A thorough workup of the client’s bone pain is prudent even with an association between bone pain and phosphorus. You would also need to assess calcium, vitamin D, PTH, and kidney function to further investigate a low phosphorus level in the blood.
It is important to try to identify why someone has low phosphorus, whether it’s been a trend, and whether it is consistently falling below the standard reference range.
Low serum phosphorus (phosphate) may be caused by a shift into the cells and out of circulation, loss of phosphate via the kidneys, GI losses, intracellular losses, and hyperparathyroidism. Excess carbohydrate ingestion (with insulin surge) can decrease serum phosphate acutely, and a vitamin D deficiency can also contribute to low serum phosphate (Pagana 2019). Malabsorption and phosphate-binding antacids may also contribute to hypophosphatemia (Assadi 2010).
There may be specific causes of bone pain that phosphorus repletion may relieve including hypophosphatemic osteomalacia (Nair 2009, Tatsumi 2016) so the full workup is warranted.
References
Assadi, Farahnak. “Hypophosphatemia: an evidence-based problem-solving approach to clinical cases.” Iranian journal of kidney diseases vol. 4,3 (2010): 195-201. [R]
Nair, Lekshmi T et al. “Following the forgotten phosphorus.” The American journal of medicine vol. 122,12 (2009): 1093-5. doi:10.1016/j.amjmed.2009.07.006 [R]
Tatsumi, Fuminori et al. “Dramatic mitigation of bone pain after phosphorus replacement therapy in a subject with FGF23-related hypophosphatemic osteomalacia.” SpringerPlus vol. 5,1 1904. 2 Nov. 2016, doi:10.1186/s40064-016-3602-6 [R]