In End-Stage Renal Disease (ESRD), parathyroid hormone (PTH) levels increase due to several factors, primarily related to the kidneys’ inability to regulate calcium, phosphorus, and vitamin D. This leads to a state called secondary hyperparathyroidism (SHPT).
Here’s a breakdown of the key reasons:
Impaired Vitamin D Activation:
Healthy kidneys convert inactive vitamin D to its active form, calcitriol, which is essential for calcium absorption in the intestines. In ESRD, this process is impaired, leading to lower active vitamin D levels and reduced calcium absorption.
Hyperphosphatemia:
Damaged kidneys cannot effectively filter phosphate from the blood, causing elevated phosphate levels. High phosphate levels can bind to calcium in the blood, further decreasing calcium levels.
Hypocalcemia:
The combination of reduced calcium absorption (due to low vitamin D) and decreased calcium levels in the blood (due to hyperphosphatemia) results in lower calcium in the blood.
Parathyroid Gland Response:
The parathyroid glands, which produce PTH, sense the low calcium levels in the blood and respond by overproducing PTH. This increased PTH secretion attempts to raise blood calcium levels by mobilizing calcium from bones.
In essence, the impaired kidney function in ESRD leads to a cascade of events that result in a chronic state of low calcium and high phosphate, which in turn stimulates the parathyroid glands to overproduce PTH, leading to SHPT.