Hyperphosphatemia

Hyperphosphatemia – Peter Thorne, Amanda Morrison

Background

  • Phosphate (PO4-3) >4.5mg/dL
  • Etiologies:
    • Cellular lysis (TLS, Rhabdomyolysis)
    • Increased intake/absorption or iatrogenic hyperphosphatemia (Over repletion, Vitamin D toxicity, use of Fleet’s enemas, etc.)
    • Decreased phosphate clearance (Acute or chronic renal disease, hypoparathyroidism, pseudohypoparathyroidism)
    • Acute extracellular shifts of phosphate (DKA, severe Lactic acidosis)

 

Presentation

  • Symptoms are usually secondary to coexistent hypocalcemia (psychosis, seizure, perioral paresthesia’s, muscle weakness)
  • Can cause Acute phosphate nephropathy with phosphate containing laxatives
  • Calciphylaxis if concurrent hypercalcemia (high Ca+2 x PO4-3product)

 

Evaluation

  • Labs: BMP (calcium, creatinine), Vit D, PTH, PTHrP, lactate

 

Management

Acute

  • If renal function normal, can often treat with IVF (promote PO4-3 excretion)
  • Consider need for calcium supplementation (see hypocalcemia section)
  • If renal function impaired and severe hypocalcemia present = consider hemodialysis

 

Chronic

  • Usually secondary to chronic renal failure, goal PO4-3 3.5-5.5 in CKD patients
  • Renal diet (low PO4-3)
  • PO4-3 binders: Ca+2 containing (calcium carbonate and calcium acetate) and non Ca+2 containing (sevelamer, lanthanum, and iron based such as ferric citrate)
      • Sevelamer is significantly more expensive than calcium containing binders
        • Given 3 times daily with meals, started at 800mg (Can be to 1,600mg TID)
        •  Should not be given if pt is not eating
      • Calcium acetate: started at 1334mg TID with meals
  • Limit dose changes to chronic binders upon discharge
  • Need to avoid calcium containing binders in patients with calciphylaxis