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SOURCE

Source: Pai AB. Disorders of calcium and phosphorus homeostasis. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 10th ed. New York, NY: McGraw-Hill; 2017. http://accesspharmacy.mhmedical.com/content.aspx?bookid=1861&sectionid=146061894. Accessed March 31, 2017.

DEFINITION

  • Serum phosphorus >4.5 mg/dL (>1.45 mmol/L)

ETIOLOGY

  • Results from chronic kidney disease (CKD), AKI, or endogenous intracellular phosphate release.

    • Tumor lysis syndrome in patients treated for leukemia or lymphoma.

    • Hemolysis.

    • Rhabdomyolysis.

PATHOPHYSIOLOGY

  • Impaired glomerular filtration rate (GFR) decreases renal tubular reabsorption, leading to phosphate retention.

    • Under normal conditions, 85–90% of filtered phosphate reabsorbed via proximal tubule.

    • Retention of phosphate decreases vitamin D synthesis and induces hypocalcemia, leading to increase in parathyroid hormone (PTH).

  • Administration of oral and rectal phosphate-containing solutions in patients with moderate to several renal insufficiencies can result in hyperphosphatemia.

EPIDEMIOLOGY

  • Rare in general population.

  • Incidence: 70% in renal insufficiency or renal failure.

    • Nearly universal finding in patients with stages 4 and 5 CKD

PREVENTION

RISK FACTORS

  • Acute or chronic renal failure.

  • Chemotherapy administration for leukemia or lymphoma.

CLINICAL PRESENTATION

  • Uncommon in patients with normal kidney function.

  • May present as hypocalcemia and tetany.

SIGNS AND SYMPTOMS

  • Acute symptoms include:

    • Gastrointestinal (GI) disturbances.

    • Lethargy.

    • Obstruction of urinary tract.

    • Seizures (rare)

  • Chronic hyperphosphatemia associated with deposition of calcium-phosphate crystals into soft tissues, intrarenal calcification, nephrolithiasis, or obstructive uropathy.

    • Likely to form when product of serum calcium and phosphate concentrations exceeds 50–60 mg2/dL2 (44.8 mmol2/L2).

    • Calciphylaxis: tissue necrosis resulting from precipitation of crystals in arteries, joints, soft tissues, and viscera.

DIAGNOSIS

MEANS OF CONFIRMATION AND DIAGNOSIS

  • Serum phosphorus >4.5 mg/dL (>1.45 mmol/L)

LABORATORY TESTS

  • Metabolic panel.

    • Serum phosphorus.

    • Serum calcium.

  • Parathyroid hormone.

  • Vitamin D level.

DIFFERENTIAL DIAGNOSIS

DESIRED OUTCOMES

  • Normalize serum phosphate concentrations (or near normal in CKD).

  • Minimize long-term cardiovascular consequences of calcium-phosphate crystal deposition.

TREATMENT: PHARMACOLOGIC THERAPY

  • Most effective way to treat nonemergent hyperphosphatemia: decrease phosphate absorption from GI tract with phosphate binders and altering the dietary content of phosphorus.

  • Severe symptomatic hyperphosphatemia manifesting as hypocalcemia and tetany treated by IV administration of calcium.

MONITORING

  • Evaluate serum calcium every 4–6 hours during IV calcium infusions.

PROGNOSIS

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