Secondary Hyperparathyroidism Due to Chronic Kidney Disease
This 79-year-old woman has secondary hyperparathyroidism caused by CKD stage G3b (eGFR 29 mL/min/1.73 m²), and the first step is to evaluate for reversible causes—specifically vitamin D deficiency, hyperphosphatemia, and inadequate calcium intake—before considering any PTH-lowering therapy. 1, 2
Diagnosis
This patient's laboratory profile is diagnostic of CKD-related secondary hyperparathyroidism:
- PTH elevation begins when eGFR falls below 60 mL/min/1.73 m² and shows a significant inverse relationship with declining renal function 3
- Normal calcium excludes primary hyperparathyroidism, which typically presents with hypercalcemia and elevated or inappropriately normal PTH 2, 4
- At CKD stage G3b (eGFR 29), PTH levels of 132 pg/mL are expected as the kidneys lose their ability to excrete phosphate and produce active vitamin D 3, 5
- The intact PTH assay measures both active 1-84 PTH and inactive 7-84 fragments, with the inactive fragments accumulating disproportionately as kidney function declines 5
Initial Evaluation—Identify Reversible Causes
Before initiating any treatment, measure the following to exclude secondary causes that can be corrected 1, 6, 2:
1. 25-Hydroxyvitamin D Level
- Target ≥30 ng/mL to exclude vitamin D deficiency, the most common reversible cause of elevated PTH 6, 2
- If 25-OH vitamin D is <30 ng/mL, supplement with cholecalciferol or ergocalciferol to achieve levels ≥30 ng/mL before considering other interventions 6, 2
- Do NOT use calcitriol or active vitamin D analogs at this stage, as they increase hypercalcemia risk and can cause adynamic bone disease 1, 7
2. Serum Phosphorus
- Check for hyperphosphatemia, which drives PTH secretion in CKD 1, 6
- If phosphorus is elevated, restrict dietary phosphate intake as the first intervention 1, 6
- Consider phosphate binders only if dietary restriction fails to control phosphorus 1
3. Dietary Calcium Intake
- Assess whether the patient is consuming 1,000–1,200 mg of elemental calcium daily 6, 2, 8
- Inadequate calcium intake causes secondary hyperparathyroidism even with normal kidney function and vitamin D levels 8
- If intake is insufficient, supplement with calcium carbonate 600 mg twice daily and recheck PTH in 2–3 weeks 8
4. Medication Review
- Discontinue thiazide diuretics if present, as they reduce urinary calcium excretion and can worsen hyperparathyroidism 7
- Review for loop diuretics, bisphosphonates, or other medications affecting calcium metabolism 6
Management Algorithm
Step 1: Correct Modifiable Factors First 1, 2
- Replete vitamin D to ≥30 ng/mL using cholecalciferol 1,000–2,000 IU daily 6, 2
- Ensure adequate calcium intake (1,000–1,200 mg/day) through diet or supplementation 6, 8
- Restrict dietary phosphate if hyperphosphatemia is present 1, 6
- Recheck PTH after 3 months of correcting these factors 6, 2
Step 2: Reassess After Correction 1, 6
- If PTH normalizes or decreases significantly, continue monitoring calcium, phosphorus, and PTH every 3–6 months 1
- If PTH remains >110 pg/mL despite correction of vitamin D, calcium, and phosphorus, the patient has persistent secondary hyperparathyroidism requiring closer monitoring 1
Step 3: Avoid Routine Active Vitamin D Therapy 1
- Do NOT routinely prescribe calcitriol or vitamin D analogs in CKD G3b not on dialysis 1
- Reserve active vitamin D (calcitriol, alfacalcidol, doxercalciferol) only for severe and progressive hyperparathyroidism (PTH persistently >300 pg/mL with rising trend) in CKD G4–G5 1
- Active vitamin D increases hypercalcemia risk and can cause adynamic bone disease, especially in elderly patients 1, 7
Monitoring Schedule 1, 2
For CKD G3b (eGFR 29):
- Measure calcium and phosphorus every 3–6 months 1
- Measure PTH every 3–6 months after initial correction of reversible factors 1, 2
- During active treatment (if initiated), check calcium and phosphorus monthly for 3 months, then every 3 months 6, 2
Critical Pitfalls to Avoid
- Do not start calcitriol or active vitamin D analogs without first correcting vitamin D deficiency, calcium intake, and hyperphosphatemia 1, 2
- Do not target PTH suppression to normal range in CKD, as mild hyperparathyroidism may be protective against adynamic bone disease 1
- Do not use calcium-based phosphate binders if calcium is >10.2 mg/dL 4
- Recognize that PTH assays vary by up to 47% between platforms, so use assay-specific reference ranges and trend values over time 2, 4
- In elderly patients with age-related GFR decline, PTH elevation is expected and does not always require aggressive intervention 2