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Lesson: 33.B. Phosphate Balance.
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BY PAUL GEDEON

Pathophysiology of phosphate balance.

Physiological function of phosphate

  • *Relatively high concentration in ICF
  • Role in cellular signaling (cAMP etc.)
  • Phosphorylation to activate or deactivate enzymes as cofactors Buffer of bodily fluids
  • Component of bones
  • Nucleic acids (DNA, RNA)
  • ATP, GTP
  • Phospholipids

Regulation of phosphate level

  • PTH: Secretion stimulated by high serum phosphate which decreases activity of NaPi transporter leading to phosphaturia. Note: PTH will have effect on both calcium and phosphate so don’t forget about calcium in all this!
  • Absorbed in GI via same NaPi transported that is present in kidney; stimulatted by Vitamin D.
  • FGF-23:Exact effect still debated but concentration of FGF-23 is proportional to PTH, Vit D and phosphate level. FGF-23 acts to inhibit Vit D action (negative feedback) and stimulate renal loss of phosphate.

 Hypophosphatemia (<0.81 mmol/l)

Causes

  • EC to IC shift o Respiratory alkalosis = H shifted out of cells and into blood in exchange for phosphate, lowering the serum phosphate
    • Refeeding syndrome = recovery from malnutrition or chronic alcoholism causes using up of phosphate in rebuilding “damaged” metabolism  o Recovery from diabetic ketoacidosis
  • Admin of any substances that stimulates glycolysis (which uses phosphate) e.g insulin,
  • Bone reservoir disturbance o Hungry bone syndrome (explained in hypocalcemia): After surgical removal of parathyroids to treat osteitis fibrosa cystica, there is rapid deposition of phosphate and calcium to form new bone.
  • Excretion disturbance in kidney (congenital vs acquired) o PHPT = increased PTH causes phosphaturia o Hyper FGF-23 (x-linked hypophosphatemic rickets) = phosphaturia
    • Fanconi syndrome = Proximal tubular defect causing loss of bicarbonate (RTA-2) and other ions.
    • NaPi transported defect
    • Osmotic diuresis = in diabetic patients with significant glucosuria, loss of not only water but other ions including phosphate.
  • Intake disturbance o Fasting  o Alcoholism
    • Antacids (with Ca, Al, Mg) = complexation with phosphate will decrease blood phosphate
    • Chronic diarrhea or steatorrhea
    • Vit D deficiency = low intestinal Pi and calcium absorption

Clinical consequences

*Depletion of IC ATP = no energy for cellular metabolic function, leading to various consequences

  • Hematological o Hemolytic anemia
    • Reduced 2,3-BPG = decreased oxygen carrying capacity since normally 2,3-DPG regulates affinity of oxygen to hemoglobin.
    • Decreased leukocyte migration o Platelet dysfunction
  • Neuromuscular o CNS: Irritability, confusion, coma
    • Peripheral neurons: Paresthesia, increased nerve conduction velocity
    • Muscle weakness: proximal myopathy, dysphagia, ileus, respiratory failure
  • Bone = osteomalacia
  • Cardiovascular o Impaired muscle function o CMP
  • Renal dysfunction o Falling GFR
    • Abnormal tubular transport (loss of Ca, Ng, bicarbonate and glucose)

Hyperphosphatemia (>1.45mmol/l)

Causes

  • IC to EC shift (extensive tissue destruction) o Tumor lysis syndromeo Rhabdomyolysis (extensive skeletal muscle breakdown) o Hemolysis  o Fulminant hepatitis  o Bowel infarction
    • Acidosis = H moved into cell and phosphate moved out in exchange
  • Bone reservoir disturbance o Osteoporosis
    • CKD as a mineral and bone disorder
  • Excretion problems (kidney) o Renal failure (most common cause) = due to falling GFR
    • PTH resistance = no stimulation of phosphaturia in kidney o HypoPTH
  • Intake problems o Per os, IV load
    • Vit D intoxication
    • Phosphate enemas

Clinical manifestations

  • Short term o Hyperphosphatemia inhibits Vit D activation (hydroxylation) causing Hypocalcemia leading to tetany.
  • Long term o Ectopic calcification

o Secondary hyperPTH and development of CKD mineral and bone disorder.

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