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When a donor receives a large volume of blood products, the citrate used as an anticoagulant in stored blood can lead to a decrease in calcium levels in the body, resulting in hypocalcemia. Sodium citrate binds calcium ions in the blood, which can temporarily lower serum calcium levels, especially in the context of massive transfusion where the amount of citrate introduced can be significant relative to the recipient's calcium stores.

This risk of hypocalcemia is particularly pronounced when citrate is metabolized, leading to a depletion of free calcium beyond the normal physiological levels. The symptoms of hypocalcemia can include muscle cramps, tetany, and cardiovascular issues, emphasizing the clinical importance of monitoring calcium levels during and after massive transfusion protocols.

In contrast, the other options do not directly involve the mechanism of citrate's action. Although hyperkalemia can occur from massive transfusions, it is more related to cellular breakdown and release of potassium rather than citrate specifically. Hyponatremia might occur in certain scenarios but is not directly linked to blood transfusion-related citrate effects, and hypomagnesemia doesn’t relate to citrate use in blood products either. Thus, hypocalcemia is the most relevant risk associated with massive blood transfusion and the administration of sodium citrate.