Potassium, Calcium, Phosphate, and Magnesium

Phosphate (PO4)

  • active and passive absorbsion by GI tract

  • mainly stored in bone and ICF

  • Kidneys reabsorb @ max rate

  • saturated basal transport = PO4 execrated in urine

  • acidosis increases excretion

PO4 reabsorption

  • @ apical side : into cell via symport w Na

    • PTH downregulates the apical transporters

    • Vit D hormones upregulates these transporters

  • @ basalateral side: out of ell via antiport w anion

  • Decreased max reabsorbsion rate

    • PTH

    • High PO4 diet

  • increased max reabsorbsion rate

    • Low PO4 diet

Parathyroid hormone & Calcitriol (Vit D3 hormone)

  • main hormones for Ca balance

  • low free Ca2 increases production of PTH & Calcitriol

  • Ca2+ receptors in the parathyroid glands sense low Ca2+ levels and cause release of PTH

    • Release of PTH requires Magnesium, so low Mg2+ leads to low Ca2

PTH action

  • Goal of PTH is to increase Ca2+ levels and Decrease PO4

  • Action of PTH

    • Bone resorption (release of Ca2+ and phosphate)

    • Kidney: Increased Ca2+ reabsorption and Phosphate excretion (decreased reabsorption)

    • Increased Calcitriol production

  • Even though PTH increases Ca2+ reabsorption, it also increases Ca2+ excretion because it increases the filtered load

    • Filtered load increases due to increased free Ca2+ via bone resorption 

Calcitriol formation

  • made from 1-𝛼-hydroxylase in PCT

  • kidney disease = low calcitriol = hypocalcemia

  • UV light req for production

Calcitriol

  • The goal of Calcitriol is to increase Ca2+ and phosphate levels

  • Actions of Calcitriol

    •  Small intestines: Increased Ca2+ and Phosphate absorption

    • Bone resorption (increase release of Ca2+ and phosphate)

    • Kidney: Increased Ca2+ and Phosphate reabsorption 

PCT Ca reabsorption

  • Ca2 is 100% filtered @ glomerulus

  • majority of Ca2 reabsorbsion occurs here

  • Ca2+ Reabsorbed passively via solvent drag = paracellular w Na and H2O

  • If plasma level is too high, Ca2+ reabsorption will decrease

    • Such as increased Na+ or water intake

Ascending loop Ca reabsorption

  •  Ca2+ reabsorbed paracellularly via electrochemical gradient generated by the NKCC transporter and ROMK

    • Positive charge generated by secretion of K+ into the ultrafiltrate pushes Ca2+ paracellular into the interstitium/blood

  • If the Ca2 sensor on the basolateral side senses increased Ca2+, it inhibits ROMK and the NKCC

  • Loop diuretics decrease Ca2+ reabsorption due to blocking NKCC, thus preventing ROMK from making the ultrafiltrate more positive

DCT Ca reabsorption

  • Ca2+ diffuses through Ca2+ channels on the apical side

  • Actively transported on the basolateral side in the Plasma membrane via Ca2+ ATPase (PMCa) and the Na+/Ca2+ Exchanger (NCX) send Ca2+ into the interstitium/blood

  • PTH increases Ca2+ reabsorption here by increasing the apical channels and PMCa activity

  • Thiazide diuretics increase Ca2+ reabsorption here because it keeps sodium in the urine, which increases NCX1 activity

Mg reabsorption

  • majority of Mg2 Reabsorption occurs in the Thick Ascending Limb

    • Loop diuretics block Mg2+ reabsorption here

  • Thiazide diuretics block Mg2+ reabsorption in DCT

K renal handling

  • 100% of filtered K is reabsorbed and can be secreted if needed

  • majority of K control occurs in DCT and colllecting duct

    • principal cells and type B cells secrete

    • Type A cells can reabsorb if K is low

  • K handling is affected by

    • blood K levels

    • aldosterone

    • tubular flow

K reabsorption

  • PCT: K+ is reabsorbed paracellularly due to solvent drag and the electrochemical gradient

  • Ascending limb: K+ is reabsorbed via the NKCC transporter

    • NH4+ can compete with K+ for this transporter

  • Collecting Duct: K+ is reabsorbed in Alpha intercalated cells via antiport with H+

    • Hypokalemia: more K+ is reabsorbed, which increases H+ secretion into the urine, causing metabolic alkalosis

    • Hyperkalemia: less K+ is reabsorbed, so less H+ is secreted, leading to metabolic acidosis

K excretion and distal Na delivery

  • Diuretics = Increased Ultrafiltrate and distal sodium delivery = increased K+ secretion

  • Late DCT: High flow as described above causes secretion of sodium via MAXI K+ (BK) channels

  • Cortical Collecting duct: K+ excretion occurs in principle cells

    • Aldosterone increases K+ excretion by increasing Na/K pump activity and adding ENaC and K+ channels