What is the recommended management for an 89‑year‑old woman with prior parathyroid adenoma resection for primary hyperparathyroidism who now has stage 3 chronic kidney disease (eGFR ≈ 45 mL/min/1.73 m²), mild albuminuria, low 25‑hydroxy‑vitamin D, elevated parathyroid hormone, normal serum calcium, normal serum phosphate, and normal alkaline phosphatase?

Management of Post-Parathyroidectomy Hungry Bone Syndrome with Secondary Hyperparathyroidism

This patient has developed hungry bone syndrome following parathyroid adenoma resection, now complicated by secondary hyperparathyroidism driven by severe vitamin D deficiency and stage 3b CKD—immediate aggressive calcium and vitamin D repletion is required, not active vitamin D therapy.

Understanding the Clinical Picture

This 89-year-old woman presents with a complex post-surgical metabolic derangement:

• Hypocalcemia (2.42 mmol/L = 9.68 mg/dL; normal ~10.2 mg/dL) with low-normal phosphate (1.0 mmol/L = 3.1 mg/dL)
• Elevated PTH (12 pmol/L ≈ 113 pg/mL) despite prior parathyroid adenoma resection
• Severe vitamin D deficiency (43.5 nmol/L = 17.4 ng/mL; target ≥30 ng/mL) 1, 2
• Stage 3b CKD (eGFR 45 mL/min/1.73 m²) with mild albuminuria (uACR 27.1 mg/mmol)
• Normal alkaline phosphatase (116 U/L), suggesting resolution of high bone turnover from primary hyperparathyroidism

The combination of hypocalcemia with elevated PTH after parathyroidectomy indicates hungry bone syndrome transitioning to secondary hyperparathyroidism driven by profound vitamin D deficiency 3, 4. The low-normal phosphate (rather than elevated) confirms this is not typical CKD mineral-bone disorder but rather post-surgical calcium avidity by previously suppressed bone 1.

Immediate Management Priorities

1. Aggressive Calcium Supplementation

Initiate calcium carbonate 1–2 g (500–1,000 mg elemental calcium) three times daily with meals to correct hypocalcemia and provide substrate for remineralizing bone 1, 5. This serves dual purposes: raising serum calcium and binding any dietary phosphate 5.

• Monitor serum calcium weekly for the first month, then every 2 weeks until stable above 9.5 mg/dL 1, 5
• Measure ionized calcium if total calcium remains low despite supplementation, as albumin status affects interpretation 1

2. Nutritional Vitamin D Repletion (NOT Active Vitamin D)

The critical error to avoid is starting calcitriol when the primary problem is nutritional vitamin D deficiency, not impaired renal 1α-hydroxylation 1, 2.

Prescribe ergocalciferol (vitamin D2) 50,000 IU weekly for 12 weeks, then monthly maintenance to correct severe deficiency (25-hydroxyvitamin D <20 ng/mL) 2, 5. This approach is specifically recommended by K/DOQI guidelines for CKD patients with documented deficiency 2.

• Target 25-hydroxyvitamin D ≥30 ng/mL to suppress secondary hyperparathyroidism 2, 1
• Recheck 25-hydroxyvitamin D at 3 months to confirm adequate response 2
• At stage 3b CKD (eGFR 45), the kidneys retain sufficient 1α-hydroxylase capacity to convert 25-hydroxyvitamin D to active 1,25-dihydroxyvitamin D 2, 6

Why ergocalciferol over cholecalciferol? K/DOQI guidelines consider vitamin D2 the best available treatment for established deficiency in CKD, though higher doses are required 2. Both are acceptable for prevention, but ergocalciferol has more extensive safety data in CKD populations 2.

3. Monitor for Resolution vs. Persistent Hyperparathyroidism

Measure PTH every 3 months for the first 6 months, then every 3 months thereafter 2, 5. The expected trajectory is:

• If PTH normalizes (target 35–70 pg/mL for stage 3 CKD) after vitamin D repletion, this confirms the diagnosis was hungry bone syndrome with reactive secondary hyperparathyroidism 5, 1
• If PTH remains >110 pg/mL after achieving 25-hydroxyvitamin D ≥30 ng/mL and calcium >9.5 mg/dL, only then consider adding low-dose calcitriol 0.25 µg daily 1, 2

The Canadian Society of Nephrology explicitly states that for stage 3 CKD, routine calcitriol use is not recommended (Grade 2B)—either supplementing with nutritional vitamin D or not supplementing are both reasonable 1. Active vitamin D should be reserved for persistent hyperparathyroidism despite nutritional repletion 1, 2.

Critical Pitfalls to Avoid

Do Not Start Calcitriol as First-Line Therapy

Starting active vitamin D (calcitriol) when the primary problem is nutritional deficiency bypasses the body's regulatory mechanisms and increases hypercalcemia risk 2, 6. At eGFR 45, this patient retains adequate renal 1α-hydroxylase activity to convert 25-hydroxyvitamin D to calcitriol once substrate is provided 2, 6.

The PRIMO and OPERA trials demonstrated that activated vitamin D increased hypercalcemia risk without cardiac or survival benefits in CKD stages 3–4 2. Recent KDIGO 2025 updates recommend against routine activated vitamin D in non-dialysis CKD 2.

Do Not Target Normal PTH Levels

Suppressing PTH to normal range (<65 pg/mL) in CKD patients causes adynamic bone disease, characterized by low bone turnover and increased fracture risk 1, 5. For stage 3b CKD (eGFR 30–59), target PTH is 70–110 pg/mL, not normal range 5, 1.

Adynamic bone disease reduces the skeleton's capacity to buffer calcium-phosphate loads, paradoxically increasing vascular calcification risk 6, 5.

Monitor Calcium-Phosphate Product

Maintain calcium × phosphate product <55 mg²/dL² (or <70 mg²/dL² by some guidelines) to prevent soft tissue calcification 2, 5. With current values (9.68 mg/dL × 3.1 mg/dL = 30 mg²/dL²), there is safe margin for calcium supplementation 2.

If phosphate rises above 4.6 mg/dL during calcium supplementation, switch from calcium carbonate to non-calcium-based phosphate binders (sevelamer, lanthanum) 1, 5.

Monitoring Protocol

Parameter	Frequency	Target
Serum calcium	Weekly × 4 weeks, then every 2 weeks	>9.5 mg/dL (2.37 mmol/L)
Serum phosphorus	Every 2 weeks × 3 months	2.7–4.6 mg/dL (0.87–1.49 mmol/L)
25-hydroxyvitamin D	At 3 months	≥30 ng/mL (≥75 nmol/L)
PTH	Every 3 months	70–110 pg/mL for stage 3b CKD
Alkaline phosphatase	Every 3 months if PTH elevated	Monitor for bone turnover
eGFR/creatinine	Every 3 months	Track CKD progression

1, 5, 2

When to Escalate Therapy

Consider adding calcitriol 0.25 µg daily only if all of the following criteria are met after 3–6 months of nutritional vitamin D repletion 1, 2:

1. PTH remains >110 pg/mL (upper limit for stage 3b CKD) 5
2. 25-hydroxyvitamin D confirmed ≥30 ng/mL 2
3. Serum calcium <9.5 mg/dL 1, 5
4. Serum phosphorus <4.6 mg/dL 1, 5

If calcitriol is initiated, measure calcium and phosphorus monthly for 3 months, then every 3 months 5, 2. Discontinue immediately if calcium rises above 10.2 mg/dL 5.

Addressing the Underlying CKD

Nephrology referral is reasonable but not urgent at eGFR 45 with stable kidney function and minimal albuminuria 1. The Canadian Society of Nephrology recommends referral threshold at eGFR <30 mL/min/1.73 m² for stable patients, though earlier referral is appropriate if eGFR declines >5 mL/min/year or proteinuria exceeds 1 g/day (ACR ≥60 mg/mmol) 1.

This patient's uACR of 27.1 mg/mmol is below the threshold requiring nephrology referral 1. Primary care can manage stage 3b CKD with focus on cardiovascular risk reduction, blood pressure control, and monitoring for progression 1.

Why This Approach Differs from Typical CKD-MBD Management

This patient does not have typical CKD mineral-bone disorder—she has post-parathyroidectomy hungry bone syndrome with superimposed nutritional vitamin D deficiency 3, 4. The key distinguishing features are:

• Hypocalcemia (not hypercalcemia) with elevated PTH after parathyroid adenoma removal 3
• Low-normal phosphate (not hyperphosphatemia typical of CKD-MBD) 1
• Severe vitamin D deficiency as the primary driver of PTH elevation 3, 4
• Normal alkaline phosphatase, indicating resolution of high bone turnover from primary hyperparathyroidism 1

A case series reported primary hyperparathyroidism associated with hypocalcemia in a patient with kidney disease and vitamin D deficiency, successfully treated with parathyroidectomy preceded and followed by intensive calcium and vitamin D supplementation 3. This mirrors the current clinical scenario.

The management priority is nutritional repletion (calcium + vitamin D2), not hormonal suppression with calcitriol 2, 3.