In this episode we’re continuing our bloodwork focus - in episode 128 we chatted all about calcium, and today we’re turning our attention to its friend-slash-enemy, phosphate.
Phosphate is one of those values most of us glance at, mentally file under 'kidney stuff', and then move on from. And while yes, kidney disease is a really big part of the phosphate story, it's not the whole of it.
Phosphate is involved in energy production in every single cell in the body. It helps red blood cells deliver oxygen to the tissues, it keeps muscles (including the diaphragm and the heart) working properly, and when we see levels change dramatically - be that increasing or decreasing - it can have significant consequences for our patients.
It's also a value that can change incredibly quickly in hospitalised patients, often as a direct result of the treatment we're giving them - especially in cases of insulin administration. And because we're the ones in the wards 24/7 closely monitoring these patients, we're often in a really good position to spot those subtle changes early.
I remember the first hypophoshataemic patient I saw - a cat with refeeding syndrome after going missing for 6 months and losing lots of weight. I didn’t really understand how it impacted my patient beyond knowing it was a thing - but I remember it being a big faff trying to source the right phosphate, calculate it, and administer it safely.
When we understand how these diseases impact our patients, we can plan nursing care to mitigate it - and know the exact steps to take when caring for them in the ward.
So that’s what we’ll do in this episode. We'll chat about what phosphate is and how the body keeps it balanced, how to take samples you can actually trust, and then - most importantly - our patients. We'll look at why they become hyper- or hypophosphataemic (including in conditions like DKA and refeeding syndrome), what it does to them, how it's corrected, and how we support them as nurses and technicians.
So what actually is phosphate, and why does it matter so much?
Firstly, I want to quickly mention terminology. You'll see 'phosphorus' and 'phosphate' used in practice - on lab reports, in textbooks, and probably by me in this episode too. Technically phosphorus is the element, and phosphate is the form it exists in within the body - so we’d feed a phosphorus-restricted food for example, to reduce our patient’s phosphate levels.
To be honest, though, we tend to use the terms interchangeably - and what our analysers measure is the inorganic phosphate in the blood.
Phosphate is the main negatively charged ion (or anion) inside our cells, and it does a LOT. It:
Forms part of ATP, the molecule our cells use for energy - so it's needed for muscle contraction, nerve conduction, and moving substances in and out of cells
Makes up part of our cell membranes (as phospholipids) and our DNA
Is needed to make a substance called 2,3-diphosphoglycerate (or 2,3-DPG) in red blood cells, which helps haemoglobin release oxygen molecules so it can be delivered to the tissues
Acts as a buffer in urine, helping the kidneys get rid of acid
And, alongside calcium, forms hydroxyapatite or calcium phosphate, which is the mineral that gives bone its strength
Where is phosphate stored in the body?
Around 80-85% of the body's phosphate is in bone. Most of the rest, around 15%, is inside cells, mainly in soft tissues like muscle. And less than 1% is in the extracellular fluid - which includes the blood we're sampling, but also other extracellular fluids such as the interstitial fluid.
If you listened to episode 128 on calcium disorders, this might sound familiar, because, just like with calcium, only a tiny fraction of the body’s supply is circulating.
But phosphate actually behaves more like potassium than calcium.
Because so much of it sits inside cells, it can move in and out of them really quickly - so the blood level can change dramatically within hours, without the total amount in the body changing at all. If we think about potassium, we see marked changes in response to things like insulin or glucose administration - and it can be the same with phosphate.
What this means in practice is that the phosphate on our blood results is actually a pretty poor reflection of how much phosphate the patient actually has overall. A patient can have a normal (or even high) blood phosphate while being really depleted elsewhere in the body, and a low result doesn't always mean the patient is depleted, either - it just means the circulating phosphate is low.
This movement of phosphate between different body fluid compartments explains some of the most common causes of hypophosphataemia - but we’ll come to those a little later in the episode.
How does the body keep phosphate balanced?
Like calcium, phosphate homeostasis is regulated in 3 main places - the gastrointestinal tract, the kidneys and the bone - plus that movement in and out of cells.
The GI tract
Most of our patients' phosphate comes from their diet, and protein-rich foods like meat and fish contain a lot of it. It's absorbed in the small intestine, mainly the jejunum, and calcitriol (the active form of vitamin D, as we mentioned in episode 128) can increase how much is absorbed.
Some things reduce absorption, too, including aluminium-containing antacids (eg aluminium hydroxide) and, of course, phosphate binders - which is exactly why we use them in kidney disease.
The kidneys
The kidneys are the main regulators of phosphate. It's filtered via the glomerulus, and normally around 80-90% of it is reabsorbed back into the blood in the proximal tubule - with the rest being excreted via the urine.
So when kidney function declines, we can’t excrete that phosphate effectively and it is retained.
Parathyroid hormone (PTH) is the most important hormone involved in this process. As we chatted about in episode 128, PTH increases calcium - but in the kidneys it does the opposite for phosphate, reducing reabsorption so that more is lost in the urine.
There's also a group of hormones called phosphatonins, and FGF-23 is one of these. We chatted about FGF-23 back in episode 126 where we looked at renal disease, as this is now something we monitor to evaluate calcium and phosphate balance in renal patients.
A few other things increase phosphate loss in the urine, including steroids, osmotic diuresis (for example due to glucosuria), and volume expansion with IV fluids. Growth hormone and thyroid hormone do the opposite and actually increase reabsorption - which is part of the reason young, growing animals and hyperthyroid cats can have naturally higher phosphate levels.
The bone
Bone basically acts like the body’s storage reservoir for phosphate. PTH releases both calcium and phosphate from bone, and when phosphate is low for a long time, the body will draw more and more phosphate out of these stores.
Movement in and out of cells
As I mentioned earlier in the episode, lots of factors cause phosphate to move in and out of the cells. This mechanism is behind most of the rapid changes we see in hospitalised patients - and a lot of them are caused by things we're doing.
Phosphate is pushed out of the bloodstream and into the cells - lowering circulating levels - by:
Insulin
Glucose
Alkalosis, particularly respiratory alkalosis, which we see in patients with hyperventilation
Catecholamines
Refeeding after a period of starvation
And things that move phosphate OUT of cells, raising the blood level, include:
Acidosis
Cell breakdown - including haemolysis, muscle damage, and tumour lysis
And of course, calcium
We can’t talk about phosphate without recapping calcium. Now we did an entire episode on this a few weeks ago, but as a quick reminder - calcium and phosphate are incredibly closely related.
When phosphate is high, it binds to calcium, and it also reduces how much vitamin D is activated - so less calcium is absorbed from the GI tract. Both of these lower the ionised calcium. And if calcium and phosphate are BOTH high at the same time, the risk of calcium phosphate being deposited in soft tissues increases significantly.
So whenever you're looking at a phosphate result, look at the calcium too (ideally the ionised calcium).
So that's how phosphate is balanced. But how do we measure it - and get a result we can actually trust?
As a rough guide, phosphate in adult dogs sits at around 0.8 to 1.9 mmol/l depending on the analyser you’re using. Adult cats tend to sit a little higher than this on average.
What is ‘normal’ for our patients is highly age-dependent. For example, young animals run MUCH higher than the adult reference ranges due to their growth.
In puppies under 8 weeks old, levels up to around 3.5 mmol/l can be completely normal, and they gradually fall into the adult range by about a year of age. The effect is less obvious in kittens, but they still tend to be higher than adult cats.
Top tips for phosphate sampling as veterinary nurses and technicians
Phosphate isn't as fussy as ionised calcium, but there are still a few things that can change the result:
Take a fasted sample where you can because results can be impacted by recent ingestion of protein or carbohydrate. Of course in our hospitalised patients a fasted sample isn't always possible - so make a note of when the patient last ate, and whether they're on any dextrose or insulin, so we can interpret the result alongside that information.
Use serum or heparinised plasma - EDTA, citrate and oxalate all interfere with phosphate testing causing inaccurate results. The main problem we see with this is filling EDTA tubes first, and inadvertently contaminating your heparin sample with EDTA. If possible, fill your EDTA tube after your biochemistry tube.
Avoid haemolysis - red blood cells contain phosphate, so a haemolysed sample can cause phosphate levels to be falsely increased.
Make a note of lipaemia, icterus or very high proteins (for example some cancers, or patients with FIP) - depending on the analyser these can interfere with the result in either direction.
Let's talk about our patients - starting with hyperphosphataemia, or high phosphate
What causes hyperphosphataemia in cats and dogs?
Reduced excretion by the kidneys
This is by far the most common cause. It includes:
Acute kidney injury - where hyperphosphataemia is typical, because the body hasn't had time to adapt unlike in cases of CKD.
Chronic kidney disease - in early CKD, the remaining nephrons can increase how much phosphate they excrete, so phosphate often stays normal. However, as the disease advances this compensation mechanism fails, and hyperphosphataemia results.
Hypoparathyroidism - with no PTH, the kidneys will retain phosphate. In these patients, though, the signs we see are usually dominated by the hypocalcaemia.
Increased intake
Phosphate-containing enemas such as fleet enemas. These are reported to have caused severe hyperphosphataemia in cats and small dogs.
Vitamin D toxicity, for example certain rodenticides and psoriasis creams. These increase calcium AND phosphate, causing widespread soft tissue mineralisation and kidney injury, often with a very rapid onset.
Overdose of urinary acidifiers or phosphate supplements, including IV phosphate.
Phosphate moving out of cells
Tumour lysis syndrome. This is uncommon, but can happen within around 48 hours of a patient's first chemotherapy treatment - especially in patients with lymphoma and a large tumour burden. As the cancer cells break down they release large amounts of potassium and phosphate into the bloodstream.
Severe tissue trauma and muscle damage (rhabdomyolysis).
Aortic thromboembolism in cats.
Haemolysis.
Metabolic acidosis, such as lactic acidosis or DKA.
What does a high phosphate actually do to our patients?
Most of the clinical signs we see in these patients come from the underlying disease - but the high phosphate has some important effects of its own. We see:
Hypocalcaemia
Phosphate binds calcium and reduces vitamin D activation, so the ionised calcium falls. So we may see the signs we chatted about in episode 128 - restlessness, facial rubbing, muscle twitching and, in severe cases, tetany.
Soft tissue mineralisation
Calcium phosphate can be deposited in the kidneys, heart, lungs and blood vessels. The risk is highest when calcium and phosphate are both increased (like vitamin D toxicity), and it can be fatal.
In CKD, renal secondary hyperparathyroidism
A persistently high phosphate means less calcitriol and a lower ionised calcium, which both stimulate PTH. Over time, this high PTH contributes to bone demineralisation and some of the effects of uraemia, and phosphate retention is associated with progression of kidney disease. This is the reason we restrict phosphate in CKD, which we chatted about in episode 126.
Also, I do want to mention that because of that link between how potassium and phosphate move in the body, hyperkalaemia can be seen in many of these patients - particularly in cases of AKI, urethral obstruction and tumour lysis syndrome. So these patients often need close monitoring, especially cardiovascular checks and perhaps even continual ECG monitoring, too.
How do we treat hyperphosphataemia?
The main treatment is always going to be managing the underlying cause - relieving the obstruction, treating the AKI, decontaminating after a toxin ingestion, and so on. Alongside this, we’ll provide supportive fluid therapy and general nursing & symptomatic care.
Fluid therapy
IV fluids help in a couple of ways. Correcting dehydration and expanding circulating volume dilutes the phosphate, and improving blood flow to the kidneys increases how much phosphate they can excrete.
As always, the overall fluid choice and rate are going to be tailored to the individual patient, so for us it's all about monitoring - urine output (ins and outs), body weight, hydration status, and watching for signs of fluid overload, especially in patients with oliguric AKI.
What about calcium administration?
Because adding calcium to a high phosphate increases the risk of mineralisation, calcium supplementation in hyperphosphataemic patients is something that needs careful consideration. And calcium gluconate should never be given subcutaneously - calcinosis cutis (calcium deposits in the skin) has been reported in dogs and cats after subcutaneous calcium gluconate.
Diet and phosphate binders
In our CKD patients, longer-term management is about reducing how much phosphate the patient absorbs. Most dietary phosphate comes from protein, so renal diets, which are protein and phosphate restricted, are a big part of this. (Remember from episode 127, though, that renal diets aren't indicated in AKI.)
If diet alone isn't enough, phosphate binders are used. They work by binding phosphate in the food within the gut, which means:
They need to be given WITH meals - mixed into the food, or given just before or just after eating.
They're split across all of the patient's meals rather than one or two of them.
They don't do much in a patient who isn't eating (which is why, as we said in episode 127, we hold off on them in AKI patients until they're eating or being tube fed).
Binders also take time to work - often weeks - because the body has a large store of phosphate to work through in the meantime. Once they’ve been introduced, we’ll monitor their effects with repeated phosphate sampling at appropriate intervals.
How can we prevent hyperphosphataemia?
There are a couple of situations where we can reduce the risk of hyperphosphataemia in the first place:
Patients with lymphoma and a large tumour burden starting chemotherapy may have IV fluids beforehand. Monitoring urine output, potassium, phosphate, calcium and kidney values over the first 48 hours helps us pick up tumour lysis syndrome early.
Check what's in your enema cupboard - phosphate-containing enemas aren't suitable for cats and small dogs, and caregivers should know not to use human enemas at home. Micralax enemas are not phosphate-based, which is why we tend to use these as our go-to in cats.
Ok, so that's hyperphosphataemia. What about when phosphate levels decrease - what does that do?
Mild to moderate hypophosphataemia is actually really common in our patients, and often isn't significant on its own, because total body phosphate levels are likely normal.
Once phosphate falls below around 0.3 mmol/l, though, it's generally considered clinically significant, and is more likely to reflect a true depletion of the body's phosphate stores.
Cats seem to be more sensitive than dogs to the effects of hypophosphataemia - problems have been reported at higher levels in cats compared with dogs, and thinking back, it has always been hypophosphataemic cats I’ve ended up nursing.
Why does low phosphate matter?
If we go back to what phosphate does, this is mostly about energy. Without enough phosphate, cells can't make enough ATP, and red blood cells can't make enough of that 2,3-DPG. The cells that use the most energy are hit hardest - red blood cells, muscle, and the brain.
This means we can see lots of changes in our patients, particularly:
Haemolysis - this is the most common complication. Red blood cells without enough ATP become fragile and break down, and in reported cases the PCV dropped within 24-48 hours of hypophosphataemia being found.
Reduced oxygen delivery to the tissues - because haemoglobin cannot release oxygen into the tissues as easily when 2,3-DPG is low.
Muscle weakness and pain, and in severe cases rhabdomyolysis - including weakness of the respiratory muscles, which can affect ventilation.
Reduced cardiac contractility and arrhythmias.
Inappetence, nausea, vomiting and ileus.
Neurological signs, such as changes in mentation, ataxia, seizures and stupor.
Poor white blood cell and platelet function, increasing the risk of infection and bleeding.
Interestingly, many patients with severe hypophosphataemia show no obvious signs at all - which is why we can't rely on clinical signs alone, and why monitoring is so important in our at-risk patients.
OK, that’s what hypophosphataemia is, and why it is so important. But what causes it?
There are three main reasons:
1. Phosphate moving into cells
This is the big one in hospitalised patients, and includes insulin therapy (especially in DKA), dextrose infusions, refeeding, respiratory alkalosis, and hypothermia.
2. Increased losses, mainly in the urine
This includes primary hyperparathyroidism - where high calcium with low phosphate is the classic pattern on bloods (another link back to episode 128). Here, the hypophosphataemia is usually mild, and often doesn't need supplementation. Hypercalcaemia of malignancy, osmotic diuresis in diabetic patients, glucocorticoids and hyperadrenocorticism, some diuretics, and eclampsia can also increase losses.
3. Reduced intake or absorption
This includes prolonged anorexia and malnutrition, excessive use of phosphate binders, and aluminium-containing antacids.
Phosphate balance in the diabetic ketoacidosis patient
Diabetic patients, and particularly those with DKA, are probably the patients we see this in most often - and they're the best example of that 'blood level vs total body' problem we talked about earlier on in this episode.
When we think about these patients, they've lost phosphate in their urine through the osmotic diuresis, they've often lost muscle mass, and many haven't been eating.
But when they arrive, their phosphate can be normal or even high. This is because a lack of insulin, together with the acidosis, moves phosphate out of the cells and into the blood.
Then we start treatment. Once insulin is given, phosphate moves back into the cells along with glucose and potassium - and the blood level can fall quickly. It usually becomes obvious within the first 24 hours of insulin therapy and is at its worst at around 24-36 hours.
So for us, just because that phosphate is normal on admission doesn’t mean it will remain normal. These patients need their phosphate rechecked alongside their potassium and glucose during the first day or two of treatment, and the vet may decide to supplement in anticipation - often by giving part of the patient's potassium supplementation as potassium phosphate.
Severe hypophosphataemia, haemolysis and seizures have all been reported in dogs and cats during DKA treatment, so keeping a close eye on the PCV and the colour of the plasma is really important too.
Refeeding syndrome and hypophosphataemia
Refeeding syndrome happens when we start feeding a patient who has been severely malnourished or hasn't eaten for a long time. It's rarely reported in our patients, but it's most often described in cats - cats with hepatic lipidosis being a classic example.
During starvation, these patients become depleted of phosphate, potassium and magnesium inside their cells - but their blood levels often look normal, because the kidneys adjust to hold on to what's there.
When feeding restarts, the carbohydrate stimulates insulin release. Insulin pushes phosphate, potassium and magnesium into the cells, and at the same time the body switches into 'rebuilding' mode, which increases demand for phosphate to make ATP.
Blood levels can then drop really quickly - hypophosphataemia is the most common and consistent abnormality (alongside hypokalaemia and hypomagnasaemia), and we can also see thiamine deficiency and fluid shifts causing oedema or heart failure.
It typically develops within 2-5 days of feeding starting, but can be seen within hours, or as late as 10 days. In tube-fed cats, phosphate has been seen to drop within 12-24 hours of feeding beginning.
This is a really big area for us as nurses, and there's so much we can do to help support these patients, including:
Identifying at-risk patients. A really thorough diet history - when did they last eat properly, and how much - along with body weight, how much weight they've lost, body condition score and muscle condition score. Patients that have lost more than 20% of their body weight (think of the cat who's been missing for six weeks) are considered high risk, and refeeding syndrome has been reported in critically ill people after only 48 hours without food.
Making sure the vet is aware of that risk before the feeding plan is put together. Fluid and electrolyte abnormalities should be corrected before feeding starts, and thiamine and electrolyte supplementation may be started beforehand.
Starting refeeding slowly. One suggested approach is to give no more than 20% of the patient's RER on the first day, then increase gradually over 4-10 days. Refeeding syndrome has been reported in cats fed as little as 6 kcal/kg/day, so the starting point needs to be very conservative.
Monitoring patients really carefully - including bodyweight, urine output, electrolytes, glucose, PCV and signs of haemolysis, alongside ECG, and cardiovascular and respiratory function.
Recording nutritional intake really accurately.
How do we treat hypophosphataemia, and what do we need to watch out for?
Where we can, prevention is better than treatment - so anticipating it in our DKA patients, refeeding patients and patients on parenteral nutrition is a really huge part of our nursing care.
In many mild cases, treating the underlying condition, correcting the acid-base status and getting the patient eating normally again is enough for phosphate to return to normal.
Where supplementation is needed, oral supplementation is safer, but it isn't suitable for patients who are vomiting and can cause diarrhoea, so it's usually given in small, divided doses. Patients with severe or symptomatic hypophosphataemia generally need IV supplementation.
IV phosphate comes as potassium phosphate or sodium phosphate. The choice depends on the patient's other electrolytes, and because many of these patients are also hypokalaemic, potassium phosphate is often used.
IV phosphate needs really careful handling:
It's concentrated and hypertonic, so it must be diluted, and it's given slowly as a CRI over hours - never as a bolus. Use an infusion pump or syringe driver, and label the bag and line clearly.
It should be given in calcium-free fluids, such as 0.9% sodium chloride. Adding phosphate to calcium-containing fluids like Hartmann's can cause calcium phosphate to precipitate. So it’s really important that we check compatibility before running it alongside anything else.
Potassium phosphate contains a lot of potassium. It needs to be included in the patient's total potassium supplementation to avoid accidental hyperkalaemia - so double-check the total potassium the patient is receiving.
Phosphate is commonly rechecked every 6-8 hours during IV supplementation (some protocols recheck more often), and monitoring continues even after it has returned to normal.
Over-supplementation is also possible - this has several risks including hyperphosphataemia, hypocalcaemia, soft tissue mineralisation and kidney injury. So we also need to monitor patients for signs of hypocalcaemia, and monitor calcium levels during phosphate treatment.
And of course, we're alao monitoring the patient's response - their PCV, plasma and urine colour, muscle strength, respiratory pattern, mentation, appetite and GI function, because phosphate abnormalities can change all of these.
So those are the things we need to know about phosphate - and what happens to our patients when it goes wrong.
This one little mineral does a LOT and when we see patients with abnormalities, they can go very wrong very quickly - and this means that, for us, knowing what to look out for is huge.
As veterinary nurses and technicians, our priorities when caring for these patients are:
Looking at phosphate results alongside the ionised calcium, potassium, magnesium, kidney values and glucose - and what's happening to the patient, when they last ate, and whether they're on dextrose or insulin.
Avoiding haemolysis, filling sample tubes appropriately, and noting any lipaemia or recent meals to help ensure results are accurate.
Knowing which patients are at risk of hypophosphataemia, and looking out for signs of it - such as our DKA patients, malnourished or long-term anorexic patients (especially cats) when feeding restarts, or patients on dextrose infusions.
Watching for signs of haemolysis.
Assessing fluid balance and urine output, especially in our hyperphosphataemic patients with AKI, urethral obstruction or tumour lysis syndrome.
Cardiovascular monitoring, particularly where potassium and calcium are abnormal too.
Looking out for neuromuscular and respiratory signs such as weakness, twitching or tetany), and changes in respiratory effort.
Giving IV phosphate safely, diluted, as a slow CRI in calcium-free fluids, and rechecked frequently.
Identifying patients at risk of refeeding syndrome, starting slowly, monitoring their intake carefully, and measuring phosphate frequently.
And then there's caregiver education, which is an enormous part of our role - especially at discharge. Talking to clients about things like when and how to use phosphate binders, how to transition to a phosphate-restricted diet, and how to manage inappetence in cats to prevent the risk of hepatic lipidosis and refeeding syndrome, is huge.
Did you enjoy this episode? If so, I'd love to hear what you think. Take a screenshot and tag me on Instagram (@vetinternalmedicinenursing) so I can give you a shout-out and share it with a colleague who'd find it helpful!
Thanks for learning with me this week, and I'll see you next time!
References and Further Reading
Chan DL. Refeeding syndrome in small animals. In: Chan DL (ed.) Nutritional Management of Hospitalized Small Animals. Wiley, 2015.
DiBartola SP, Willard MD. Disorders of phosphorus: hypophosphatemia and hyperphosphatemia. In: DiBartola SP (ed.) Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice, 4th ed. Saunders, 2012.
eClinPath. Phosphate, available from https://eclinpath.com/chemistry/minerals/phosphate/, 2026.
Elliott DA. Nutritional support in acute kidney injury in dogs and cats. In: Chan DL (ed.) Nutritional Management of Hospitalized Small Animals. Wiley, 2015.
Grünberg W. Overview of disorders of phosphorus metabolism in animals, available from https://www.msdvetmanual.com/metabolic-disorders/disorders-of-phosphorus-metabolism/overview-of-disorders-of-phosphorus-metabolism-in-animals, 2026.
Grünberg W. Hyperphosphatemia in animals, available from https://www.msdvetmanual.com/metabolic-disorders/disorders-of-phosphorus-metabolism/hyperphosphatemia-in-animals, 2026.
Grünberg W. Hypophosphatemia in animals, available from https://www.msdvetmanual.com/metabolic-disorders/disorders-of-phosphorus-metabolism/hypophosphatemia-in-animals, 2026.
O'Dwyer L. Disorders of phosphorus. In: Randels-Thorp A, Liss D (eds) Acid-Base and Electrolyte Handbook for Veterinary Technicians. Wiley, 2017.
