K+/Ca++ Secretion and Excretion

  1. Majority of potassium is stored intracellularly
  2. Often easier to transport potassium into cells rather than out of the body
  3. Insulin, epinephrine increase intracellular potassium uptake (Na+/K+ ATPase inducer)
  4. Crush injuries often cause hyperkalemia due to a release of intracellular potassium into the extracellular space
  5. Chemotherapy can cause hyperkalemia from cell damage leading to potassium release
  6. Acidosis can cause hyperkalemia as the kidneys preferentially excrete H+ ions
  7. Aldosterone has a short half-life of 10-20 minutes, and is released by Angiotensin II and increased plasma K+ levels
  8. Aldosterone increases K+ secretion and Na+ reabsorption
  9. 100% of K+ filtered load is reabsorbed before distal tube
  10. By stimulating Na/K ATPase and increasing the number of K+ channels, more potassium moves in the lumenal direction
  11. Aldosterone has much more of an impact of K+ excretion, even at low doses, with higher levels of plasma K+
  12. hyperkalemia is defined as K+ > 5.5 mEq/L
  13. Causes of hyperkalemia include kidney disease, acidosis, tissue damage, digitalis, hypoaldosteronism, insulin deficiency
  14. Hypokalemia can develop from alkalosis, decreased K+ intake, diarrhea, diuretics, hyperinsulinemia, hyperaldosteronism, increased epinephrine activity
  15. Calcium is moved from bone to plasma by Parathyroid hormone
  16. 50-60% of plasma Ca++ is filtered, rest bound to albumin, 2/3 reabsorbed in proximal tubule
  17. PTH causes reabsorption of calcium in the distal tubule in response of low plasma Ca++
  18. Klotho promotes uptake of calcium into the blood, and is a target of PTH
  19. PTH operates in a negative feedback loop
  20. Thyroid C cells release calcitonin
  21. PTH will also encourage excretion of phosphate
  22. PTH stimulates osteoclasts
  23. Vitamin D is necessary for calcium reabsorption from the gut
  24. Hyperparathyroidism can be a cause of hypercalcemia, or a secondary consequence of trying to overcome hypocalcemia
  25. Magnesium moves transcellularly and paracellularly, but levels off quickly transcellularly due to saturation
  26. Magnesium is mostly handled in the distal tubule and thick ascending loop
  27. Phosphate is handled in the proximal tubule by a sodium-phosphate symporter
  28. In the distal tubule, Magnesium is moved through the TRPM receptor, calcium through the TRPV