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Difficulty: EasyEndocrinology and Metabolism

Match each of the following clinical conditions with its classic initial presentation of serum laboratory findings (calcium, phosphorus, and intact parathyroid hormone [PTH]).

  • Primary hyperparathyroidismElevated calcium, decreased phosphorus, elevated PTH
  • HypoparathyroidismDecreased calcium, elevated phosphorus, decreased PTH
  • Chronic kidney disease (secondary hyperparathyroidism)Decreased calcium, elevated phosphorus, elevated PTH
  • Vitamin D deficiencyDecreased calcium, decreased phosphorus, elevated PTH

Answer

Primary hyperparathyroidism matches with elevated calcium, decreased phosphorus, elevated PTH. Hypoparathyroidism matches with decreased calcium, elevated phosphorus, decreased PTH. Chronic kidney disease matches with decreased calcium, elevated phosphorus, elevated PTH. Vitamin D deficiency matches with decreased calcium, decreased phosphorus, elevated PTH.
Calcium and phosphorus levels are primarily regulated by PTH and vitamin D. Understanding the primary defect allows prediction of the compensatory response and the resulting laboratory pattern. Primary hyperparathyroidism is driven by autonomous PTH excess (high Ca, low P). Hypoparathyroidism is defined by a lack of PTH (low Ca, high P). Chronic kidney disease features primary phosphorus retention and impaired vitamin D activation (low Ca, high P, high PTH). Vitamin D deficiency features poor gut absorption with intact renal function (low Ca, low P, high PTH).

Step-by-Step Solution

1
Analyze the laboratory profile for primary hyperparathyroidism.
Autonomous PTH production raises calcium and lowers phosphorus.
Excess PTH acts on the kidneys to reabsorb calcium and excrete phosphorus, and acts on bone to release calcium.
2
Analyze the laboratory profile for hypoparathyroidism.
Absent or low PTH results in low calcium and high phosphorus.
Without adequate PTH, the kidneys cannot adequately reabsorb calcium or excrete the daily phosphorus load.
3
Analyze the laboratory profile for chronic kidney disease.
Renal failure causes phosphorus retention and low 1,25-dihydroxyvitamin D, resulting in low calcium, high phosphorus, and compensatory high PTH.
The failing kidney cannot excrete phosphorus or properly activate vitamin D, leading to secondary hyperparathyroidism.
4
Analyze the laboratory profile for vitamin D deficiency.
Poor intestinal absorption leads to low calcium and low phosphorus, with a compensatory high PTH.
Secondary hyperparathyroidism in response to low calcium attempts to normalize serum calcium but simultaneously wastes phosphorus in the urine.

Key Concept

Calcium and Phosphorus Homeostasis
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Topics

Endocrinology and Metabolism

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