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Hyperphosphatemia

Peter Thorne and Amanda Morrison

Background

  • Phosphate (PO4-3) >4.5mg/dL

  • Etiologies:

    • Cellular shifts: Cellular lysis (TLS, Rhabdomyolysis), Acidemia

    • 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)

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), VBG, 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