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11/13/24, 7\:34 PM Guide | U&E interpretation

U&E interpretation

Table of contents

Introduction

The urea & electrolytes (U&E) pro
. A
standard urea and electrolytes pro
Serum creatinine
Estimated glomerular
Serum urea
Serum sodium
Serum potassium
This guide gives an overview of the U&E panel and provides a structured approach to U&E interpretation.

Why check U&Es

U&Es are commonly ordered to assess renal (kidney) function. The kidney excretes urea and creatinine, and these can be
used as surrogate markers of renal function. Sodium and potassium are included in the panel, as renal dysfunction can lead to
electrolyte derangements.
Other reasons to order U&Es include suspected electrolyte disturbances due to non-renal causes, medication monitoring
(e.g. after starting ACE inhibitors), or assessing urea levels in the case of suspected upper gastrointestinal haemorrhage.
Drug monitoring
Common drugs which require monitoring of U&Es include\:
Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs)
Diuretics\: spironolactone, thiazide diuretics (e.g. indapamide), loop diuretics (e.g. furosemide)
Direct-acting oral anticoagulants (DOACs)
Carbamazepine
Lithium
Digoxin

Reference ranges

Table 1. Urea & electrolytes pro
Test Reference range
Men 59–104 μmol/L
Creatinine
Women 45–84 μmol/ L
eGFR >90ml/min/1.73m
2
Urea 2.5 – 7.8 mmol/L
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Sodium 135–146 mmol/L
Potassium 3.5–5.3 mmol/L
These reference ranges can vary between laboratories, so always check local guidelines.

Creatinine

Creatinine is a waste product of muscle metabolism excreted entirely by the kidney.
1
Serum creatinine level is naturally higher in individuals with greater skeletal muscle mass (thus generally higher in males than
females). However, the primary determinant of serum creatinine is the kidney’s ability to
Therefore, a raised creatinine level is an indicator of kidney dysfunction.

Estimated Glomerular Filtration Rate (eGFR)

The eGFR is a mathematically derived number based on a patient’s serum creatinine in conjunction with age, sex and race.
2
eGFR aims to estimate the glomerular
creatinine rises, the eGFR will decrease, indicating worsening kidney dysfunction.
2
A ‘normal’ glomerular
roughly equated to a percentage of kidney function.
This is particularly relevant in chronic kidney disease (CKD), where the eGFR is used to ‘stage’ the disease\:
Stage 1\: eGFR >90 (normal), with other tests showing signs of kidney damage (e.g. proteinuria)
Stage 2\: eGFR of 60 to 89 ml/min, with other tests showing signs of kidney damage (e.g. proteinuria)
Stage 3a\: eGFR of 45 to 59 ml/min
Stage 3b\: eGFR of 30 to 44 ml/min
Stage 4\: eGFR of 15 to 29 ml/min
Stage 5\: eGFR \<15 ml/min
Problems with eGFR
The most common equations used to calculate eGFR are the MDRD and CKD-EPI equations. The CKD-EPI di
the MDRD equation because it does not add a race factor to the calculation.
Both equations are well-validated. However, in some circumstances, the eGFR can vary signi
glomerular
amputees). The equations are also not valid for those under 18 years of age.

Urea

Urea is a waste product of protein breakdown produced in the liver. 3
The kidneys predominantly excrete urea, and it can be
used as a surrogate marker of renal function. However, this is fairly non-speci
Causes of a raised serum urea (uraemia) include\:
Renal dysfunction\: decreased excretion of urea into the urine.
Dehydration\: urea rises quickly in dehydration, even in the presence of normally functioning kidneys. This is physiologically
mediated by anti-diuretic hormone (ADH), released from the posterior pituitary gland in response to intravascular volume
depletion. ADH increases urea and water reabsorption in the collecting ducts.
Upper gastrointestinal bleeding\: blood in the upper GI tract is broken down into proteins, which are transported to the liver
via the portal vein and metabolised into urea.
Low serum urea levels are non-pathological, associated with pregnancy and those on a low-protein diet.
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Sodium

Sodium is the main determinant of plasma osmolality, and serum levels are closely related to hydration (volume) status.
Serum sodium levels are normally regulated by antidiuretic hormone (ADH), amongst other homeostatic mechanisms.
Symptoms of both hypernatremia and hyponatremia are primarily neurological. Mild symptoms include fatigue, weakness and
confusion, but can progress to severe symptoms such as seizures and coma.
4
The severity of symptoms is related to the severity of sodium derangement and the pace of the change in serum sodium
concentration (rapid changes lead to severe symptoms).

Hypernatraemia

Hypernatraemia is de
unreplaced skin or GI losses of hypotonic
5
Rarer causes of hypernatraemia include\:
Diabetes insipidus
Drugs (e.g. loop diuretics)
Osmotic diuresis (e.g. in hyperglycemic states)
Extreme levels of salt ingestion
In most cases, where there is a clear history implicating dehydration (e.g. vomiting/diarrhoea), treatment involves gentle
rehydration with intravenous hypotonic
It is essential to monitor sodium levels during treatment, as correcting the hypernatraemia too rapidly can lead to
intracerebral
demyelination syndrome).

Hyponatraemia

SIADH).
6
Hyponatraemia is de
Treatment can vary according to the underlying cause and the patient's . Again, it is important to regularly monitor
sodium levels to avoid rapid correction.
For more information, see our guide to hyponatraemia.

Potassium

Derangements in potassium levels are common in hospital inpatients. Under physiological conditions, potassium is stored
almost entirely intracellularly and is excreted by the kidneys. Derangements in potassium levels cause myocardial
instability, leading to risks of potentially fatal arrhythmias.

Hyperkalaemia

Hyperkalaemia is de
Resuscitation Council guidelines\:
Mild\: 5.5-5.9 mmol/L
Moderate\: 6.0-6.4 mmol/L
Severe\: >6.5 mmol/L
Causes of hyperkalaemia can be varied\:
Renal\: decreased renal excretion (e.g. AKI or CKD)
Medications\: ACE inhibitors, potassium-sparing diuretics, potassium supplements
Tissue damage\: burns, rhabdomyolysis
Metabolic\: diabetic ketoacidosis
Endocrine\: Addison’s disease
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Severe hyperkalaemia is a medical emergency requiring immediate management. If ECG changes occur, the most critical
initial step is administering intravenous calcium gluconate, stabilising the myocardium. Once this is administered, treatment
focuses on lowering the serum potassium concentration, often via insulin/dextrose infusion.
For more information, see our guide to hyperkalaemia.
ECG features of hyperkalaemia
The cardinal features of hyperkalaemia on the ECG are peaked T waves, prolonged PR interval and widened QRS
complexes.

Hypokalaemia

Hypokalaemia is de
\<3.0mmol/L, which can destabilise the myocardium.
ECG changes associated with hypokalaemia include PR prolongation, widespread ST depression / T wave
prominent U waves.
Causes of hypokalaemia
Gastrointestinal potassium loss
Lower gastrointestinal losses are relatively high in potassium, and prolonged diarrhoea can cause signi
Upper gastrointestinal losses are relatively low in potassium. However, prolonged vomiting can also lead to hypokalaemia. This
occurs due to metabolic alkalosis secondary to gastric acid loss. Excess potassium is excreted from the kidney as part of the
renal compensatory mechanism to correct the alkalosis.
Renal potassium loss
Renal potassium wasting occurs most commonly due to the e
thiazide diuretics (e.g. indapamide). Other causes include increased mineralocorticoid activity or renal tubular acidosis (type I /
II).
Intracellular potassium accumulation
High extracellular pH (alkalosis), elevated beta-adrenergic activity or increased availability of insulin will act to drive potassium
into cells.
Management
8
cause\:
Management of hypokalaemia involves intravenous or oral potassium replacement alongside treatment of the underlying
If potassium is >3mmol/L, the patient is asymptomatic, and there are no ECG changes, oral potassium replacement can be
given.
indicated.
If potassium is \<3mmol/L (severe hypokalaemia) or ECG changes are present, intravenous potassium replacement is

Approach to U&E interpretation

Step 1\: Assess urea, creatinine & eGFR

Assessing the urea and creatinine in conjunction can allow you to determine whether there is potential kidney injury/damage. If
both are raised, this suggests renal dysfunction and the eGFR will be low.
Remember, an isolated raised urea can indicate dehydration or upper gastrointestinal bleeding.

Step 2\: Compare to previous creatinine / eGFR

Without a factor leading to an inaccurate eGFR calculation (e.g. obesity), a high creatinine and low eGFR suggest renal
dysfunction.
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It is then important to assess whether this is acute (i.e. acute kidney injury) or longstanding (i.e. chronic kidney disease).
AKI vs CKD
Acute kidney injury (AKI) is a rapid worsening of renal function and a common complication among hospital inpatients. It
is most commonly diagnosed when there is a creatinine rise of 1.5x from baseline and can be staged according to the
severity of the creatinine rise.
Chronic kidney disease (CKD) can be diagnosed when two blood tests, three months apart, show a reduction in renal
function, leading to health implications. Again, the severity of creatinine rise (and thus eGFR fall) is used to stage the
disease.

Step 3\: Assess electrolytes

Both AKI and CKD can be associated with electrolyte disturbances, which can be life-threatening (e.g. severe hyperkalaemia).
Once you have established a diagnosis of AKI or CKD, assessing sodium and potassium levels and appropriately managing
abnormalities is important.
Tip\: In renal dysfunction, there can also be signi
request a bone pro.

References

1. UpToDate. A s s e s s m e n t o f k i d n e y f u n c t i o n . March 2023. Available from\: [LINK]
2. UK Kidney Association. A b o u t e G F R . June 2023. Available from\: [LINK]
3. South Tees Hospitals NHS Foundation Trust. U r e a . April 2022. Available from\: [LINK]
4. UpToDate. M a n i f e s t a t i o n s o f h y p o n a t r e m i a a n d h y p e r n a t r e m i a i n a d u l t s . January 5. UpToDate. T r e a t m e n t o f h y p e r n a t r e m i a i n a d u l t s . Sept 2021. Available from\: [LINK]
6. UpToDate. D i a g n o s t i c e v a l u a t i o n o f a d u l t s w i t h h y p o n a t r e m i a . June 2022. Available 7. UpToDate. C a u s e s o f h y p o k a l e m i a i n a d u l t s . May 2022. Available from\: [LINK]
8. UpToDate. C l i n i c a l m a n i f e s t a t i o n s a n d t r e a t m e n t o f h y p o k a l e m i a i n a d u l t s . November 2022. Available from\: [LINK]
from\: [LINK]
2021. Available from\: [LINK]
Source\: geekymedics.com
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