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Serum phosphorus is probably the least ordered blood test among all electrolytes and minerals. Excessive phosphorus is toxic to the body by causing kidney and bone damage, vascular calcification, and premature ageing.
further reported the long-term outcomes associated with serum phosphorus levels in almost 100,000 patients without significant chronic kidney disease (estimated glomerular filtration rate >60 mL/min) or cardiovascular disease. They found that about 10% of this cohort died, and 0.1% developed end-stage renal disease, over an average follow-up time of 3 years. The risk of end-stage renal disease and mortality increases 40% and 9%, respectively, for every increment of 0.5 mg/dL of serum phosphorus above 3.1 mg/dL.
It is likely that excessive dietary phosphorus intake is the culprit of mildly elevated serum phosphorus levels in patients with relatively normal kidney functions. Today, the average American male has a daily phosphorus intake of about 1500 mg, and females 1200 mg, while the recommended daily allowance is 700 mg in healthy adults.
The absorption of inorganic phosphorus from food additives is >90%, while the absorption of organic phosphorus is about 40%-60%. For organic phosphorus from animal products, the absorption is 40% higher than that from plant-based foods,
The serum phosphorus level is regulated tightly by the body. Our knowledge of phosphorus homeostasis has been expanded significantly thanks to the discovery of 2 important molecules: Klotho and fibroblast growth factor 23 (FGF23).
When we ingest excessive amounts of phosphorus, both PTH and FGF23 are released. PTH removes sodium phosphate cotransporter from the apical membrane of the proximal tubule and causes phosphaturia. FGF23 and its cofactor, Klotho, bind to epidermal growth factor receptors in the proximal tubule and shut down the synthesis of sodium phosphate cotransporter and the vitamin D activating enzyme, 1-α-hydroxylase. As a result, more phosphorus is excreted in urine and less phosphorus is absorbed from the intestine, so the serum phosphorus level is reduced.
FGF23 is essential for phosphorus homeostasis; however, long-term elevation of FGF23 is harmful. FGF23 has been implicated in the “trade off” mechanism of secondary hyperparathyroidism due to chronic kidney disease.
It is likely that initially, elevated FGF23 may suppress activation of vitamin D and render PTH unsuppressed. More importantly, elevated FGF23 levels are associated with left ventricular hypertrophy in patients with chronic kidney disease. In fact, FGF23 directly induces left ventricular hypertrophy via a Klotho-independent pathway.
Therefore, it is likely that elevated FGF23 levels are responsible for bone and mineral complications and cardiovascular disease in patients with chronic kidney disease.
We may now consider phosphorus, in addition to sodium, sugar, and fat, another devil in our diet. By avoiding processed food and soft drinks, we can reduce dietary phosphorus significantly. The soda ban in New York City aimed at lowering sugar intake will help to reduce phosphorus intake simultaneously. Mandating phosphorus content of foods to be included on the nutrition facts label and regulating phosphorus-containing food additives are logical steps toward healthier food. It is particularly important for people of low socioeconomic status because poverty is linked to higher serum phosphorus levels, probably due to the high intake of inexpensive fast foods and soft drinks.
To detect mild elevation of serum phosphorus levels, we may have to measure the levels more often than what we are currently practicing. It is possible that the current “normal ranges” of serum phosphorus levels are biased because of excessive phosphorus intake in the general population. Further studies are needed to establish accurate normal ranges of serum phosphorus levels to better guide our management of high phosphorus burden and its consequences.
Phosphate toxicity: new insights into an old problem.