How to manage a PTH level of 135?

Management of PTH 135 pg/mL

A PTH level of 135 pg/mL requires investigation to determine the underlying cause—whether this represents primary hyperparathyroidism (with elevated calcium), secondary hyperparathyroidism (with normal/low calcium), or is within acceptable range for patients with CKD on dialysis—before initiating any treatment.

Initial Diagnostic Approach

Measure serum calcium, phosphorus, and 25-hydroxyvitamin D levels immediately to differentiate between primary and secondary hyperparathyroidism and guide management 1, 2.

• If serum calcium is elevated: This suggests primary hyperparathyroidism; surgical consultation for parathyroidectomy should be considered if the patient meets criteria (symptomatic hypercalcemia, inability to undergo surgery requires medical management) 1, 3
• If serum calcium is normal or low: This indicates secondary hyperparathyroidism; proceed with evaluation for underlying causes 1, 2
• Assess kidney function (eGFR) to determine if CKD is contributing 2, 4

Management Based on Clinical Context

For Patients WITHOUT CKD (Nutritional/Malabsorption Causes)

First, correct vitamin D deficiency if 25-hydroxyvitamin D is <30 ng/mL using ergocalciferol or cholecalciferol 2, 4.

• Dosing should be based on severity of deficiency, with higher doses for levels <5 ng/mL 2
• Target 25-hydroxyvitamin D levels >30 ng/mL, though recent evidence suggests levels >125 nmol/l may be needed for optimal PTH suppression 5
• Provide calcium supplementation if dietary intake is inadequate, using calcium citrate in malabsorption syndromes 2
• Recheck 25-hydroxyvitamin D, calcium, phosphorus, and PTH in 3 months 2
• Once vitamin D repletion is achieved, continue maintenance supplementation and reassess annually 2

For Patients WITH CKD Not on Dialysis (Stages 3-4)

PTH of 135 pg/mL in CKD stages 3-4 warrants treatment, as approximately 40% of stage 3 and 80% of stage 4 CKD patients develop secondary hyperparathyroidism 4.

Implement the following stepwise approach:

1. Control serum phosphorus first through dietary phosphorus restriction and phosphate binders if needed, targeting normal range 1, 4
2. Correct vitamin D deficiency with ergocalciferol or cholecalciferol if 25-hydroxyvitamin D <30 ng/mL 2, 4
3. Initiate active vitamin D therapy (calcitriol, paricalcitol, or doxercalciferol) to suppress PTH 1, 4
   • Paricalcitol effectively suppresses PTH with minimal impact on calcium and phosphorus 4
   • Calcitriol has a narrow therapeutic window at higher doses due to hypercalcemia/hyperphosphatemia risk 4
   • Low-dose active vitamin D can be helpful as supplement to nutritional vitamin D and dietary phosphate restriction 5

Monitoring schedule: Check calcium and phosphorus every 2 weeks for 1 month after initiating therapy, then monthly; measure PTH every 1-3 months until target achieved 1

Important caveat: Cinacalcet is NOT indicated for CKD patients not on dialysis due to increased hypocalcemia risk 3. Limited data exist for its use in stages 3-4 CKD 4.

For Patients WITH CKD on Dialysis

PTH of 135 pg/mL in dialysis patients is BELOW the target range of 150-300 pg/mL recommended by K/DOQI guidelines 5, 3.

This low-normal PTH may indicate:

• Over-suppression from excessive vitamin D therapy, which can decrease bone turnover and compromise bone health 5
• Risk of adynamic bone disease with low bone turnover 5

Management approach:

• Do NOT initiate cinacalcet, as it is indicated for PTH levels that need lowering, not for already-controlled levels 3
• Consider reducing or holding active vitamin D therapy if patient is currently receiving it 5
• Reduce phosphate binder doses if appropriate, as excessive phosphate control combined with vitamin D can over-suppress PTH 5
• Monitor PTH monthly for 3 months, then every 3 months once stable 5
• Target PTH levels of 150-300 pg/mL for dialysis patients, though the 2025 KDIGO conference acknowledges uncertainty about optimal PTH targets 5, 3

Critical consideration: The optimal PTH level in dialysis patients remains controversial, with observational data showing U- or J-shaped curves between PTH and mortality 5. Some patients may have low bone turnover even with normal-range PTH 5.

Special Populations

X-Linked Hypophosphatemia (XLH)

If PTH elevation occurs in XLH patients on conventional therapy (phosphate supplementation and active vitamin D):

• Optimize active vitamin D dose (increase) and reduce phosphate dose first 5
• Consider cinacalcet with close monitoring if PTH does not normalize after optimization, though it is not licensed for this indication and carries risk of hypocalcemia and QT prolongation 5
• Parathyroidectomy should be considered for tertiary hypercalcemic hyperparathyroidism 5, 1

Monitoring for Complications

Watch for hypocalcemia if initiating any PTH-lowering therapy:

• Symptoms include paresthesias, myalgias, muscle spasms, tetany, seizures, QT prolongation, and ventricular arrhythmia 3
• Life-threatening events and fatal outcomes have been reported with cinacalcet-induced hypocalcemia 3

For dialysis patients, if calcium falls below 8.4 mg/dL but remains above 7.5 mg/dL: Use calcium-containing phosphate binders and/or vitamin D sterols to raise calcium 3

If calcium falls below 7.5 mg/dL: Withhold PTH-lowering therapy until calcium reaches 8 mg/dL, then reinitiate at lower dose 3