Every month a key biomarker is assessed in patients on dialysis to help assess mineral and bone health, that marker is serum phosphate. And unfortunately, more often than not, the numbers don’t look good. In one study by Antonio and colleagues published in 2022, 66% of patients in a cohort of 2,176 patients had hyperphosphatemia.

But what does that mean for the person with elevated phosphate levels?
Elevated serum phosphate triggers a cascade of harmful events that will go on to compromise parathyroid function, bone health, and cardiovascular health. Read on to learn more.

Parathyroid Function

Parathyroid glands produce parathyroid hormone (PTH) when serum calcium levels drop below the desired range of 8.5 to 10.2 mg/dL. Phosphate has a high affinity for binding with calcium, which is what can occur within the bloodstream when serum phosphate levels are elevated. As the calcium and phosphate bind together, serum calcium levels drop and PTH production is stimulated.

Due to other ESRD complications, including decreased calcium absorption related to inadequate vitamin D levels, the body struggles to optimize serum calcium and PTH production goes into overdrive. This can lead to the development of secondary hyperparathyroidism and parathyroid hyperplasia.

Bone Health

One of the causes of renal osteodystrophy is elevate phosphate levels. Renal osteodystrophy is the weakening of bones that can cause
bone pain and fracture.

As mentioned above, elevated phosphate leads to increased production of PTH. One of the actions of PTH is to stimulate bone resorption to free stored calcium and raise serum calcium levels. Pulling too much calcium from the bones lead to weakening and susceptibility to fracture.

Cardiovascular Health

Elevated phosphate levels are a key contributor to the initiation and progression of vascular calcification. Vascular calcification is a complex process in which bone begins to form in arterial tissue. This leads to arterial stiffness and occlusion which lends to increased blood pressure, reduced coronary perfusion, left ventricular hypertrophy, increased risk of myocardial infarction and heart failure, and ultimately increased cardiovascular morality.

It is well understood and widely accepted that a combination of dialysis, dietary phosphate reduction, and use of phosphate binders are required to control phosphate levels in people with end stage real disease (ESRD) on dialysis.

To support better management of mineral and bone markers, Patient Care America has put together a set of resources for both patients and clinicians including a patient handout on phosphate additives, a quick guide to mineral and bone labs, and a reference on phosphate binders which can be found via our Clinician Login .

For malnourished patients, PCA also provides supplementary phos-free protein in the form of IDPN for hemodialysis and IPN for peritoneal dialysis. To learn more about these supplemental therapies, visit our website, pcacorp.com .

References

  • Antonio, M. D., et al. “Hyperphosphatemia in Dialysis Patients National Multicenter Study.” Int J Nephrol Kidney Fail 8.2 (2022).
  • Jablonski, K. L., & Chonchol, M. (2013). Vascular calcification in end-stage renal disease. Hemodialysis international. International Symposium on Home Hemodialysis, 17 Suppl 1(0 1), S17–S21. https://doi.org/10.1111/hdi.12084
  • Wheeler, D. C., & Winkelmayer, W. C. (2017). KDIGO 2017 clinical practice guideline update for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease-mineral and bone disorder (CKD-MBD) foreword. Kidney International Supplements, 7(1), 1-59.
  • Mosbah, O. (2019). Chronic kidney disease-mineral and bone disorders (CKD-MBD). Arch Nephrol Urol, 2(2), 033-51.

Thank you to our guest blogger, Kathleen Meyer, RD, LD for sharing her knowledge and writing this blog post.