicine review core curriculum, 2017-2018. CO Springs, CO: MedStudy.
Therapeutic Guidelines. Melbourne: Therapeutic Guidelines Limited. https://www.tg.org.au [Accessed 2021].