Hyperphosphatemia during chemotherapy is explained by which mechanism?

Hyperphosphatemia during chemotherapy is explained by which mechanism?

• A. Massive cellular lysis that releases intracellular phosphate
• B. Inability to excrete phosphate
• C. Increased calcium citrate complexation
• D. Crush injury releasing phosphate

Answer: (A)

Rapid tumor cell death from chemotherapy releases a large amount of intracellular phosphate into the bloodstream. When many cancer cells lyse, their stored phosphate enters circulation faster than the body can excrete it, leading to hyperphosphatemia—classic tumor lysis syndrome. This rise in phosphate can bind calcium, causing hypocalcemia and potential renal complications from calcium phosphate precipitation. The primary driver here is the sudden release of phosphate from lysed tumor cells, not simply a failure to excrete phosphate. Other options describe unrelated or less likely mechanisms in this context, such as a non-specific excretion problem, calcium–phosphate chemistry not driven by this scenario, or phosphate release from non-chemo injuries.

Rapid tumor cell death from chemotherapy releases a large amount of intracellular phosphate into the bloodstream. When many cancer cells lyse, their stored phosphate enters circulation faster than the body can excrete it, leading to hyperphosphatemia—classic tumor lysis syndrome. This rise in phosphate can bind calcium, causing hypocalcemia and potential renal complications from calcium phosphate precipitation. The primary driver here is the sudden release of phosphate from lysed tumor cells, not simply a failure to excrete phosphate. Other options describe unrelated or less likely mechanisms in this context, such as a non-specific excretion problem, calcium–phosphate chemistry not driven by this scenario, or phosphate release from non-chemo injuries.