What leads to hypocalcemia in patients with end-stage renal disease (ESRD)?

Hypocalcemia in patients with end-stage renal disease (ESRD) is primarily attributable to the decreased conversion of vitamin D. In healthy individuals, the kidneys play a critical role in converting vitamin D into its active form, calcitriol. In patients with ESRD, kidney function is severely impaired, leading to reduced levels of calcitriol. This active form of vitamin D is essential for the absorption of calcium from the gastrointestinal tract and for ensuring adequate calcium reabsorption in the kidneys. As a result, insufficient calcitriol levels lead to decreased intestinal absorption of calcium, contributing to lower serum calcium levels and subsequently causing hypocalcemia.

While factors like excessive calcium supplementation or deficient dietary intake could theoretically influence calcium levels, they are not the primary cause of hypocalcemia in ESRD. Increased renal excretion of calcium is often not a characteristic of ESRD; instead, patients typically exhibit altered calcium and phosphate metabolism primarily due to the inability of their kidneys to produce adequate active vitamin D. Understanding this primary mechanism aids in the management of calcium levels in patients with ESRD and highlights the importance of monitoring and potentially supplementing vitamin D in these individuals.