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The Cause and Solutions for High Calcium in Your Bloodwork

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Parathyroid disease and kidney disease, Vitamin D and calcium

The Cause and Solution for High Calcium in Bloodwork

There is a significant link between the parathyroid glands and chronic kidney disease (CKD). If you have CKD, it is crucial to have your parathyroid hormone (PTH), calcium, and vitamin D levels checked. High calcium levels (hypercalcemia) and CKD are closely interconnected, with each condition potentially influencing the other.

Understanding the Parathyroid Glands

The parathyroid glands consist of four tiny glands located on the posterior surface of the thyroid gland, arranged in two pairs, each about the size of a grain of rice. They play a crucial role in regulating calcium and phosphorus levels in the blood by producing parathyroid hormone (PTH), which helps maintain the balance of these minerals by influencing their absorption from the intestines, reabsorption from the kidneys, and release from bones.

parathyroid gland and CKD

Source Parathyroid glands | healthdirect

The Role of Parathyroid Hormone

PTH is essential for calcium regulation. In normal kidney function, PTH levels remain within a narrow range to ensure optimal calcium and phosphorus levels. When calcium levels drop, the parathyroid glands release PTH, which stimulates calcium release from the bones, enhances calcium reabsorption in the kidneys, and activates vitamin D (necessary for calcium absorption in the intestines). Conversely, when calcium levels rise, PTH production decreases, leading to reduced calcium release from the bones and increased excretion via the kidneys. PTH acts on three primary target organs: bones, kidneys, and the gastrointestinal tract.

Bones

PTH stimulates osteoclasts (cells responsible for bone resorption), releasing calcium and phosphate into the bloodstream and increasing blood calcium levels. It also indirectly stimulates osteoblasts (bone-forming cells) to produce signalling molecules that promote osteoclast formation and activity. Osteoblasts work with other bone cells to maintain bone balance and ensure adequate bone remodelling.

Kidneys

  • Calcium reabsorption: PTH increases calcium reabsorption in the distal convoluted tubules within the kidneys, reducing the amount of calcium excreted in the urine and conserving calcium in the body.
  • Phosphate excretion: PTH decreases phosphate reabsorption in the proximal tubules of the kidneys, leading to an increase in phosphate excretion in the urine, helping maintain the balance between calcium and phosphate in the blood.
  • Vitamin D: PTH stimulates the action of 1α-hydroxylase in the kidneys, which converts 25-hydroxyvitamin D into its active form, 1,25-dihydroxyvitamin D (calcitriol). Active vitamin D is essential for calcium absorption in the intestines.

Gastrointestinal Tract

The active form of vitamin D (calcitriol) enhances calcium absorption from the diet within the small intestine. Renal production of calcitriol is stimulated in response to PTH, low calcium, and low phosphate levels. Calcitriol plays a vital role in plasma calcium regulation by supporting the absorption of dietary calcium and phosphate from the gastrointestinal tract.

The Impact of Chronic Kidney Disease on Parathyroid Hormone

The parathyroid glands and kidneys are closely linked through their roles in regulating calcium and phosphorus balance. The progressive decline in kidney function due to CKD disrupts this balance. As kidney function declines, the kidneys’ ability to convert vitamin D to its active form is impaired, leading to decreased calcium absorption from the intestines and reduced calcium reabsorption in the kidneys. These changes trigger a response from the parathyroid glands, leading to excessive secretion of PTH, a condition known as secondary hyperparathyroidism.

hyperparathyroidism and CKD

Source Everything To Know About Hyperparathyroidism! (cherishsisters.com)

Secondary Hyperparathyroidism

Secondary hyperparathyroidism is a common complication of CKD. It occurs due to low calcium levels caused by another disease. The increase in parathyroid hormones is the body’s attempt to maintain calcium homeostasis.

Symptoms of Secondary Hyperparathyroidism:

  • Feeling thirsty and urinating more than usual
  • Abdominal pain
  • Fatigue
  • Muscle weakness
  • Depression, forgetfulness, or mild confusion
  • Nausea, vomiting, or loss of appetite
  • Constipation

If left untreated, it may cause:

  • Bone deformities, fractures, and swollen joints
  • Kidney stones
  • Bone pain or tenderness
  • Joint pain
  • Irregular heartbeat
  • High blood pressure

Secondary Hyperparathyroidism and its Consequences

  1. Bone disorders: Excessive PTH production leads to increased bone resorption, resulting in bone loss, weakened bones, and an increased risk of fractures.
  2. Mineral imbalances: Elevated PTH levels contribute to an imbalance of calcium and phosphorus, leading to hypercalcemia (high calcium levels) and hypophosphatemia (low phosphorus levels).
  3. Vascular calcification: Secondary hyperparathyroidism contributes to vascular calcification due to calcium deposits in blood vessels, increasing the risk of cardiovascular events and complications.
  4. Renal Osteodystrophy: CKD-Mineral and Bone Disorder (CKD-MBD) describes the complex interplay of mineral and bone abnormalities in CKD. Secondary hyperparathyroidism is a key factor in the development of renal osteodystrophy, characterized by bone abnormalities and increased fracture risk.

parathyroid calcium and renal disease and vitamin D

Source Secondary Hyperparathyroidism in Chronic Kidney Disease: Pathophysiology and Management – PMC (nih.gov)

Management & Treatment Options

Treatment aims to manage secondary hyperparathyroidism in CKD, normalize PTH levels, and restore calcium and phosphorus balance. Treatment options include:

  1. Dietary modifications: Controlling dietary intake of calcium and phosphorus through restrictions and careful monitoring can help manage secondary hyperparathyroidism. Education on low phosphorus diets, appropriate calcium intake, and adherence to prescribed medication and protocols is essential.
  2. Support groups: Support groups and counselling for those with chronic health concerns can help maintain treatment adherence.
  3. Vitamin D supplementation: Active forms of vitamin D or vitamin D analogs may be prescribed to CKD patients to improve calcium absorption, reduce PTH secretion, and support bone health.
  4. Phosphate binders: Medications that bind dietary phosphorus, preventing its absorption and reducing the stimulus for PTH secretion. These include calcium acetate, calcium carbonate, sevelamer, lanthanum carbonate, and aluminium hydroxide.
  5. Calcimimetics: Medications that mimic the actions of calcium on the parathyroid glands, activating calcium-sensing receptors to suppress PTH secretion and production.
  6. Parathyroidectomy: In severe cases of hyperparathyroidism that do not respond to medical treatment, surgical removal of the parathyroid glands may be considered to normalize PTH levels and restore calcium and phosphorus balance.

Regularly monitoring PTH, calcium, and phosphorus levels is crucial in managing secondary hyperparathyroidism in CKD. Collaboration between nephrologists, endocrinologists, and other healthcare providers is essential for effective management and appropriate treatment adjustments.

The link between hyperparathyroidism, CKD, and consequences such as vascular calcification, bone disorders, and anemia requires further research. It would be beneficial to combine holistic therapeutic approaches to reduce the need for parathyroidectomy and its complications.

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