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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.

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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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