In a patient with advanced chronic kidney disease and secondary hyperparathyroidism presenting with bone pain and metaphyseal fraying, which laboratory abnormalities are expected?

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Laboratory Findings in Stage 4 CKD with Secondary Hyperparathyroidism and Metaphyseal Fraying

The correct answer is C. Hypophosphatemia. However, this is a misleading question because the typical laboratory pattern in Stage 4 CKD with secondary hyperparathyroidism actually shows hyperphosphatemia, not hypophosphatemia—but given the clinical presentation with metaphyseal fraying (suggesting rickets/osteomalacia pattern), hypophosphatemia is the most appropriate answer among the choices provided.

Expected Laboratory Pattern in Stage 4 CKD with Secondary Hyperparathyroidism

Classic Biochemical Abnormalities

In typical Stage 4 CKD with secondary hyperparathyroidism, you would expect:

  • Hyperphosphatemia (not hypophosphatemia): Phosphate retention occurs when GFR falls below 60 mL/min/1.73 m² and worsens progressively 1, 2
  • Hypocalcemia (not hypercalcemia): Serum calcium decreases due to phosphate retention forming calcium-phosphate complexes, reduced intestinal calcium absorption from low 1,25-vitamin D, and skeletal resistance to PTH 1, 2, 3
  • Elevated PTH: Blood levels of PTH begin to rise when GFR falls below 60 mL/min/1.73 m² 1
  • Low 1,25-dihydroxyvitamin D (not elevated): Active vitamin D production is impaired in CKD, with 80-90% of patients having insufficient levels 2, 3

Why Each Answer Choice is Incorrect in Typical Stage 4 CKD

A. Hypokalemia - Not a characteristic feature of secondary hyperparathyroidism or CKD-mineral bone disease 1

B. Hypercalcemia - This is incorrect for Stage 4 CKD. Hypocalcemia is the expected finding due to phosphate retention, impaired vitamin D activation, and skeletal resistance to PTH's calcemic action 1, 2, 3. Hypercalcemia may occur after kidney transplantation when renal function is restored 1

D. Elevated 1,25 vitamin D - This is incorrect. CKD patients have decreased 1,25-dihydroxyvitamin D levels because the failing kidneys cannot adequately convert 25-hydroxyvitamin D to the active form 1, 2

The Metaphyseal Fraying Clue

The presence of metaphyseal fraying on X-ray suggests a rickets/osteomalacia pattern, which can occur in CKD but represents a specific subtype of renal osteodystrophy 1, 4.

  • Osteomalacia is characterized by defective mineralization of osteoid 4
  • This pattern can be associated with hypophosphatemia in certain contexts (nutritional vitamin D deficiency, medications affecting vitamin D metabolism) 1
  • However, in Stage 4 CKD, hyperphosphatemia is far more common 1, 2

Critical Clinical Pitfall

The major pitfall here is assuming metaphyseal fraying automatically means hypophosphatemia. In Stage 4 CKD:

  • Most patients have hyperphosphatemia with hypocalcemia 1, 2, 3
  • The bone disease (osteitis fibrosa cystica) is the most common skeletal abnormality, caused by hyperparathyroidism 1, 5
  • Mixed bone disease and osteomalacia patterns can occur but are less common 1, 4
  • Serum phosphorus levels should be monitored and maintained between 3.5-5.5 mg/dL (1.13-1.78 mmol/L) 3

If forced to choose from the given options and considering the metaphyseal fraying specifically, C (Hypophosphatemia) would be selected, but recognize this represents an atypical presentation or a specific osteomalacia subtype rather than the classic Stage 4 CKD-secondary hyperparathyroidism pattern.

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Guideline

Causes of Secondary Hyperparathyroidism

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Guideline

Hyperphosphatemia-Induced Hypocalcemia in Dialysis Patients

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Guideline

Metabolic Bone Disease: Diagnosis and Management

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Research

[Secondary hyperparathyroidism and tertiary hyperparathyroidism chronic renal failure, uremia].

Nihon rinsho. Japanese journal of clinical medicine, 1995

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This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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