Phosphorus & Kidney Disease
Phosphorus is an element on the periodic chart and humans are dependent on its dietary intake for survival. It is required by every cell in the human body and it plays a dominating role over human hormones and diseases. Knowing what phosphorus does in the human body is not important for the general public, but knowing what happens if you get too much or too little is.
A phosphorus deficiency is associated with impaired intestinal absorption found with Crohn’s and Celiac disease, prolonged use of anti-acids, laxative abuse, and chronic diarrhea. But of course, the above health conditions would impair intestinal absorption of all essential nutrients, and would result in malnutrition.
Notwithstanding the above, it’s very unlikely a phosphorus deficiency would result from an inadequate diet because phosphorus is a chemical component in all food. Additional amounts, and different types of phosphorus, are added to ready-to-eat foods as preservatives and flavor enhancers. The additive forms of phosphorus amplify the negative effects of excessive phosphorus and represent a hidden burden on the human body that genetically programed human defense mechanisms did not anticipate.
The public’s total and type of exposure to phosphorus, makes toxicity from phosphorus more common and a bigger concern than phosphorus deficiencies. Primary complications from prolonged intake of excess dietary phosphorus, is calcification of organs and most commonly the kidneys.
The deterioration of the human kidneys leads to the retention of many waste products, of which phosphorus may be the most important because phosphorus is the most destructive. In kidney disease and dialysis patients, the therapeutic strategies aimed at controlling blood levels of phosphorus includes medical advice to restrict dietary intake between dialysis treatments and use of prescriptions.
In America, the amount of phosphorus absorbed daily from ingested food is larger than the amount of phosphorus that can be eliminated through a conventional four hour dialysis treatment. In response, pharmaceutical manufacturers have successfully created a line of medication known as phosphorus binders. Binders react with the phosphorus in food, rendering the phosphorus unavailable to the human body.
Dialysis treatments and prescriptions have reduced human suffering for millions of Americans and have prolonged lives for many years. However, despite the advancements in technology only 50% of the dialysis population meets their targeted goal. In short, technology has not been able to completely offset the adverse effects of a phosphorus rich diet.
Historically, a barrier to balancing phosphorus has been blamed on the patient’s inability to restrict dietary intake of phosphorus between dialysis treatments. Until now, patients have never been given the tools to do so.
The phosphorus in a person’s blood is not the result of an infection, and phosphorus is not made by your body. Phosphorus comes from the food you eat and the liquid you drink and from nowhere else. A dietary phosphorus intervention may be the missing link for better phosphorus control between dialysis treatments for the kidney diseased population.
When blood levels of phosphorus become too high relative to calcium, the excess phosphorus bonds with calcium forming calcium-phosphate compounds. Salts of these compounds precipitate out of the blood, become localized, and attach to the soft tissues of vital organs. This is a condition known as calcification. Many years ago it was referred to as hardening of the arteries. Cells of tissues that will become calcified will be chemically transformed into bone-forming-like cells to accept the calcium deposits simultaneously while the body is losing calcium from bone. Although many tissues are known to become calcified the blood vessels, heart valves, and the kidneys seem particularly susceptible.
Calcification is an actively regulated process that takes place daily throughout a lifetime and the extent of calcification is influenced by the amount, type, and duration of dietary intake of phosphorus. Calcification of tissues is known to start in an early age and is documented in young adults. Calcification progresses slowly and silently for many years at a subclinical level without any symptoms. Because of calcification’s slow evolution it has been referred to as age-related which means it’s predictable.
Reference of a disease to such a term as age-related may give a false impression that the diseases identified to be linked with calcification are unavoidable. Age-related does not mean that someone is helpless and cannot prevent calcification. We’re talking about normal body chemistry being changed in a negative way by diet with no infections being involved.
Calcification is well documented in the scientific community and is expected to occur over time as a result of elevated phosphorus levels. It is believed to indicate activity of an ongoing disease. Calcification leads to a group of biochemical abnormalities commonly referred to as age-related diseases, such as bone disease, cardiovascular disease, and kidney disease.
A common denominator found in all three of the above diseases is the existence of calcification deposits. Normally, the kidneys keep levels of phosphorus in balance with excretion. When calcification strikes the kidneys, however, a level of blockage occurs. This blockage interferes with the kidney’s ability to filter phosphorus at its initial normalized rate and excrete phosphorus from the body. Although small in the beginning, historically, the calcification blockage has appeared to be permanent.
If dietary intake of phosphorus remains constant, while the kidney is losing the ability to filter phosphorus, each time the kidney’s filtration rate drops a notch, an incremental amount of phosphorus will be permanently retained by the body. This may take years or even decades, but it is sure to happen if daily intake of phosphorus is far above the RDA.
Kidney damage will progressively intensify since the body requires less phosphorus to induce further damage after each drop in the filtration rate. Over time, the decline in excretion of phosphorus will lead to a buildup of toxic levels of phosphorus in the blood, known as hyperphosphatemia.
To make things worse, many critical body functions are totally dependent on calcium blood levels being strictly maintained within a very narrow range. If calcium is removed from the blood and deposited in tissues as calcification then blood levels of calcium could become too low and with time could result in a condition known as hypocalcemia. Hypocalcemia is the medical term used to describe dangerously low levels of calcium.
Hyperphosphatemia is a documented cause of hypocalcemia, and when full blown clinical symptoms of hypocalcemia appear a person will require emergency medical attention.
Excessive blood levels of phosphorus in addition to causing calcification, has been proven to inhibit the kidney’s production of the biological active form of vitamin-D. A reduction in vitamin D reduces the absorption of calcium from food. This in turn reduces blood levels of calcium contributing to the mild hypocalcemia state that was already festering. This temporary mild hypocalcemia state will trigger the body to elevate its calcium-regulating hormone levels, known as the parathyroid hormones. This will take place within hours after each phosphorus rich meal and without noticeable changes in blood levels of phosphorus.
Thus, more than one phosphorus rich meal during a day will create episodes of transient hypocalcemia states. And these overlapping episodes will cause the parathyroid hormones to linger in circulation longer than normal. Therefore, meal-to-meal phosphorus rich meals, on a daily bases, will result in persistent elevated levels of the parathyroid hormones, and a continuous slow erosion of bone.
The sole purpose of the parathyroid hormone is to prevent hypocalcemia by leaching calcium from bone to replace any lost circulating calcium. Unfortunately, as genetically programed, the bone will continue to release calcium as long as the parathyroid hormone levels stay elevated.
Overall, we have a loss of calcium circulating throughout the body due to calcification caused by excessive phosphorus. We cannot replenish the lost calcium from the food we eat because absorption of calcium has been shut down, due to a lack of vitamin-D, caused by excessive phosphorus. Additionally, we have a loss of calcium from bone due to the lingering high parathyroid hormone levels caused by excessive phosphorus.
A compounding problem, in addition to excessive intake of phosphorus, is that blood levels of phosphorus considered to be clinically acceptable may be unsafe for the general public and an unreliable indicator of any existing or ensuing diseases.
As mentioned earlier, a high dietary intake of phosphorus elevates the parathyroid hormones without changing blood concentrations of phosphorus; thus, laboratory test of blood levels of phosphorus will not reflect the damage being caused by excessive dietary intake of phosphorus. Since calcification precedes any clinical symptoms, the kidneys will calcify long before elevated levels of phosphorus can be detected in a laboratory. Finally, since hyper-phosphatemia has no clinical symptoms of its own, its evolution and damage also goes unnoticed.
In addition, to the damaged organs being able to go unnoticed, if using blood levels of phosphorus as a gage, the blood levels of phosphorus considered to be acceptable has been shown not to be acceptable for a per cent of the population.
Despite having kidney filtrations rates low enough to be defined as chronic kidney disease, in a study of 1077 males, averaging 69 years old, over 50% of the study group had blood levels of phosphorus measurements within the range considered to be normal. In 2005, a study reported phosphorus levels on the high side but still within a normal range was associated with an increased risk of heart failure in patients with coronary disease. A study in 2007 demonstrated phosphorus blood levels above 3.5 milligrams per deciliter, although within the range deemed to be acceptable, were still associated with an increased risk of cardiovascular disease. This occurred in a community of men and women who had no prior cardiovascular disease or kidney disease. In 2008 and again in 2009 blood levels of phosphorus within the range considered to be normal are associated with increased atherosclerosis and vascular calcification in the general population. Finally, in 2013, phosphorus levels are linked with increased mortality in healthy Americans.
Fortunately, one study has suggested the possibility that calcification might be reversible with diet. In 2011, a study reported phosphorus concentrations at the lower end of the normal range appeared to correlate with a decline in artery calcification in individuals with normal renal functions.
Strong clinical evidence exist that controlling dietary intake of phosphorus early in the course of kidney failure may greatly retard or even halt progression of kidney disease. Animal studies have shown dietary phosphorus restriction prevents calcification of the kidneys, and kidney patients who started their phosphorus management early after initial diagnosis had a more favorable outcome than those who failed to comply with dietary medical advice.
In view of the frequency with which hyperphosphatemia and calcification deposits have been found within the kidney disease population, phosphorus’s contribution to the destruction of the kidneys is beyond questioning.
Long-term intake of excessive phosphorus, even if it does not cause hyperphosphatemia, is still considered to be a risk factor for cardiovascular disease in the general population. One cardiology group studying lesions reported that phosphorus levels confer a cardiovascular risk similar to that of smoking and calcification has been implicated in the mechanical failure of transplanted heart valves.
Thus, dietary phosphorus is associated with cardiovascular disease in individuals who have no kidney disease, but cardiovascular disease appears to occur earlier in life, is more severe, and progresses more rapidly in those individuals who have kidney disease. The arteries of patients with kidney disease have more calcification deposits than the arteries of healthy individuals of the same age group.
Because dietary phosphorus is deemed to be a risk factor for cardiovascular disease in healthy persons as well as in the kidney disease population, the advice to restrict dietary intake of phosphorus has been extended to include the general population.
On a final note, because phosphorus is a naturally occurring structural chemical component of all protein matter, phosphorus rich foods will naturally be rich in protein. Based on this principal, there has been concern that a strict phosphorus restriction with a proportional decline in protein could outweigh the benefits by leading to malnutrition. In order to ensure a phosphorus restriction does not compromise the nutritional protein intake, a dietary ratio of phosphorus / protein can be used to identify foods that are lowest in phosphorus but still high in protein. The lower the value of the phosphorus/protein dietary ratio the more appropriate the food choice is for incorporating into a routine diet for dialysis and kidneys disease patients. A dietary ratio of phosphorus/ protein equal to 10 mg / g or below has been considered for management of phosphorus.
To summarize all the above, blood levels of phosphorus will not reflect the damage being caused to the kidneys by dietary intake of phosphorus, and high blood levels of phosphorus reduce blood levels of calcium by calcification, drive the initiation and progression of vascular calcification, is an independent determinant of severe coronary calcification, calcifies the kidneys and is a predictor of mortality in kidney disease patients, inhibits absorption of calcium, leaches calcium from bone, inhibits the body’s synthesis of vitamin D, and elevates blood levels of the parathyroid hormones. Furthermore, blood levels of phosphorus on the high side of what is consider a normal range, has been associated with increased risk of atherosclerosis, cardiovascular disease, and mortality in healthy U.S. adults.
Recommend Daily Intakes Levels for Phosphorus