Immediate Questions

A. Does patient have tetany or other signs of acute hypocalcemia? Many patients with acute and severe hyperphosphatemia develop hypocalcemia and tetany. The hypocalcemia must be recognized and treated while measures to bring down the phosphate level are being initiated.

B. Does patient have acute or chronic renal failure? Renal failure is a significant risk factor for hyperphosphatemia and may dictate therapy. In acute situations, such as tumor lysis syndrome, the hyperphosphatemic patient may require dialysis.

C. What medication(s) does patient take? Excessive amounts of Vitamin D cause increased intestinal absorption of phosphate. Phosphate-containing enemas also may increase phosphate levels.

III. Differential Diagnosis. Phosphate is similar to other compounds, such as potassium and magnesium, which are largely intracellular and levels of which are dependent on renal excretion. Hyperphosphatemia is usually the result of decrease in renal excretion, shift from intracellular to extracellular pools, and intake of amounts beyond what the kidney can regulate.

Decreased Renal Excretion

1. Renal failure a. Acute renal failure. If associated with other mechanisms, can lead to severe, life-threatening hyperphosphatemia.

b. Chronic renal failure. Phosphate retention issues are routine.

2. Parathyroid disorders. Parathyroid hormone (PTH) stimulates the renal tubule to excrete phosphate. Decreased PTH effect results in hyperphosphatemia.

a. Hypoparathyroidism. Can be congenital (DiGeorge syndrome) or acquired (autoimmune polyglandular candidi-asis ectodermal dystrophy syndrome).

b. Pseudohypoparathyroidism. Renal tubules are resistant to PTH.

3. Other causes a. Physiologic phosphate levels in infants. Due to high phosphate reabsorption by proximal tubule.

b. Tumoral calcinosis. Transcellular Shifts From Intracellular to Extracellular Pools

1. Tumor lysis syndrome. Look for hyperkalemia, hyperuricemia, and acute renal failure.

2. Rhabdomyolysis.

3. Hemolysis.

4. Malignant hyperpyrexia. After anesthesia.

5. Diabetic ketoacidosis.

6. Respiratory acidosis. Increased Intake of Phosphate or Vitamin D

1. Enteric. Phosphate-containing laxatives and enemas.

2. High-phosphate formulas in newborns. See discussion of neonatal hypocalcemia in Chapter 46, Hypocalcemia, p. 219.

3. Vitamin D intoxication. Miscellaneous

1. Intermittent hyperphosphatemia. Rare condition.

2. Artifact.

IV. Database

A. Physical Exam Key Points. See Chapter 46, Hypocalcemia, p. 220, for signs of parathyroid disorders that can also cause hyperphos-phatemia.

1. Vital signs and general appearance a. Temperature. Hyperthermia after anesthesia; malignant hyperpyrexia.

b. Respiratory rate. Increased rate may be sign of respiratory acidosis.

c. Body mass. Obesity is associated with pseudohy-poparathryroidism.

2. Neuromuscular. Look for tetany as a sign of hypocalcemia. Muscle tenderness may be a sign of rhabdomyolysis.

3. Skeletal. Look for short metacarpals, metatarsals of pseudohypoparathyroidism (Albright hereditary osteodystrophy). Masses around large joints are a sign of tumoral calcinosis.

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