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