Secondary Hyperparathyroidism – Causes and Treatment
Secondary hyperparathyroidism is an overactivity of the parathyroid glands caused by persistent low calcium or vitamin D deficiency, most commonly associated with chronic kidney disease.
Things worth knowing about "Secondary Hyperparathyroidism"
Secondary hyperparathyroidism is an overactivity of the parathyroid glands caused by persistent low calcium or vitamin D deficiency, most commonly associated with chronic kidney disease.
What is Secondary Hyperparathyroidism?
Secondary hyperparathyroidism (sHPT) is a reactive overactivity of the parathyroid glands. Unlike primary hyperparathyroidism -- where the glands produce excess parathyroid hormone (PTH) without an external trigger -- secondary hyperparathyroidism develops as a compensatory response to persistently low blood calcium levels (hypocalcemia) or a deficiency in active vitamin D. The parathyroid glands attempt to restore normal calcium levels by increasing PTH secretion, which mobilizes calcium from bones, enhances calcium reabsorption in the kidneys, and promotes activation of vitamin D.
Causes
The most common cause of secondary hyperparathyroidism is chronic kidney disease (CKD). Damaged kidneys are unable to excrete phosphate adequately and can no longer activate vitamin D (calcitriol) sufficiently. This creates a cycle of hyperphosphatemia, hypocalcemia, and vitamin D deficiency that chronically stimulates the parathyroid glands.
- Chronic kidney disease: the most frequent cause, particularly from CKD stage 3 onwards
- Vitamin D deficiency: due to insufficient sun exposure, malabsorption, or inadequate dietary intake
- Malabsorption syndromes: such as celiac disease, Crohn's disease, or short bowel syndrome
- Liver diseases: impairing the first activation step of vitamin D
- Rickets and osteomalacia: bone mineralization disorders caused by vitamin D or calcium deficiency
Symptoms
In early stages, secondary hyperparathyroidism is often asymptomatic. As the condition progresses, the following symptoms may appear:
- Bone pain and increased bone fragility (renal osteodystrophy)
- Muscle weakness and muscle cramps
- Fatigue and general exhaustion
- Itching (pruritus), especially in patients with kidney failure
- Vascular calcifications due to elevated calcium-phosphate deposits
- Symptoms related to the underlying condition (e.g., kidney failure)
Diagnosis
Diagnosis of secondary hyperparathyroidism is based on a combination of laboratory tests and imaging studies:
- Blood tests: elevated intact PTH (iPTH), low calcium, elevated phosphate, reduced 25-OH vitamin D and 1,25-OH vitamin D levels
- Urine tests: assessment of urinary calcium excretion
- Bone density scan (DXA): to detect bone mineral loss
- Imaging: ultrasound or scintigraphy of the parathyroid glands when hyperplasia is suspected
- Evaluation of kidney function (creatinine, GFR) to assess the underlying disease
Treatment
Treatment is guided by the underlying cause and the severity of sHPT. The goal is to reduce PTH levels, normalize calcium and phosphate balance, and prevent organ damage.
Conservative Treatment
- Vitamin D supplementation: native vitamin D (cholecalciferol) or active vitamin D (calcitriol, alfacalcidol) depending on the cause and kidney function
- Phosphate binders: for hyperphosphatemia (e.g., sevelamer, calcium carbonate) to lower phosphate levels
- Calcimimetics: e.g., cinacalcet increases the sensitivity of calcium receptors in the parathyroid glands, reducing PTH secretion
- Calcium supplementation: correcting calcium deficiency through diet or supplements
- Treatment of the underlying condition: e.g., optimization of renal replacement therapy (dialysis)
Surgical Treatment
In cases of severe, therapy-resistant parathyroid overactivity (tertiary hyperparathyroidism), a parathyroidectomy (surgical removal of the parathyroid glands) may be necessary.
Prognosis and Outlook
When diagnosed early and managed consistently, secondary hyperparathyroidism can be well controlled. If left untreated, it can lead to serious complications including bone loss, vascular calcifications, and increased cardiovascular risk. Regular monitoring of PTH, calcium, and phosphate levels is essential, particularly in dialysis patients.
References
- Kidney Disease: Improving Global Outcomes (KDIGO) - CKD-MBD Update Guideline 2017. Kidney International Supplements, 7(1):1-59.
- Goltzman D. - Approach to hypocalcemia. In: UpToDate, Post TW (ed.), Wolters Kluwer, 2023.
- Drüeke T.B., Massy Z.A. - Changing bone patterns with progression of chronic kidney disease. Kidney International, 2016; 89(2):289-302.
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