High Potassium Explained: What a High Potassium Blood Test Means, Causes, Symptoms and When It Matters

This article is for general health education only.

It does not diagnose hyperkalaemia, kidney disease, adrenal disease, heart disease, diabetic ketoacidosis or any other medical condition. It does not provide personalised treatment advice.

Do not stop ACE inhibitors, ARBs, spironolactone, eplerenone, potassium supplements or other prescribed medicines because of information in this article unless instructed by an appropriate healthcare professional.

A significantly elevated potassium result can be medically urgent even when the person feels well.

Seek urgent professional assessment for an unexpectedly very high potassium result or symptoms such as:

• severe muscle weakness
• paralysis
• significant palpitations
• fainting
• chest pain
• severe breathlessness
• marked deterioration
• or symptoms associated with severe kidney or metabolic illness.

Blood tests frequently contain values flagged slightly above or below a reference interval. Many of those abnormalities can be reviewed routinely.

Potassium is different.

That is because the difference between the concentration of potassium inside and outside cells helps create the electrical gradients that allow nerves and muscles - including the heart - to function correctly.

South Tees Hospitals notes that potassium is predominantly an intracellular ion, with only a small proportion present in extracellular fluid. Maintaining that relatively low extracellular concentration is important for normal neuromuscular and cardiac activity.

A small absolute shift in the amount circulating in the blood can therefore have substantial physiological consequences.

Suppose a blood report shows a potassium of 5.8 mmol/L flagged HIGH. The immediate question should not simply be "what foods did I eat?" or "is 5.8 dangerous?". The more useful questions are:

• Is this result genuine?
• What was the previous potassium?
• How are the kidneys functioning?
• Which medicines is the person taking?
• Is there an acute illness?
• Is there acidosis, insulin deficiency or major tissue injury?
• Is the potassium stable or rapidly rising?
• Are there ECG abnormalities?

This is what converts an isolated laboratory flag into clinically meaningful information.

Potassium is one of the body's major electrolytes. It is found predominantly inside cells.

Its functions include helping regulate:

• nerve impulse transmission
• skeletal muscle contraction
• cardiac electrical activity
• transport of nutrients into cells
• movement of waste products out of cells
• cellular fluid balance

The NHS specifically describes potassium as important for communication between nerves and muscles and for healthy heart function.

Because the extracellular potassium concentration is tightly controlled, the body relies on several overlapping systems to maintain balance. These include kidney excretion, hormonal regulation, movement of potassium between intracellular and extracellular compartments, and gastrointestinal intake and loss.

There is no single universal laboratory reference interval. Examples from current NHS laboratories include:

Other laboratories may use an upper limit of around 5.0, 5.2 or 5.3 mmol/L depending on their methodology and local population. This means a result of 5.2 mmol/L might be flagged in one laboratory but remain within range in another.

Hyperkalaemia means potassium concentration in the blood is higher than normal. The European Resuscitation Council classification cited in current NICE materials categorises hyperkalaemia as:

These categories are useful clinically, but they do not tell the entire story.

A potassium level of 6.2 mmol/L that has developed rapidly during acute kidney injury can be more concerning than the same concentration that has been present chronically in a closely monitored patient. Similarly, ECG abnormalities can change urgency.

The overall assessment therefore considers both the potassium concentration and the person behind the potassium concentration.

Every heartbeat is coordinated by electrical signals moving through cardiac muscle cells. Potassium contributes to the electrical membrane potential required for those signals.

When extracellular potassium rises substantially, the electrical properties of cardiac cells change. As hyperkalaemia becomes more severe, possible ECG changes include:

• tall or "tented" T waves
• PR prolongation
• flattening or disappearance of P waves
• QRS widening
• sine-wave patterns
• malignant arrhythmias
• cardiac arrest

The UK Kidney Association's acute hyperkalaemia guideline illustrates the progressive ECG abnormalities that can occur as potassium rises. However, this progression is not perfectly predictable. A patient can have a dangerously high potassium level without every textbook ECG feature appearing.

Yes.

The relationship between potassium concentration and ECG findings varies between individuals. Current clinical guidance warns that even severe hyperkalaemia may sometimes produce relatively limited ECG abnormalities, particularly when the increase has developed gradually.

A normal ECG does not reliably exclude clinically important hyperkalaemia. Likewise, the presence of ECG abnormalities increases concern but does not independently explain the cause.

Yes - but hyperkalaemia can also be asymptomatic. When symptoms occur, NHS guidance describes possibilities including:

• muscle weakness
• tiredness
• numbness
• muscle cramps
• palpitations
• irregular pulse
• chest discomfort
• paralysis in severe cases

These symptoms are nonspecific. Many other conditions can cause weakness, fatigue or palpitations. That means symptoms cannot diagnose hyperkalaemia. Equally importantly, no symptoms does not prove the potassium level is safe.

High potassium generally develops through one or more of four broad mechanisms: the kidneys cannot excrete potassium efficiently; medicines interfere with potassium regulation; potassium moves from inside cells into the bloodstream; or the laboratory result is artificially high.

Less commonly, excessive potassium intake or administration contributes substantially, particularly when normal excretion is already impaired.

Royal Devon NHS guidance groups causes into excessive intake, reduced renal excretion, transcellular shifts and technical causes of pseudohyperkalaemia.

The kidneys are central to potassium balance. They filter blood and regulate how much potassium is ultimately excreted in urine.

The NHS identifies kidney disease as the most common cause of high potassium levels and lists potassium measurement as an important part of diagnosing or monitoring kidney disease.

Hyperkalaemia may occur with acute kidney injury, advanced chronic kidney disease, dialysis dependence, reduced effective kidney perfusion, or combinations of kidney dysfunction and potassium-raising medications. The risk becomes particularly important when kidney function deteriorates suddenly.

Acute kidney injury - AKI - means kidney function worsens over a relatively short period. If potassium excretion falls rapidly, potassium can accumulate. Royal Devon NHS guidance lists acute kidney injury among major risk factors for hyperkalaemia.

This is one reason potassium and creatinine are commonly reviewed together. A potassium of 6.1 mmol/L alongside a substantially increased creatinine and a reduced eGFR is a very different pattern from a potassium of 5.4 mmol/L with unchanged creatinine, stable eGFR and a sample reported as haemolysed.

People with chronic kidney disease may have reduced capacity to excrete potassium, particularly as kidney function becomes more impaired.

The challenge is that some of the medicines that protect the kidneys and heart can also increase potassium. This creates an important clinical balancing act.

NICE's chronic kidney disease guidance states that RAAS inhibitors should not routinely be started when pretreatment potassium is above 5.0 mmol/L and recommends stopping RAAS inhibitor treatment if potassium rises to 6.0 mmol/L or more after other potassium-raising medicines have been addressed.

These are clinician-management recommendations, not instructions for patients to stop medicines themselves.

Medication review is essential whenever hyperkalaemia is identified. Commonly implicated medicine groups include:

• ACE inhibitors
• angiotensin receptor blockers
• mineralocorticoid receptor antagonists
• potassium-sparing diuretics
• potassium supplements
• some NSAIDs
• certain combinations of the above

NHS guidance specifically notes that spironolactone can raise potassium and that potassium supplements, some heart medicines and NSAIDs can increase the risk further.

NICE's current heart-failure guideline recommends measuring kidney function and electrolytes 1-2 weeks after starting ACE inhibitors, ARNI, ARBs or MRAs, 1-2 weeks after each dose increase, every 3-6 months once the maximum tolerated dose has been reached, and whenever kidney function may be compromised.

If potassium rises above 5.5 mmol/L, NICE advises following local guidance. This demonstrates why potassium is routinely monitored even when a patient feels completely well.

Spironolactone blocks aldosterone action, which can reduce potassium excretion.

The NHS lists hyperkalaemia as a recognised important adverse effect and notes possible symptoms including muscle weakness, tiredness, numbness and arrhythmia. Spironolactone users are also advised to discuss potassium-rich foods and potassium-containing salt substitutes where appropriate because those can add to overall potassium exposure.

This does not mean everyone taking spironolactone needs an extremely low-potassium diet. Dietary decisions depend on kidney function, potassium levels and individual treatment plans.

ACE inhibitors and angiotensin receptor blockers alter the renin-angiotensin-aldosterone system. They are valuable treatments for conditions including hypertension, chronic kidney disease, heart failure and certain cardiovascular conditions.

But reduced aldosterone signalling can also reduce potassium excretion. This is why potassium is typically checked before and after initiation or dose changes.

NICE emphasises the need to balance the benefits of RAAS inhibition against the risk of hyperkalaemia rather than treating the potassium number in isolation.

The adrenal glands produce aldosterone, a hormone that helps regulate sodium and potassium balance. In primary adrenal insufficiency - Addison's disease - aldosterone deficiency can contribute to hyperkalaemia.

Royal Devon and NHS Scotland guidance both list Addison's disease or hypoaldosteronism among causes of hyperkalaemia. This is far less common than kidney disease or medication-related hyperkalaemia. A high potassium result by itself does not indicate Addison's disease.

Insulin helps move potassium from the extracellular fluid into cells. In severe insulin deficiency, potassium can move out of cells and raise blood potassium concentration.

This is one reason hyperkalaemia can occur in diabetic ketoacidosis (DKA) even when the body's total potassium stores may eventually be depleted. The NHS specifically lists suspected DKA as a reason potassium testing may be performed. Royal Devon guidance also identifies diabetes and DKA among important clinical contexts for hyperkalaemia.

Acid-base disturbances can influence potassium distribution between cells and blood.

South Tees Hospitals notes that hyperkalaemia can occur when potassium movement out of cells exceeds excretion and highlights acidosis - particularly when kidney filtration is impaired - as an important context.

The underlying mechanism can be multifactorial. A critically ill person may simultaneously have acidosis, kidney dysfunction, tissue injury, medications and reduced circulating volume.

Because most potassium is stored inside cells, major cellular destruction can release potassium into the circulation. Recognised causes include rhabdomyolysis, crush injury, severe burns, tumour lysis syndrome and major trauma.

Royal Devon NHS guidance lists several of these causes. These conditions are very different from a mildly high outpatient potassium result and usually occur within a significant clinical illness.

Tumour lysis syndrome occurs when large numbers of cancer cells break down rapidly, releasing intracellular contents including potassium. It is primarily associated with certain cancers and cancer treatments, and it can cause severe electrolyte disturbances and acute kidney injury.

Tumour lysis syndrome is therefore an important but specialised and uncommon explanation for hyperkalaemia in the general population. NHS clinical hyperkalaemia guidance includes tumour lysis syndrome among recognised causes.

One of the most important concepts in interpreting an unexpectedly high potassium result is pseudohyperkalaemia. This means the blood sample reports high potassium, but the person's true circulating potassium is not actually elevated to the same degree. It can happen because potassium leaks out of blood cells after the blood has been taken.

Red blood cells contain potassium. If they rupture during or after blood collection - a process called haemolysis - potassium can leak into the serum or plasma. The laboratory may then report an artificially elevated potassium concentration.

Newcastle Hospitals lists sample haemolysis as an important cause of spurious hyperkalaemia. Common pre-analytical problems can include difficult blood collection, traumatic venepuncture, sample handling issues and prolonged delay before processing.

Whether a specific sample is affected should be determined by the laboratory rather than assumed by the patient.

Newcastle Hospitals also identifies delay before centrifugation, potassium-EDTA contamination and potassium-oxalate contamination as potential causes of falsely high potassium.

This is why an unexpected result may need confirmation. NICE itself notes that serum potassium tests can sometimes incorrectly identify hyperkalaemia and therefore often require confirmation.

Marked thrombocytosis and leukocytosis can sometimes produce pseudohyperkalaemia. Potassium may leak from platelets during the clotting process or from fragile white cells during sample handling.

Newcastle Hospitals specifically warns that thrombocytosis and leukocytosis can cause spurious hyperkalaemia. This becomes particularly relevant when a patient has a high potassium alongside an extremely high platelet or white-cell count but the clinical picture does not fit hyperkalaemia.

This is one of the most persistent misconceptions about potassium. Bananas contain potassium, as do many healthy foods.

The NHS lists potassium-rich foods including fruit, vegetables, pulses, nuts and seeds, milk, fish, meat and bread.

In people with healthy kidney function and normal hormonal regulation, dietary potassium is generally handled efficiently. Diet becomes more clinically important when potassium excretion is impaired - for example in advanced kidney disease - or when medications interfere with potassium regulation.

High potassium is usually not simply "because you ate a banana".

Some reduced-sodium salt substitutes replace sodium chloride with potassium chloride. This can matter in people at risk of hyperkalaemia.

The NHS specifically warns people taking spironolactone that salt substitutes such as Lo-Salt may raise potassium further. This is an important reason medication and dietary history need to be considered together.

No. Dietary intervention should depend on the cause and clinical circumstances.

Someone with a falsely high result does not need a low-potassium diet. Someone with acute kidney failure needs treatment of the acute condition. Someone with persistent CKD-related hyperkalaemia may benefit from targeted dietary assessment.

NICE's current 2026 hyperkalaemia technology appraisal describes dietary changes as part of usual management for persistent hyperkalaemia in selected patients with chronic kidney disease or heart failure.

The goal is not indiscriminate elimination of nutritious foods. It is appropriate potassium control while preserving overall nutritional quality.

The commonly referenced classification is:

However, this table needs three major caveats. The rate of change matters, because a rapid rise can be particularly dangerous. The ECG matters, because electrical abnormalities increase urgency. And the underlying condition matters, because acute kidney injury, metabolic illness or severe tissue breakdown may require immediate treatment even while the diagnostic work-up continues.

In acute severe hyperkalaemia, medical treatment has several broad objectives: protect the heart, temporarily shift potassium from the blood into cells, remove excess potassium from the body, and identify and treat the underlying cause.

The exact treatment depends on potassium concentration, ECG findings, kidney function and clinical circumstances. The UK Kidney Association has a dedicated guideline for acute hyperkalaemia management because it can be a time-critical medical problem.

This article intentionally does not provide medication doses or emergency treatment instructions because severe hyperkalaemia requires professional management.

For selected patients with persistent hyperkalaemia, potassium-binding medicines may be considered. Current NICE guidance includes patiromer and sodium zirconium cyclosilicate for specific populations and clinical circumstances.

NICE recommends patiromer for selected adults with persistent hyperkalaemia and stage 3b-5 CKD or heart failure when potassium is confirmed at 6.0 mmol/L or above and RAAS inhibitor therapy cannot otherwise be optimised, as well as use alongside standard care in acute life-threatening hyperkalaemia.

NICE's April 2026 updated appraisal of sodium zirconium cyclosilicate also addresses persistent hyperkalaemia management in CKD and heart failure.

These drugs are not treatments for a single incidental mildly raised potassium reading.

ACE inhibitors, ARBs and related RAAS medicines can protect heart and kidney function. However, they can also increase potassium. This creates a trade-off.

NICE's hyperkalaemia discussions specifically acknowledge that clinicians may want treatment strategies that allow people to remain on beneficial RAAS therapy where safely possible.

This explains why "potassium is high, therefore stop every RAAS medicine" is an oversimplification. Treatment decisions depend on severity of hyperkalaemia, kidney function, the indication for the drug, other medications, whether the elevation is recurrent or one-off, and the availability of alternative approaches.

Dehydration itself is not a universal direct explanation for hyperkalaemia. However, severe volume depletion can reduce kidney perfusion and contribute to acute kidney injury, which may then impair potassium excretion.

The context therefore matters. A mildly dehydrated healthy person and a severely volume-depleted patient with falling kidney function are not equivalent.

During muscle activity, potassium moves temporarily out of muscle cells. After exercise, regulatory mechanisms usually restore balance. Routine physical activity therefore does not normally cause sustained clinically important hyperkalaemia in healthy people.

Major muscle injury, however, is different. Conditions such as rhabdomyolysis can release large amounts of intracellular potassium and are recognised causes of hyperkalaemia.

Yes. Persistent hyperkalaemia may occur in people with chronic kidney disease, heart failure, diabetes, hypoaldosteronism or certain long-term medicines.

Management differs substantially from emergency treatment of sudden severe hyperkalaemia. NICE specifically distinguishes persistent chronic hyperkalaemia from acute life-threatening presentations.

Myth 1: "High potassium always means kidney failure." Fact: Kidney dysfunction is a major cause, but medicines, hormonal disorders, acidosis, tissue injury and laboratory artefact can also raise potassium.

Myth 2: "If I feel well, my potassium cannot be dangerous." Fact: Hyperkalaemia may cause few or no symptoms even when clinically important.

Myth 3: "A normal ECG proves my potassium is safe." Fact: Severe hyperkalaemia can occasionally occur without classic ECG abnormalities.

Myth 4: "One high potassium result always means true hyperkalaemia." Fact: Haemolysis, delayed processing, contamination, thrombocytosis and leukocytosis can cause pseudohyperkalaemia.

Myth 5: "A banana caused my potassium to become dangerously high." Fact: Severe hyperkalaemia usually reflects impaired regulation or excretion rather than one potassium-containing food.

Myth 6: "Everyone with potassium above 5.0 needs emergency treatment." Fact: Clinical severity depends on the actual concentration, confirmation, trend, ECG, symptoms and underlying cause.

Myth 7: "A potassium of 6.0 and 5.1 are basically the same because both are high." Fact: Magnitude matters. NICE and resuscitation guidance distinguish mild, moderate and severe hyperkalaemia.

Myth 8: "If a medicine raises potassium, it should always be stopped permanently." Fact: Some potassium-raising medicines provide substantial heart and kidney benefits. Clinicians balance these benefits against hyperkalaemia risk.

Myth 9: "Low-potassium diets are appropriate for everyone." Fact: Dietary restriction is relevant only in selected clinical circumstances and should avoid unnecessary nutritional restriction.

Myth 10: "Potassium is just another routine blood-test value." Fact: Severe abnormalities can directly affect cardiac electrical activity and become life-threatening.

What is considered high potassium? The laboratory's own reference range should be used. Several NHS laboratories use an adult upper limit around 5.3 mmol/L.

Is potassium 5.4 high? It is above the reference interval used by many laboratories but would generally fall below the 5.5 mmol/L threshold used in the ERC mild-hyperkalaemia classification. Context and confirmation matter.

Is potassium 5.5 dangerous? It is classified as mild hyperkalaemia in the ERC framework referenced by NICE. It warrants appropriate clinical assessment but does not carry the same implications as severe hyperkalaemia.

Is potassium 6.0 serious? A potassium of 6.0 mmol/L falls into the moderate hyperkalaemia category referenced by NICE and generally requires prompt clinical assessment.

Is potassium 6.5 dangerous? Yes. 6.5 mmol/L or above is classified as severe hyperkalaemia and may threaten cardiac electrical stability.

Can potassium be falsely high? Yes. Pseudohyperkalaemia can result from haemolysis, sample delays, contamination or very high blood-cell counts.

Why might my potassium test be repeated? Because unexpectedly high potassium often needs confirmation before treatment decisions are made, particularly when pseudohyperkalaemia is possible.

What does "haemolysed sample" mean? It means red blood cells were damaged in the specimen. Potassium can leak from those cells and artificially raise the measured concentration.

What is the most common cause of high potassium? The NHS identifies kidney disease as the most common major cause.

Can CKD cause high potassium? Yes. Reduced kidney excretion makes hyperkalaemia more likely, particularly in advanced CKD or when potassium-raising drugs are used.

Can acute kidney injury cause high potassium? Yes. AKI is an important cause and risk factor for hyperkalaemia.

Can ACE inhibitors raise potassium? Yes. RAAS inhibitors can increase potassium and require monitoring, especially in CKD and heart failure.

Can spironolactone cause high potassium? Yes. Hyperkalaemia is an important recognised adverse effect.

Can ibuprofen affect potassium? NSAIDs can contribute to potassium elevation in susceptible individuals, particularly when combined with other potassium-raising medicines or kidney dysfunction. NHS spironolactone guidance specifically warns about NSAID interactions.

Can potassium supplements cause hyperkalaemia? Yes, particularly when kidney excretion is impaired or potassium-raising medicines are also present.

Can salt substitutes cause high potassium? Potassium-containing salt substitutes can increase potassium exposure. The NHS specifically cautions people taking spironolactone about products such as Lo-Salt.

Can high potassium cause palpitations? Yes. Palpitations and irregular pulse are recognised possible symptoms.

Can high potassium cause muscle weakness? Yes. Muscle weakness is a recognised manifestation of hyperkalaemia.

Can high potassium cause tiredness? Tiredness may occur but is nonspecific and can also reflect the underlying kidney, cardiac or metabolic condition.

Can high potassium cause numbness? Numbness is listed by the NHS among possible symptoms of hyperkalaemia related to spironolactone.

Can high potassium cause cardiac arrest? Severe hyperkalaemia can produce dangerous arrhythmias and cardiac arrest.

Does ECG always change when potassium is high? No. Significant hyperkalaemia may sometimes occur without classic ECG abnormalities.

Why is creatinine checked with potassium? Kidney function is central to potassium excretion, so creatinine and eGFR help determine whether impaired renal clearance may be contributing.

Can Addison's disease cause high potassium? Yes. Aldosterone deficiency in primary adrenal insufficiency is a recognised cause.

Can diabetes cause high potassium? Diabetes can contribute through kidney disease, medications and severe insulin deficiency such as diabetic ketoacidosis.

Can DKA cause high potassium? Yes. Severe insulin deficiency and acidosis can shift potassium from cells into the blood.

Can muscle damage raise potassium? Yes. Rhabdomyolysis, crush injury and major trauma can release intracellular potassium.

Can chemotherapy cause high potassium? Certain cancer treatments can cause tumour lysis syndrome, which may release large amounts of intracellular potassium.

Does high potassium automatically require dialysis? No. Dialysis is used in selected severe or refractory cases, particularly where kidney failure prevents adequate potassium removal.

What are potassium binders? They are medicines that bind potassium in the gastrointestinal tract, allowing more potassium to leave the body in stool. NICE recommends agents such as patiromer and sodium zirconium cyclosilicate in selected patients.

Should I stop my ACE inhibitor if potassium is high? Do not stop prescribed medication based on an online article. NICE provides specific clinician guidance balancing potassium concentration against the cardiovascular and renal benefits of treatment.

Should I avoid bananas? Not automatically. Dietary potassium restriction should be individualised according to kidney function, medicines and repeated potassium measurements.

Why would potassium suddenly become high after years of normal results? Possible explanations include acute kidney injury, dehydration severe enough to impair renal perfusion, new medicines, dosage changes, acute illness, tissue damage or a falsely high laboratory specimen.

What matters more: the potassium number or the ECG? Both matter. Neither should be considered alone.

What is the most important first question after an unexpected high potassium result? Whether the result is genuine and confirmed, followed rapidly by assessment of its severity, kidney function, medicines and clinical context.

Step 1 - Check the laboratory reference interval A potassium concentration should first be interpreted against the range printed beside the result.

Step 2 - Check whether the sample was haemolysed A laboratory comment such as "haemolysed sample - potassium may be falsely elevated" can substantially change interpretation.

Step 3 - Compare previous results A sequence of 4.2, 4.4, 4.5 then 5.8 is not equivalent to 5.3, 5.4, 5.3, 5.4. The first suggests a significant new change; the second may represent a persistent borderline elevation.

Step 4 - Check kidney function Look at creatinine, eGFR, previous kidney function and any evidence of acute kidney injury.

Step 5 - Review medicines Pay particular attention to ACE inhibitors, ARBs, spironolactone, eplerenone, potassium supplements, potassium-containing salt substitutes, NSAIDs and combinations of potassium-raising treatments.

Step 6 - Look for an acute illness Consider dehydration with kidney dysfunction, diabetic ketoacidosis, sepsis, major tissue injury, rhabdomyolysis, tumour lysis or severe metabolic acidosis.

Step 7 - Assess severity A potassium of 5.6 and a potassium of 7.0 are not equivalent. Use the actual number and clinical situation rather than simply the red HIGH flag.

Step 8 - Consider the ECG and symptoms Severe hyperkalaemia may require cardiac monitoring and urgent treatment. But do not assume a normal ECG makes a significantly high potassium harmless.

Consider a laboratory portal showing a potassium of 5.9 mmol/L flagged HIGH. Alone, that is incomplete. Now add the wider timeline:

Now the result carries considerably more meaning. Alternatively, consider a very different pattern:

The same initial potassium value created a completely different final interpretation. That is the value of longitudinal health intelligence.

Potassium is a perfect example of why isolated blood tests can be misleading. Seeing a potassium of 5.8 mmol/L flagged HIGH can create immediate concern. But the more useful questions are longitudinal: was it 4.3 last month, has creatinine increased, did eGFR fall, was spironolactone recently added, was the sample haemolysed, has potassium been mildly high for years, did it return to normal on repeat testing?

A sequence of 4.2, 4.4, 4.9, 5.6, 6.0 alongside creatinine moving 82, 84, 92, 119, 148 tells a very different health story from 4.4, 4.3, 6.1, 4.5 where the 6.1 result was labelled "haemolysed specimen".

Healio360 is designed around this principle. Health data becomes more useful when results are connected across time rather than read as isolated red and green numbers.

Instead of asking only "why is my potassium high?", you can begin asking when it changed, what else changed at the same time, whether kidney function moved with it, whether a medication change preceded the rise, whether the test was repeated, and whether this is a real biological trend or a sample artefact.

Bring laboratory reports, medical results, imaging and health data into one longitudinal view so changes become easier to understand and discuss with healthcare professionals.

Healio360 provides educational interpretation and health-information organisation. It does not diagnose hyperkalaemia, determine its cause or replace professional clinical assessment.