Secondary hyperparathyroidism
Secondary hyperparathyroidism is an appropriate, physiologic rise in parathyroid hormone driven by hypocalcemia or impaired vitamin D activation, most commonly from chronic kidney disease and less often from vitamin D deficiency or malabsorption. Management targets the underlying stimulus with dietary phosphorus restriction, phosphate binders, vitamin D repletion or active vitamin D analogs, and calcimimetics, reserving parathyroidectomy for disease refractory to medical therapy.
- Topic reviewThe full article, organized the way the exam asks it.
- ABIM-format MCQsVignettes with an explanation for every wrong answer.
- Key factsThe numbers and thresholds worth memorizing, up front.
- AI tutorMedBrain answers the question you're stuck on.
What this article covers
- Overview
Definition: secondary hyperparathyroidism is a physiologic, appropriate increase in parathyroid hormone (PTH) secretion driven by a sustained hypocalcemic or hypovitaminosis-D stimulus, most commonly chronic kidney disease (CKD).
- Epidemiology
Nearly universal in advanced CKD: the prevalence and severity of mineral and bone disorder rise as GFR falls, becoming clinically significant by CKD stage 3b to 4 (GFR below 45 mL/min/1.73m2) and prominent by stage 5.
- Risk factors
Advanced chronic kidney disease: the single dominant risk factor, with risk rising as GFR declines below 45 mL/min/1.73m2.
- Pathophysiology
The CKD cascade: declining GFR reduces renal phosphate excretion (raising serum phosphorus), reduces renal 1-alpha-hydroxylation of 25-hydroxyvitamin D to calcitriol (lowering 1,25-dihydroxyvitamin…
- Clinical features
Often asymptomatic early, detected on routine CKD monitoring labs: calcium, phosphorus, and PTH are checked periodically as kidney disease progresses.
- Differential diagnosis
Primary hyperparathyroidism: hypercalcemia with an elevated or inappropriately normal PTH, unlike the low or normal calcium in secondary hyperparathyroidism (primary hyperparathyroidism).
- Diagnosis
The diagnostic basis is biochemical, not a formal criteria set: an elevated PTH with a low or low-normal calcium and, in renal disease, an elevated phosphorus, in a patient with an identified…
- Management
First, restrict dietary phosphorus intake in any patient with hyperphosphatemia from CKD, as the foundation of therapy before adding a binder.
- Complications
Renal osteodystrophy: high-turnover bone disease (osteitis fibrosa), adynamic bone disease from over-suppression of PTH, or mixed disease, all increasing fracture risk.
- Prognosis
Tracks with control of the underlying CKD-mineral and bone disorder: early, sustained control of phosphorus, calcium, and PTH reduces bone and vascular complications.
- Prevention
Monitor calcium, phosphorus, and intact PTH regularly starting at CKD stage 3 (GFR below 60 mL/min/1.73m2), with increasing frequency as CKD advances toward stage 5.
Read the whole article
Subscribing to Internal Medicine opens every article, the full question bank and MedBrain, on the web, iPhone and Android.
Related articles
- Primary hyperparathyroidism
Primary hyperparathyroidism is autonomous PTH oversecretion, most often from a solitary parathyroid adenoma, producing hypercalcemia with an elevated or inappropriately normal PTH and low or low-normal phosphorus. Most patients are asymptomatic and identified on routine labs; parathyroidectomy is curative and is first-line for symptomatic disease or when specific biochemical, skeletal, or renal criteria are met, while observation with annual monitoring suffices for mild, asymptomatic disease.
- Tertiary hyperparathyroidism
Tertiary hyperparathyroidism is autonomous parathyroid hormone hypersecretion that develops after long-standing, poorly controlled secondary hyperparathyroidism, most often in end-stage kidney disease, causing eucalcemia or hypercalcemia despite hyperplastic glands that no longer respond to normal feedback. Cinacalcet is first-line medical therapy, and subtotal or total parathyroidectomy with autotransplantation is reserved for disease refractory to medical management or a markedly elevated PTH.
- Hypocalcemia
Hypocalcemia is a low serum calcium concentration, most often from insufficient parathyroid hormone action (postsurgical or autoimmune hypoparathyroidism, hypomagnesemia, or PTH resistance) or from vitamin D deficiency and chronic kidney disease. Severe or symptomatic disease requires urgent intravenous calcium, while chronic disease is managed with oral calcium, vitamin D repletion, and calcitriol when PTH is absent or the kidney cannot activate vitamin D.
- Osteoporosis
Osteoporosis is low bone strength that raises fragility fracture risk, diagnosed by a hip or spine T-score of -2.5 or less or by a fragility fracture itself. First-line treatment is an oral bisphosphonate, alendronate or risedronate, alongside adequate calcium and vitamin D intake.