E450 Diphosphates and Bakery Additives: Health Effects, Kidney Function and Laboratory Tests

Introduction: from a bakery label to the clinical laboratory

Look at the ingredient list on a packet of cake rusk, bread, biscuits, sponge cake or another packaged bakery product and you may see:

Raising agents: E450, E500

For many people, an E-number can sound more concerning than a familiar chemical name. However, an E-number is primarily a regulatory identification code. It does not indicate how toxic or dangerous a substance is.

E450 refers to a family of diphosphates, while E500 refers to sodium carbonates, including sodium bicarbonate. These compounds have useful technological roles in food production.

In baking, certain diphosphates provide an acidic component that reacts with sodium bicarbonate to release carbon dioxide. This gas helps cakes, biscuits and other products develop the required volume and texture.

The more interesting question from a biomedical science perspective is:

What happens to these substances after we eat them, and can laboratory tests show whether they are affecting our health?

To answer this properly, we need to follow the pathway:

Food intake → gastrointestinal absorption → physiological regulation → kidney handling → biochemical change → laboratory measurement → clinical interpretation

This makes bakery additives a useful example of how food chemistry connects with human physiology and clinical biochemistry.

What are food additives and E-numbers?

Food additives are substances intentionally added to foods for a technological purpose during manufacture, preparation, processing or storage.

In the UK, authorised additives are regulated under food-additives legislation and assessed for permitted uses and conditions. The Food Standards Agency provides information for consumers and manufacturers on authorised additives and E-numbers. ^1,2

An E-number therefore represents an identified and authorised additive, not a ranking of health risk.

For example:

• E300 – ascorbic acid, or vitamin C
• E322 – lecithins
• E450 – diphosphates
• E471 – mono- and diglycerides of fatty acids
• E500 – sodium carbonates

Manufacturers use additives for several reasons.

These include:

• raising dough or batter;
• preserving foods;
• preventing oxidation;
• stabilising mixtures;
• emulsifying fat and water;
• controlling acidity;
• improving flour performance;
• maintaining texture;
• adding or maintaining colour.

The important scientific questions are therefore not simply:

“Does this food contain an E-number?”

More useful questions are:

What substance is present? Why is it used? How much exposure occurs? How is it metabolised? Does the person have a condition that changes how the substance is handled?

The chemistry of bakery raising agents

E450 diphosphates

E450 represents several related diphosphate compounds.

One important example is:

E450(i) – disodium diphosphate, also known as disodium dihydrogen diphosphate and commonly described in food technology as sodium acid pyrophosphate.

It can act as the acidic component of a chemical raising system.

E500 sodium carbonates

E500 includes sodium carbonate compounds, including:

sodium bicarbonate, commonly known as bicarbonate of soda or baking soda.

When sodium bicarbonate encounters an acidic ingredient in the presence of moisture, an acid-base reaction occurs.

A simplified representation is:

Acidic component + sodium bicarbonate → carbon dioxide + water + salts

The carbon dioxide forms bubbles within the dough or batter.

These bubbles:

• become trapped in the food structure;
• expand during baking;
• increase volume;
• produce a lighter texture;
• contribute to the final crumb structure.

This is the basic principle behind many chemical raising systems.

Does sodium bicarbonate in bakery food alter blood pH?

Sodium bicarbonate is alkaline, and large medicinal doses can influence systemic acid-base balance.

However, this should not be confused with ordinary dietary exposure from baked foods.

Much of the bicarbonate used in baking reacts during food preparation, and the quantities involved in normal bakery consumption are very different from therapeutic bicarbonate doses.

In healthy people, blood pH is also tightly controlled by respiratory and renal mechanisms.

Therefore, normal consumption of foods prepared using E500 is not expected to produce clinically significant systemic alkalosis.

E500 may nevertheless contribute some sodium to the diet, which should be considered as part of total dietary sodium intake.

What happens to phosphate additives after we eat them?

Phosphorus is not foreign to the human body.

It is an essential nutrient.

Phosphorus is required for:

• ATP and cellular energy metabolism;
• DNA and RNA;
• phospholipid cell membranes;
• intracellular signalling;
• phosphorylation reactions;
• bone and tooth mineralisation;
• acid-base buffering.

Most phosphorus in the body is present in the skeleton. Much of the remainder is intracellular, while only a relatively small proportion is present in extracellular fluid and measured as circulating inorganic phosphate.

This distinction is important.

Dietary phosphorus is not the same as serum phosphate.

Similarly:

• dietary phosphate intake;
• inorganic phosphate additives;
• intracellular phosphate;
• serum phosphate;
• hyperphosphataemia;

are related concepts but should not be used interchangeably.

Intestinal absorption of phosphate

Dietary phosphorus exists in several forms.

Phosphate from food additives is predominantly inorganic and tends to be relatively readily available for intestinal absorption.

Naturally occurring phosphorus behaves differently depending on the food source.

For example, phosphorus within plant phytate may be less readily absorbed because humans have limited ability to digest phytate.

Phosphorus in animal-derived foods is generally more accessible.

This means that two foods containing similar total quantities of phosphorus may not necessarily deliver the same absorbable phosphate load. ^3,4

How is phosphate regulated?

The body maintains phosphate balance through interaction between:

• the intestine;
• kidneys;
• bone;
• parathyroid glands;
• vitamin D;
• fibroblast growth factor 23.

Kidneys

The kidneys are central to long-term phosphate balance.

Phosphate is filtered at the glomerulus. A substantial proportion is normally reabsorbed by the renal tubules, while the remainder is excreted in urine.

When phosphate intake increases in a person with healthy kidneys, renal phosphate excretion can increase.

Parathyroid hormone

Parathyroid hormone (PTH) is an important regulator of calcium and phosphate.

Among its actions, PTH reduces renal tubular phosphate reabsorption, thereby promoting phosphate excretion in urine.

Fibroblast growth factor 23

Fibroblast growth factor 23 (FGF23) is produced mainly by bone cells.

FGF23:

• reduces renal tubular phosphate reabsorption;
• increases urinary phosphate excretion;
• influences vitamin D metabolism.

Vitamin D

Active vitamin D promotes intestinal absorption of calcium and phosphate.

Kidney disease can interfere with vitamin D metabolism, which contributes to abnormalities of calcium, phosphate and PTH regulation.

Why do phosphate additives receive particular attention?

Phosphorus occurs naturally in many foods, including:

• meat;
• fish;
• dairy products;
• beans;
• nuts;
• seeds;
• cereals.

However, phosphate additives receive particular attention because inorganic phosphate is generally more readily absorbed than some naturally bound dietary phosphorus. ^3,4

Added phosphate may be found in products such as:

• processed meat;
• processed cheese;
• some bakery products;
• cola drinks;
• convenience foods;
• certain fast foods;
• processed food mixtures.

The important nutritional concept is therefore the total dietary phosphate burden.

It would be misleading to suggest that one biscuit, slice of bread or serving of cake containing E450 causes phosphate toxicity.

Instead, the concern becomes more relevant when readily absorbable phosphate is consumed repeatedly from several processed food sources, particularly in people who cannot excrete phosphate efficiently.

What about healthy individuals?

In people with:

• normal renal function;
• normal mineral metabolism;
• a balanced diet;

the body is generally able to adapt to variations in dietary phosphate intake.

One of the most important adaptations is increased renal phosphate excretion.

The European Food Safety Authority has evaluated phosphate food additives and established a group acceptable daily intake of 40 mg phosphorus/kg body weight/day, covering phosphorus from all dietary sources. This is not an additive-only allowance or an individual intake target, and it does not apply to people with moderate to severe reduction in kidney function. ⁵

Therefore:

Occasional consumption of a bakery product containing E450 should not be interpreted as phosphate poisoning or as evidence that kidney damage will occur.

The overall dietary pattern remains more important.

Phosphate and chronic kidney disease

Phosphate becomes much more clinically important in chronic kidney disease (CKD).

As renal function declines, the kidneys become progressively less able to maintain phosphate balance.

In earlier stages of CKD, increases in FGF23 and PTH can help surviving nephrons excrete more phosphate.

For this reason, serum phosphate may remain within the laboratory reference interval during earlier CKD even though phosphate regulation is already changing.

As CKD advances, compensatory mechanisms can become inadequate.

This can lead to:

• phosphate retention;
• hyperphosphataemia;
• secondary hyperparathyroidism;
• abnormalities of calcium balance;
• disturbances of vitamin D metabolism;
• abnormal bone turnover;
• vascular and soft-tissue calcification.

These abnormalities form part of:

Chronic kidney disease-mineral and bone disorder

CKD-MBD describes the systemic abnormalities of mineral and bone metabolism associated with CKD.

It may involve abnormalities in:

• phosphate;
• calcium;
• PTH;
• vitamin D;
• bone turnover;
• bone mineralisation;
• vascular or soft-tissue calcification.

International kidney guidelines recommend assessing these markers together and following changes over time rather than relying on a single isolated laboratory value. ⁶

Why may phosphate additives matter more in CKD?

A person with normal kidney function can usually increase renal phosphate excretion in response to increased intake.

A patient with advanced CKD cannot do this as effectively.

Readily absorbed inorganic phosphate additives may therefore become relevant when attempting to control total phosphate exposure.

Renal dietitians may advise some patients to reduce foods containing added phosphate.

This should not be interpreted as meaning that every patient with CKD must avoid every food containing E450.

Dietary management depends on:

• CKD stage;
• serum phosphate;
• nutritional status;
• PTH;
• calcium;
• medication;
• protein requirements;
• overall diet.

Dietary advice should therefore be individualised by the renal and dietetic team.

Cardiovascular disease and phosphate

Disturbed phosphate metabolism has also been studied in relation to cardiovascular disease.

Potential mechanisms include:

• vascular calcification;
• changes in vascular smooth-muscle cells;
• endothelial dysfunction;
• arterial stiffness;
• abnormal FGF23 signalling.

Observational studies have reported associations between increased serum phosphate and poorer cardiovascular outcomes, particularly in CKD. ⁷

However, an association is not the same as proven causation.

Three different types of evidence need to be distinguished.

Mechanistic evidence

Laboratory and experimental studies may show biological pathways through which abnormal phosphate metabolism could influence vascular tissue.

Observational evidence

People with higher serum phosphate may experience more cardiovascular events.

However, these individuals may also have more advanced renal disease or other risk factors.

Interventional evidence

The strongest evidence would show that lowering phosphate directly reduces cardiovascular events or mortality.

Evidence here remains less definitive than the observational association. ⁸

It would therefore be scientifically inappropriate to state:

“E450 causes heart attacks.”

Current evidence does not support that conclusion.

Bone and mineral metabolism

Calcium, phosphate, PTH, vitamin D, FGF23, the kidneys and the skeleton function as an interconnected system.

In advanced CKD:

1. phosphate excretion becomes impaired;
2. FGF23 rises;
3. vitamin D metabolism changes;
4. calcium balance may be affected;
5. PTH may increase;
6. bone turnover may become abnormal.

Persistent secondary hyperparathyroidism can contribute to renal bone disease.

Again, phosphate-containing additives may contribute to total dietary exposure, but they are only one part of this much larger physiological process.

Laboratory Investigations

Laboratory testing is where food chemistry and clinical physiology become measurable.

There is no single “E450 blood test”.

Instead, the laboratory evaluates phosphate homeostasis, kidney function, calcium balance, endocrine regulation and bone metabolism.

Serum phosphate

Serum or plasma phosphate measures circulating inorganic phosphate.

It may be requested when investigating:

• chronic kidney disease;
• hyperphosphataemia;
• hypophosphataemia;
• bone disease;
• calcium abnormalities;
• refeeding syndrome;
• renal phosphate wasting;
• major cellular breakdown.

Important interpretation points

Serum phosphate is influenced by:

• kidney function;
• age;
• PTH;
• FGF23;
• vitamin D;
• dietary intake;
• time of day;
• medications;
• cellular shifts.

Reference intervals vary between laboratories.

The result should therefore always be interpreted using the reference interval reported by the analysing laboratory.

Serum calcium

Laboratories commonly measure total calcium.

Because some circulating calcium is bound to albumin, laboratories may also use or report an albumin-adjusted calcium, depending on local practice.

In selected situations, ionised calcium can provide a more direct assessment of physiologically active calcium.

Calcium should be interpreted alongside:

• phosphate;
• albumin;
• PTH;
• renal function;
• vitamin D.

Parathyroid hormone

PTH plays a major role in calcium and phosphate regulation.

In CKD, PTH may rise in response to disturbances including:

• phosphate retention;
• altered vitamin D metabolism;
• changes in calcium balance.

A single raised PTH result should not automatically be interpreted in isolation. Trends and the wider biochemical picture are important.

Vitamin D

The usual laboratory marker of vitamin D status is:

25-hydroxyvitamin D [25(OH)D]

It should not be confused with 1,25-dihydroxyvitamin D, the hormonally active form, which is used for more specialised investigations.

Vitamin D status is relevant because vitamin D contributes to intestinal calcium and phosphate absorption and interacts with PTH physiology.

Renal function

Kidney function is critical when interpreting phosphate.

Common investigations include:

• serum creatinine;
• estimated glomerular filtration rate (eGFR);
• urea where clinically appropriate.

An elevated phosphate result in a patient with advanced CKD has a different significance from a similar result occurring in someone with normal renal function.

Alkaline phosphatase

Alkaline phosphatase (ALP) originates principally from liver and bone.

An increased ALP can therefore have several explanations.

In an appropriate renal or endocrine setting, increased ALP may reflect increased bone turnover.

It should be interpreted alongside:

• liver tests;
• calcium;
• phosphate;
• PTH;
• vitamin D;
• clinical history.

Magnesium

Magnesium interacts with calcium and PTH physiology.

Significant magnesium abnormalities can contribute to disturbances in mineral metabolism and may be measured when investigating complex calcium, phosphate or PTH disorders.

FGF23

FGF23 has an important physiological role in phosphate regulation.

However:

FGF23 is not routinely measured in most NHS clinical chemistry laboratories.

It is mainly used for specialist metabolic investigation, for example where renal phosphate wasting or particular hypophosphataemic disorders are suspected.

Urinary phosphate

Urinary phosphate measurement can help investigate renal phosphate handling.

Depending on the clinical question, investigations may include:

• spot urinary phosphate;
• 24-hour urinary phosphate;
• fractional excretion of phosphate;
• tubular phosphate handling;
• tubular maximum phosphate reabsorption relative to GFR, or TmP/GFR.

These investigations are used for specific renal or metabolic problems.

They are not routine screening tests performed simply because somebody has eaten food containing E450.

Laboratory Medicine Perspective

A phosphate result is only clinically useful when the result is analytically reliable and interpreted in context.

Biomedical Scientists contribute through:

• accurate phosphate analysis;
• validated analytical methods;
• internal quality control;
• external quality assessment;
• appropriate analyser maintenance;
• recognition of haemolysis;
• correct specimen handling;
• appropriate reference intervals;
• reliable renal and bone-profile testing;
• investigation of unexpected results.

This is an important example of the Biomedical Scientist’s role in linking analytical science with patient care.

Laboratory interpretation case study

Consider a patient with Stage 4 chronic kidney disease.

Laboratory results show:

How might these results fit together?

Step 1 – Reduced renal phosphate excretion

Advanced CKD reduces the kidney’s ability to eliminate phosphate efficiently.

Step 2 – Phosphate retention

As kidney function declines, phosphate begins to accumulate despite compensatory mechanisms.

Step 3 – Altered vitamin D physiology

Reduced kidney function alters activation and regulation of vitamin D.

Step 4 – Secondary hyperparathyroidism

Changes in phosphate, vitamin D and calcium contribute to increased PTH secretion.

Step 5 – Increased bone turnover

Persistently increased PTH may stimulate bone turnover, which may contribute to an increased ALP.

Step 6 – CKD-MBD

Taken together, the results support a disturbance of mineral and bone metabolism associated with CKD.

A diet containing phosphate additives could contribute to overall phosphate intake, but it would be incorrect to attribute this entire biochemical pattern to E450.

Can a blood test tell whether someone has eaten too much E450?

No.

There is no routine laboratory investigation that tells us:

“This patient consumed too much E450.”

Serum phosphate does not measure E450 exposure from a particular food.

Laboratory tests instead assess:

• phosphate homeostasis;
• renal clearance;
• calcium-phosphate balance;
• endocrine regulation;
• bone turnover;
• consequences of abnormal mineral metabolism.

A person with normal kidney function can consume a phosphate-containing meal and still have serum phosphate within the reference interval because phosphate is tightly regulated.

This illustrates an important principle:

Dietary intake and serum concentration are not necessarily the same thing.

Pre-analytical considerations for phosphate measurement

Biomedical Science students should also understand that an abnormal phosphate result may not always reflect true disease.

Haemolysis

Red blood cells contain intracellular phosphate.

Significant haemolysis can therefore increase the measured phosphate concentration and potentially produce a misleading result.

Delayed separation

Prolonged contact between cells and serum or plasma can affect biochemical measurements.

Samples should therefore be processed according to the laboratory’s validated procedures.

Time of day

Serum phosphate shows diurnal variation.

This means concentrations can vary according to sampling time.

Recent dietary intake

Food intake can influence circulating phosphate.

Fasting is not required for every routine phosphate request, but standardised sampling conditions may be useful for particular metabolic investigations.

Age

Children and adolescents normally have higher phosphate concentrations than adults because of skeletal growth.

Age-specific reference intervals are therefore important.

Kidney function

Renal function is one of the most important factors affecting phosphate interpretation.

Medication

Phosphate concentrations may also be affected by:

• vitamin D preparations;
• phosphate supplements;
• phosphate binders;
• antacids;
• diuretics;
• other medicines affecting renal or endocrine physiology.

Other bakery additives

Bakery products may contain several other authorised additives.

E471 – mono- and diglycerides of fatty acids

E471 is widely used as an emulsifier.

Emulsifiers help mixtures containing fat and water remain stable and can improve:

• texture;
• dough properties;
• softness;
• product consistency.

Mono- and diglycerides are composed of glycerol attached to one or two fatty acids.

During digestion, they enter pathways similar to ordinary dietary fat digestion, producing fatty acids and glycerol-related products.

Regulatory safety assessments have not established that E471 is inherently toxic at authorised food uses. ⁹

Some more recent observational studies have examined possible relationships between intake of certain emulsifiers and chronic disease.

Such research can identify potential associations but cannot by itself establish that a specific additive directly causes disease.

Other relevant bakery additives

E341 – calcium phosphates

These compounds may be used for several technological purposes and contribute calcium and phosphate.

E451 and E452

Triphosphates and polyphosphates can contribute additional inorganic phosphate and may be particularly relevant when a patient has specifically been advised to reduce phosphate additives.

E322 – lecithins

Lecithins act as emulsifiers and consist largely of phospholipid-related substances.

E481 and E482

Sodium and calcium stearoyl lactylates are emulsifiers used to influence dough structure and product texture.

E300 – ascorbic acid

E300 is ascorbic acid, or vitamin C.

In bread making it may also be used as a flour treatment agent.

This is a useful reminder that an E-number does not automatically identify a harmful substance.

Sorbates and propionates

Sorbic acid and permitted sorbates are used to inhibit microbial growth in appropriate foods.

Propionates such as E282 calcium propionate are widely used to reduce mould growth in bakery products.

Colours

Colours may be used in cakes, decorative coatings, fillings and other bakery products.

As with all additives, risk assessment depends on the individual substance, authorised use and exposure rather than simply the presence of an E-number.

Bakery foods and metabolic health

There is a wider nutritional issue that is often more important than one specific additive.

Frequent consumption of some highly processed bakery products may contribute:

• high energy intake;
• refined carbohydrates;
• added sugar;
• saturated fat;
• sodium;
• relatively low fibre.

Over time, the overall dietary pattern can be more important for metabolic health than whether one product contains E450.

Where clinically appropriate, laboratory assessment may include:

• HbA1c;
• glucose;
• total cholesterol;
• HDL cholesterol;
• LDL cholesterol;
• triglycerides;
• liver enzymes;
• renal function.

Blood pressure, body weight and waist circumference may also provide useful clinical information.

These investigations should be requested because of clinical risk or symptoms.

They should not be performed simply because somebody eats cake, biscuits or bread.

How to identify phosphate additives on food labels

People who have specifically been advised to reduce phosphate intake can check ingredient lists for terms containing:

“phosphate”

and for relevant E-numbers such as:

• E338 – phosphoric acid
• E339 – sodium phosphates
• E340 – potassium phosphates
• E341 – calcium phosphates
• E343 – magnesium phosphates
• E450 – diphosphates
• E451 – triphosphates
• E452 – polyphosphates

This information may be particularly useful for people with advanced CKD who have received dietary phosphate-restriction advice.

It does not mean that the general population needs to avoid all phosphate-containing foods.

Frequently Asked Questions

1. Is E450 dangerous?

E450 should not automatically be considered dangerous. It is an authorised family of phosphate additives. Total phosphate exposure becomes more important in people who have difficulty excreting phosphate, particularly those with advanced kidney disease.

2. Is disodium diphosphate the same as E450?

E450 describes a family of diphosphates.

E450(i) is disodium diphosphate, also known as disodium dihydrogen diphosphate.

3. Does E450 contain phosphorus?

Yes.

Diphosphates contain phosphorus and can contribute to dietary inorganic phosphate.

4. Is phosphate naturally present in food?

Yes.

Phosphorus occurs naturally in many foods including meat, fish, dairy products, pulses, cereals, nuts and seeds.

5. Are phosphate additives absorbed more readily than natural dietary phosphorus?

Generally, inorganic phosphate additives are readily absorbed.

Phosphorus bound within plant phytate is less readily available, while absorption from animal-derived foods tends to be higher.

6. Can E450 damage healthy kidneys?

There is no good evidence that normal consumption of an authorised E450-containing bakery product directly causes kidney disease in people with normal kidney function.

7. Should people with CKD avoid phosphate additives?

Some people with CKD may be advised to reduce readily absorbed phosphate additives.

This decision should be based on their kidney function, laboratory results and advice from the renal and dietetic team.

8. Can serum phosphate show how much phosphate I have eaten?

No.

Serum phosphate measures circulating inorganic phosphate at the time of sampling.

It does not quantify recent E450 intake.

9. Why can phosphate be high when calcium is low?

High phosphate, altered vitamin D metabolism and CKD can disturb calcium regulation and stimulate PTH.

The pattern should be interpreted using the wider biochemical picture.

10. Which laboratory tests are used in CKD-MBD?

Common investigations include:

• serum phosphate;
• calcium;
• PTH;
• ALP;
• renal function;
• 25-hydroxyvitamin D where appropriate.

11. Are all E-numbers harmful?

No.

An E-number identifies an authorised additive.

For example:

• vitamin C is E300;
• lecithins are E322;
• sodium carbonates are E500.

12. Is sodium bicarbonate E500 harmful?

Sodium bicarbonate belongs to the E500 group.

Normal quantities used in baked food are not expected to significantly alter systemic acid-base balance in healthy people, although they can contribute some sodium to overall dietary intake.

Key take-home messages

1. E-numbers are regulatory identifiers, not toxicity ratings.

2. E450 refers to a family of diphosphates. E450(i) is disodium diphosphate.

3. Diphosphate raising agents can react with sodium bicarbonate to release carbon dioxide and help bakery products rise.

4. Phosphorus is an essential nutrient required for ATP, DNA, cell membranes, signalling, buffering and bone.

5. Inorganic phosphate additives tend to be more readily absorbed than phosphorus bound within some natural foods.

6. Phosphate exposure is particularly important in people with significantly impaired renal function because kidney phosphate excretion is reduced.

7. There is no routine laboratory test that specifically measures E450 consumption.

8. Serum phosphate should be interpreted alongside renal function, calcium, PTH, vitamin D, ALP and the wider clinical picture.

9. Overall diet quality is usually more meaningful than focusing on one authorised food additive.

Educational disclaimer

This article is intended for education and does not replace individual medical or dietary advice. Patients with kidney disease or disorders of calcium/phosphate metabolism should follow advice from their renal, medical and dietetic teams.

References and Further Reading

1. Food Standards Agency. Approved additives and E numbers. London: Food Standards Agency. Available from: https://www.gov.uk/government/publications/approved-additives-and-e-numbers/approved-additives-and-e-numbers

2. European Parliament and Council. Regulation (EC) No 1333/2008 on food additives. Available from: https://www.legislation.gov.uk/eur/2008/1333

3. Calvo MS, Uribarri J. Contributions to total phosphorus intake: all sources considered. Semin Dial. 2013;26(1):54-61. View source

4. St-Jules DE, Jagannathan R, Gutekunst L, Kalantar-Zadeh K, Sevick MA. Examining the proportion of dietary phosphorus from plants, animals, and food additives excreted in urine. J Ren Nutr. 2017;27(2):78-83. View source

5. EFSA Panel on Food Additives and Flavourings. Re-evaluation of phosphoric acid-phosphates-di-, tri- and polyphosphates (E338-341, E343, E450-452) as food additives and the safety of proposed extension of use. EFSA J. 2019;17(6):5674. Available from: https://www.efsa.europa.eu/en/efsajournal/pub/5674

6. Kidney Disease: Improving Global Outcomes CKD-MBD Update Work Group. KDIGO 2017 clinical practice guideline update for the diagnosis, evaluation, prevention and treatment of chronic kidney disease-mineral and bone disorder. Kidney Int Suppl. 2017;7(1):1-59. View source

7. Palmer SC, Hayen A, Macaskill P, et al. Serum levels of phosphorus, parathyroid hormone, and calcium and risks of death and cardiovascular disease in individuals with chronic kidney disease: a systematic review and meta-analysis. JAMA. 2011;305(11):1119-1127. View source

8. Lioufas NM, Pascoe EM, Hawley CM, et al. Systematic review and meta-analyses of the effects of phosphate-lowering agents in non-dialysis chronic kidney disease. J Am Soc Nephrol. 2022;33(1):59-76. View source

9. EFSA Panel on Food Additives and Nutrient Sources added to Food. Re-evaluation of mono- and diglycerides of fatty acids (E471) as food additives. EFSA J. 2017;15(11):5045. View source

10. Kidney Care UK. Natural phosphate and added phosphate: what you need to know. Available from: https://kidneycareuk.org/get-support/healthy-diet-support/natural-phosphate-and-added-phosphate-ckd/

11. British Dietetic Association. Phosphate and kidney disease dietary information. Birmingham: British Dietetic Association. Available from: https://www.bda.uk.com/specialist-groups-and-branches/kidney-dietitian-specialist-group/non-renal-dietitians-section/phosphate.html

12. University Hospitals Birmingham NHS Foundation Trust. Phosphate (serum): laboratory test information. Available from: Phosphate (serum)

13. South Tees Hospitals NHS Foundation Trust. Vitamin D: pathology test information. Available from: https://www.southtees.nhs.uk/services/pathology/tests/vitamin-d/

LabPathPro Learning Point

When interpreting nutrition-related laboratory results, avoid the assumption:

Food contains phosphate → serum phosphate must be high.

The more accurate pathway is:

Dietary phosphate source and quantity → intestinal bioavailability → absorption → hormonal regulation → renal handling → distribution between blood, cells and bone → laboratory measurement → clinical interpretation.

This relationship is central to understanding both phosphate physiology and evidence-based clinical biochemistry.

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