A client with acute kidney injury reports twitching and tingling of fingers and toes. Which process would the nurse consider in her explanation?

A client with acute kidney injury reports twitching and tingling of fingers and toes. Which process would the nurse consider in her explanation?

• A. Acidosis
• B. Calcium depletion
• C. Potassium retention
• D. Sodium chloride depletion

Answer: (B)

Tingling and twitching in this context point to low calcium affecting nerve and muscle excitability. In acute kidney injury, calcium can become depleted because phosphate builds up and binds calcium, lowering free calcium in the blood, and the kidneys’ reduced ability to activate vitamin D decreases calcium absorption from the gut. When calcium levels fall, nerve membranes become more easily depolarized, leading to paresthesias and muscle twitching or tetany. That direct link between hypocalcemia and neuromuscular irritability makes calcium depletion the best explanation for the symptoms. Acidosis, potassium retention, and sodium chloride depletion can occur with kidney injury, but they don’t explain the specific neuromuscular symptoms as directly as hypocalcemia does.

Tingling and twitching in this context point to low calcium affecting nerve and muscle excitability. In acute kidney injury, calcium can become depleted because phosphate builds up and binds calcium, lowering free calcium in the blood, and the kidneys’ reduced ability to activate vitamin D decreases calcium absorption from the gut. When calcium levels fall, nerve membranes become more easily depolarized, leading to paresthesias and muscle twitching or tetany. That direct link between hypocalcemia and neuromuscular irritability makes calcium depletion the best explanation for the symptoms.

Acidosis, potassium retention, and sodium chloride depletion can occur with kidney injury, but they don’t explain the specific neuromuscular symptoms as directly as hypocalcemia does.