Hyperphosphatemia

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

• Calcium and phosphate product should be <55 mg²/dL² (4.4 mmol²/L²) per National Kidney Foundation Dialysis Outcomes Quality Initiative.

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 (4–4.8 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

• Tumor lysis syndrome.

• Hypocalcemia

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