Urea and Electrolytes (U&Es): How to Read Sodium, Potassium, Creatinine and eGFR

Urea and electrolytes, usually shortened to U&Es, are among the blood results you will see most often on placement. They are sometimes called “kidney bloods”, but that description is too narrow. U&Es can give you clues about kidney function, fluid balance, electrolyte disturbance, acute illness and the effects of medicines.

The important skill is not memorising a list of numbers. It is learning to ask: What has changed, why might it have changed, and does it fit what I am seeing in the patient?

A typical U&E profile includes sodium, potassium, urea and creatinine. Many laboratories also report chloride and bicarbonate, and an estimated glomerular filtration rate (eGFR) is commonly reported with creatinine in adults. Exact tests and reference intervals vary between laboratories, so always use the range shown alongside the patient’s result.

Before you interpret anything: look at the whole panel

Start with four simple checks:

1. Is anything outside the laboratory reference range?
2. Is it new? Compare with previous results whenever they are available.
3. Is the change clinically important? A trend may matter even when a value has not moved dramatically.
4. Does it fit the patient? Think about observations, urine output, fluid balance, symptoms, medicines and recent illness.

This stops U&Es becoming a number-reading exercise. A creatinine of 140 micromol/L means something very different in a patient whose usual creatinine is 135 compared with someone whose creatinine was 65 yesterday.

Sodium: think water balance, not simply salt

Serum sodium is a concentration. It reflects the relationship between sodium and water, so an abnormal result does not simply tell you that the patient has eaten too much or too little salt.

Low sodium: hyponatraemia

Hyponatraemia can occur in several different fluid states. Causes include gastrointestinal losses, medicines such as some diuretics, heart failure, liver disease, kidney disease, adrenal insufficiency and syndrome of inappropriate antidiuresis (SIADH). The underlying mechanism matters, which is why treatment cannot be decided from the sodium result alone.

High sodium: hypernatraemia

Hypernatraemia most often reflects water deficit relative to sodium. Consider poor access to water, impaired thirst, fever, gastrointestinal losses, excessive urinary water loss and diabetes insipidus.

What should make you concerned? Acute or severe sodium disturbance can affect neurological function. New confusion, reduced consciousness, seizures or significant clinical deterioration require prompt escalation. Sodium correction must be clinically managed because overly rapid correction can itself cause serious neurological harm.

Potassium: the result you should never ignore

Potassium is essential for normal nerve, skeletal muscle and cardiac electrical activity. The kidneys have a major role in regulating it, so potassium disturbance frequently accompanies impaired kidney function.

High potassium: hyperkalaemia

Hyperkalaemia may occur with acute kidney injury (AKI), chronic kidney disease, acidosis, tissue breakdown and medicines that reduce renal potassium excretion. Clinically important hyperkalaemia can cause dangerous cardiac conduction abnormalities and arrhythmias.

Low potassium: hypokalaemia

Hypokalaemia may occur with vomiting or diarrhoea, diuretic therapy, poor intake or shifts of potassium into cells. It can cause weakness and cardiac rhythm disturbance.

Do not decide urgency from a memorised potassium cut-off alone. Consider the actual result, symptoms, ECG, kidney function, rate of change and local critical-result or hyperkalaemia pathway.

Could a high potassium be false?

Yes. Haemolysis can release intracellular potassium into the sample and produce a falsely raised result. Difficult venepuncture, prolonged tourniquet time, repeated fist clenching and problems with sample handling or processing can contribute.

Look for a laboratory comment such as haemolysed sample. But never simply assume a high potassium is false. Report and escalate the result appropriately and follow the clinical plan for assessment, ECG and/or repeat sampling.

Urea: useful, but not a diagnosis

Urea is produced during protein metabolism and is removed mainly through the kidneys. It can rise when renal clearance falls, but it can also rise with dehydration, gastrointestinal bleeding, tissue breakdown and increased protein load.

This is why a raised urea does not automatically mean “the patient is dehydrated”. Interpret it alongside creatinine, urine output, fluid balance, observations and the clinical assessment.

Creatinine: always ask what the baseline was

Creatinine is produced from normal muscle metabolism and is filtered by the kidneys. When kidney filtration falls, serum creatinine commonly rises. However, creatinine is influenced by factors including muscle mass, age, diet and some medicines.

The most useful question is often not “Is the creatinine high?” but “How different is this from the patient’s baseline?”

A patient with low muscle mass may have significant kidney impairment without a striking creatinine result. Creatinine can also lag behind an acute deterioration in kidney function, so concerning oliguria or clinical deterioration should never be ignored simply because creatinine has not yet risen substantially.

Recognising possible acute kidney injury

AKI is an acute reduction in kidney function. NICE advises detecting AKI using changes in serum creatinine and/or urine output. In adults, criteria include a rise in serum creatinine of 26 micromol/L or more within 48 hours, a rise to 1.5 times or more the baseline value within the previous 7 days, or urine output below 0.5 mL/kg/hour for more than 6 hours.

For a student nurse, this means that trend and urine output matter. You may be the person who notices that the creatinine has climbed since yesterday or that urine output has remained low for several hours.

eGFR: useful for chronic kidney disease, less useful in rapidly changing kidney function

Estimated glomerular filtration rate (eGFR) uses serum creatinine together with other information to estimate kidney filtration. It is particularly useful in the assessment and monitoring of chronic kidney disease (CKD).

eGFR should not be interpreted in isolation. NICE uses both GFR category and urine albumin-to-creatinine ratio (ACR) when assessing CKD and its associated risk. A single reduced eGFR does not automatically establish CKD; chronicity and/or other evidence of kidney damage are important.

eGFR is also less reliable when kidney function is changing rapidly, including during AKI, and its accuracy can be affected at extremes of muscle mass. Do not independently alter medicine doses from an eGFR result. Renal dosing may require a different estimate of kidney function and should follow prescribing guidance and local policy.

Chloride and bicarbonate: what are they telling you?

If your laboratory includes them, chloride and bicarbonate add information about fluid and acid-base balance. A low bicarbonate may be seen with metabolic acidosis, while a raised bicarbonate may occur with metabolic alkalosis or compensation for chronic respiratory acidosis.

These values are not interpreted in isolation. If an acid-base disorder is suspected, the wider biochemical picture, clinical assessment and, where indicated, a blood gas are needed.

A simple way to read U&Es on placement

When the results appear, work through them in the same order each time:

1. Sodium: Is it abnormal, and does the patient have a plausible water-balance problem?
2. Potassium: Is it abnormal or rapidly changing? Is there a haemolysis comment? Could an ECG or urgent review be needed?
3. Urea: Is it raised, and what does the wider clinical picture suggest?
4. Creatinine: Compare it with previous values. Has it changed enough to raise concern for AKI?
5. eGFR: Use it mainly as part of the wider assessment of renal function, particularly CKD, rather than as a stand-alone number.
6. Patient: Check urine output, fluid balance, observations, symptoms and medicines.

Worked example: put the numbers back into the patient

Imagine you are caring for Mr Fraser, admitted with vomiting and poor oral intake. His creatinine today is 146 micromol/L. Yesterday it was 112 and his previous baseline was around 82. His urine output has been below 0.5 mL/kg/hour for seven hours and his blood pressure is lower than usual.

The important finding is not simply “creatinine 146”. You have a significant rise from baseline plus sustained low urine output in an acutely unwell patient. That combination should make you think about possible AKI and prompt escalation.

A useful handover sounds like this:

“Mr Fraser’s creatinine has risen from a baseline of about 82 to 146 micromol/L. His urine output has been below 0.5 mL/kg/hour for seven hours. He has had ongoing vomiting and his blood pressure is lower than baseline. I’m concerned about possible acute kidney injury and would like him reviewed.”

That is much more useful than saying, “His kidney bloods are abnormal.”

Read U&Es beside the patient

Before escalating an abnormal result, gather the information you can safely obtain:

• previous U&E results and baseline kidney function
• urine output and fluid balance
• blood pressure, pulse, perfusion, weight and oedema where relevant
• vomiting, diarrhoea, poor intake, fever or bleeding
• relevant prescribed medicines
• ECG findings or whether an ECG has been requested when potassium is abnormal
• laboratory comments, particularly haemolysis

Remember: a normal-looking U&E panel does not cancel clinical deterioration, and an abnormal panel does not tell you the cause on its own.

Your role as a student nurse

You are not expected to diagnose the cause of every biochemical abnormality or independently prescribe treatment. You are expected to recognise when something does not fit, collect accurate clinical information, identify trends, communicate concerns and follow up appropriately.

Useful actions within your role include checking previous results, maintaining accurate fluid-balance records, measuring and reporting urine output, checking whether a sample was haemolysed, obtaining observations, recognising deterioration and escalating concerns to your supervising registered nurse or appropriate clinician.

The skill you are building is not simply learning what sodium or creatinine means. It is learning to connect blood result + trend + patient assessment.

Continue with Fluid Balance Charts and Urine Output and Oliguria.

References

National Institute for Health and Care Excellence (NICE) (2019, updated 2024) Acute kidney injury: prevention, detection and management. NICE guideline NG148. Available at: https://www.nice.org.uk/guidance/ng148 

National Institute for Health and Care Excellence (NICE) (2021) Chronic kidney disease: assessment and management. NICE guideline NG203. Available at: https://www.nice.org.uk/guidance/ng203 

UK Kidney Association (2023) Clinical practice guideline: treatment of acute hyperkalaemia in adults. Available at: https://guidelines.ukkidney.org/hyperkalaemia/ 

Association for Laboratory Medicine (n.d.) Urea and electrolytes. Lab Tests Online UK. Available at: https://labtestsonline.org.uk/tests/ue 

Nursing and Midwifery Council (NMC) (2018) The Code: Professional standards of practice and behaviour for nurses, midwives and nursing associates. Available at: https://www.nmc.org.uk/standards/code/