Cardiac Lab Interpretation and Troponin

Cardiac Lab Interpretation and Troponin

If you work in the hospital – it is essential that you know and understand cardiac labs like troponin.

Cardiac labs are life and death, and knowing these labs inside and out will help you in the clinical setting.

Cardiac labs are used to identify cardiac conditions and will often guide diagnostic and treatment courses for your patients – so buckle up because you’re about to become an expert!

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Troponin is the most important cardiac lab that you will see, and it is also the most common.

But what exactly is Troponin?

Troponin is a family of enzymes or proteins found within muscle cells. Two members of this family, Troponin-I and Troponin-T, are found pretty much exclusive to cardiac tissue.

When heart damage occurs, the cells of the heart lyse or split apart, releasing this troponin. 

Since the heart is really the only tissue to have this type of troponin, the presence of troponin the bloodstream signifies myocardial necrosis or cell death.

The higher the level of troponin – the more cell death has occurred. As you can see – this can come in handy when diagnosing heart attacks.

Troponin is the preferred blood test in evaluating patients for a myocardial infarction (heart attack).

Normal Troponin Levels

Normal levels of Troponin (whether T or I) are zero, as or close to zero as you can get.

Labs may utilize different assays which may have different specific cutoffs, but generally, you will find that levels should be:

Troponin-I = < 0.04 ng/mL

Troponin-T = ≤ 0.01 ng/mL

Pattern of Troponin

Both types of Troponin will typically show up within 2-3 hours after cell death has begun – but they may not be detectable until 6-12 hours later.

It will peak in 24 hours but can take up to 1-2 weeks for the troponin to return back to non-detectable levels.

Significance of Troponin

As stated above – Troponin signifies myocardial cellular death.

The prime example of this is during a Myocardial infarction (whether STEMI or NSTEMI… see below).

However, there are other causes that can cause mild elevations in troponin, such as:

  • Demand-ischemia: Sepsis, hypovolemia, shock, arrhythmias, CHF exacerbation.
  • Other cardiac damage: Various forms of carditis, aortic dissection, post-cardiac surgery, post-cardiac cath, CPR, defibrillation, chest trauma.
  • Kidneys: Renal damage, Acute Kidney Injury, Chronic Kidney Disease (especially if on dialysis).
  • Vascular: Pulmonary embolism and Stroke.

This isn’t a complete list, but most of these may cause minor elevations in the Troponin.

When cardiac damage is sustained, the troponin level should rise significantly.  


It doesn’t matter what the Troponin level is during a STEMI – if it’s new-onset – expect the troponin to be negative. Remember – it can take time for the troponin to become positive.

If the EKG reads STEMI – you need to hook your patient up to the defibrillator, establish 2 large-bore IVs, give aspirin, possibly another antiplatelet medication like Brlinta, pain relief, nitro, and get that pt to the Cath lab ASAP.


This is really where troponin shine. NSTEMIs are a type of myocardial infarction that don’t have ST elevation on the EKG (Non-ST-Elevation-MI).

Serial checks of the troponin can determine whether or not the pt is actually having a heart attack.

It will vary based on the facility, but most facilities will check the troponin Q6-8hrs at least 2-3 times. 2-3 negative troponins in a row basically rule out any type of acute coronary syndrome (heart attack).

This doesn’t mean that the patient does not have a high-grade blockage of their coronary arteries.  Stress tests and cardiac caths are needed to definitively detect significant cardiac blockages.

Is there a specific level that a troponin has to rise to be considered an NSTEMI?

Not really, it just needs to be above the 99th percentile – which is any positive number. However, just because there is an elevation in troponin doesn’t mean it is an NSTEMI (See above for other causes of troponin elevation).

These patients should be having some symptoms of an MI (chest pain, SOB, nausea), and/or EKG changes (ST-depressions or T-wave inversions).

Something important to remember is that NOT ALL PATIENTS EXPERIENCE CLASSIC SYMPTOMS of an MI.

Diabetics are well-known to be at higher risk for “silent” MIs, and women can have atypical symptoms as well.

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So you’re on your unit and your patient’s troponin level comes back elevated.

What do you do?

It will depend on the patient’s symptoms and what unit you are on, but in general, you should:

  1. Remain calm.
  2. Communicate it to the Provider (Physician or APP).
  3. Make sure the patient is connected to the heart monitor and is getting frequent vital signs. Apply oxygen if SPO2 < 94%.
  4. Obtain an EKG if they have not had one recently – worry about the order later.
  5. Monitor your patient and follow the orders given by the Provider.

Cardiac Biomarkers | Learn about troponin, CK, CK-MB, and BNP (and NT-ProBNP)


CK and CK-MB are cardiac labs that are somewhat outdated and have been replaced – for the most part – by troponin.

But there are still some important clinical situations in which using these labs may be beneficial.

CK, or Creatine Kinase, is found within most muscle cells and is released into the bloodstream when muscular cellular necrosis or damage occurs.

This includes the heart – so with the same principle as troponin – elevations in CK could indicate heart muscle damage. However – CK is NOT specific.

This is why a more specific isoenzyme – CK-MB (Creatine Kinase Muscle/Brain), is used to help differentiate musculoskeletal muscle damage from heart damage. CK-MB is found in higher concentrations within the heart.

Current Indications

CK and CK-MB have mostly been replaced by troponin, but they can be used in certain instances.

These include:

  • Suspected heart attack after heart instrumentation (CABG or PCI)
  • To detect a second MI – since troponins have such a long half-life and do not return to baseline levels until 1-2 weeks after the initial incident.


The reason CK-MB can be useful is that while the onset is similar to troponin (can take 4-12 hours to be detectable), the half-life is shorter and levels drop back down to undetectable levels in 36-48 hours.

Troponin levels can take 10-14 DAYS to return to normal. This means that if a patient has a 2nd heart attack >2 days after the first, an elevated CK-MB level can indicate a 2nd MI.

The same principle is related to myocardial instrumentation. If someone had a stent placed or especially a CABG, their Troponin will be expected to be elevated from the irritation within the heart.

If it has been >48 hrs, an elevated CK-MB could indicate further myocardial injury.

Normal Levels

CK Male Normal: 39-308 U/L
CK Female Normal: 26-192 U/L
CK-MB Normal: 5-25 IU/L

Myocardial Infarction: Levels should be >2x the patient’s baseline.

Remember that CK and even CK-MB are not as specific as troponin-I or T to the heart. In the presence of musculoskeletal injury – the usefulness of these tests diminishes greatly.

Any type of muscular damage or surgery can increase CK. Rarely, chronic muscle disease, hypothyroidism, and alcoholism can increase CK-MB.

Also check out:


BNP stands for Brain Natriuretic Peptide – however, it is primarily released by the ventricles of the heart.

This hormone impacts how the kidneys manage fluid and sodium. When the ventricles experience high-pressures, the cells release this enzyme.

BNP has a diuretic (fluid out) , natriuretic (salt out) , and hypotensive effect. BNP has actually been found to be somewhat protective in cardiac remodeling (cardiomyopathies).

What’s confusing about BNP is that some hospital labs utilize BNP, and some utilize NT-ProBNP – basically an inactive byproduct of the enzymatic reaction that occurs to produce BNP.

It is important to know which kind of BNP your hospital utilizes in order to be able to understand and interpret the results.

While BNP levels can assist in the diagnosis of HF if it is uncertain, they are especially helpful in evaluating treatment response as the BNP half-life is only about 20 minutes.

This means that BNP levels will quickly go down if ventricular pressures improve.

BNP levels infographic | BNP heart failure exacerbation

Regular BNP

Baseline BNP levels – no matter which kind – are affected by genetic variation. However, people with Heart Failure will have baseline elevations along with increases during exacerbations.

Baseline levels tend to increase in age and are higher in women over men, and lower in obesity.

Levels <100 pg/mL have a great negative predictive value – meaning they likely are NOT in an exacerbation.

Levels >400 pg/mL have a high likelihood that they ARE in an acute HF exacerbation.

Levels between these (100-400 pg/mL) is the gray zone – meaning they may or may not be in an acute exacerbation.

It is ALWAYS important to take the clinical exam into account.

Do they have clinical signs or symptoms of HF? These symptoms include:

  • Dyspnea
  • Pulmonary crackles
  • Peripheral edema
  • JVD

Never rely only on labs – especially with BNP levels. BNP levels should be used as an adjunct to, and not a substitute for, clinical assessment.


NT-ProBNP levels rise much higher than regular BNP levels.

They also have a longer half-life (25-70min), which means they do not fluctuate as quickly. It is also impacted by renal failure more-so than regular BNP levels.

All ages: Levels <300 pg/mL –  you can be almost completely sure they are not in a heart failure exacerbation.
Age <50: Levels >450 pg/mL indicate acute exacerbation.
Age 50-75: Levels >900 pg/mL indicate acute exacerbation.
Age >75: Levels >1800 pg/mL indicate acute exacerbation.

With any BNP level, obesity can decrease the results, and age and renal failure can increase them.

Non-HF causes of elevated BNPs include renal failure, constrictive pericarditis, valvular disease, pulmonary hypertension, and sepsis.

And those are the main cardiac lab tests used to evaluate the heart. An EKG should always be performed for these patients above, and they should all be admitted with continuous cardiac monitoring as well.

Whether you’re a nurse, nurse practitioner, or physician – it’s very important to understand these labs and be able to interpret them to provide the best care for your patients.

Check out some of my other articles:

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Arterial Blood Gas (ABG) Interpretation

Arterial Blood Gas (ABG) Interpretation

Arterial Blood Gases (ABGs) are obtained within the hospital setting by nurses or respiratory therapists, after a physician or advanced practice provider orders them. As the name implies, this arterial blood sample is sent to the lab to evaluate the “gases” within the arterial blood – looking at acid-base disturbances or evaluate adequacy of oxygenation/ventilation. Brace yourselves – this is going to be a long confusing topic but once you understand the concepts, it can really help you manage your patient’s acid-base disturbance like a pro. 

Oxygen (O2) and carbon dioxide (CO2) are the main gases within the blood, and these are two of the main components evaluated in an ABG. However, an ABG sample also provides levels of blood pH, as well as bicarbonate. Of all of the measurements, the most important levels to look at are the CO2, the Bicarb, and the pH in determining acid-base balance.

The ability to interpret an ABG is essential for advanced practice providers and physicians, but it is also important for the nurse to be able to have a good understanding of how to interpret ABGs, especially those working in critical care (ER, ICU, etc). This can give you valuable insights into your patient’s medical status and overall condition.

Unfortunately, ABGs can be difficult to understand. Acid-Base balance is exactly that – a balance. A rise in one level will affect other levels – and this can make it difficult to understand the underlying picture. The purpose of this article is to help you be able to master ABG interpretation in order to help you become a better nurse, clinician, or provider.

So… When Should an ABG be Obtained?

As stated above, ABGs are very useful in evaluating acid-base disturbances within a patient. This can come in handy for patients with Diabetic Ketoacidosis (DKA), other forms of metabolic acidosis (kidney failure, sepsis, etc), and CO2 retention (COPD). Patients with active respiratory failure, usually with underlying COPD or CHF, often have an ABG to evaluate their CO2 retention, their O2 saturation, and their acid-base balance – as all of these factors will affect each other.

The Measurements


The pH is the first measurement that will give you the overall picture of the patient: are they acidotic or alkalotic? pH is simply the acidity of the blood. Normal values for arterial blood pH is 7.35-7.45, which is a narrow window where body homeostasis works best.
Low pH (<7.35): Indicates acidosis (metabolic or respiratory), and is termed acidemia.

High pH (>7.45): Indicates alkalosis (metabolic or respiratory), and is termed alkalemia.

pH may be normal or near-normal in the presence of chronic acid-base disturbances from compensation, or the patient can have multiple different acid-base disturbances playing a factor.

Arterial Partial Pressure Carbon Dioxide (PaCO2)

The PaCO2 is the partial pressure of Carbon Dioxide within the arterial blood. Normal values for PaCO2 is 35-45 mmHg.

Did your parent or guardian ever tell you that holding your breath would cause your blood to boil, and that’s why you can’t hold it for long? This tidbit has helped me always remember that hypoventilation (not breathing enough) causes acidosis (boiling blood), and hyperventilation (breathing too much) causes the opposite.

High PaCO2: levels greater than 45mmHg are considered high and termed “hypercapnia”.

A high PaCO2 indicates a primary respiratory acidosis (blood boiling! pH<7.35), but can also indicate compensation for metabolic alkalosis. You see, acid-base is regulating by two organs in your body – your kidneys (metabolic) and your lungs (respiratory). These always hang in balance, and when the scale tips one way (metabolic acidosis), the body will attempt to compensate by increasing production and retention of bicarbonate to act as a buffer to normalize pH (respiratory compensation). This means the compensation will always be in the opposite direction from the primary acid-base disturbance. If one becomes too acidic – the other becomes basic, and vice versa. This is another perfect example of the body performing homeostasis to maintain balance and health. Respiratory compensation tends to occur quickly, as the pt is able to change their ventilation pattern almost instantly.

Low PaCO2: levels less than 35mmHg is considered low and termed “hypocapnia”.

Low PaCO2 indicates a primary respiratory alkalosis, which means the pH must be alkalotic as well (>7.45). Or it could also mean respiratory compensation for metabolic acidosis. If a patient is breathing fast (tachypneic) but doesn’t have a respiratory complaint – you may want to investigate their acid-base to assess for respiratory compensation. This was something I did NOT catch as a new nurse on a telemetry floor. My patient was breathing fast all night and I didn’t know why – by morning her pH was 6.9! A better understanding of acid-base physiology would have helped me recognize the signs of respiratory compensation (Kussmaul respirations), and my patient would have been better off for it.

Arterial Bicarbonate Concentration (HCO3)

HCO3 is the serum bicarb within arterial blood. Bicarb acts as a buffer to make acidity less acidic. Think of it as the opposite of H+. The less bicarb there is, the more acidic the blood is. To get technical, Bicarb reacts with H+ to form carbonic acid, which the body breaks down into CO2 and water – which it breaths out. Normal levels vary but typically are somewhere around 22-26 mEq/L.

High HCO3: Levels greater than 26mEq/L are considered high.

High HCO3 indicates a primary metabolic alkalosis (pH >7.45) – meaning for whatever reason the body is losing its acidity (See specific causes in the next section). However, just as in the case of PaCO2, abnormal HCO3 levels could indicate compensation as well. A high HCO3 level could indicate metabolic compensation for respiratory acidosis – the body is trying to buffer more acid to normalize the pH. Compensation from the kidneys can take a few hours to kick in, but won’t typically reach their peak compensatory effect until a couple of days into the acid-base disturbance.

Low HCO3: Levels less than 22mEq/L are considered low.

Low HCO3 levels indicate primary metabolic acidosis (pH <7.35). This is an acid-base disturbance you will see often – although they are all fairly common. There is an accumulation of acid within the body, and the kidneys are unable to get rid of it quickly enough. Just as with the others, low HCO3 could indicate metabolic compensation for respiratory alkalosis.

Arterial Partial Pressure of Oxygen (PaO2)

PaO2 is the partial pressure of oxygen within arterial blood. This basically measures the actual oxygen content of the blood. Normal values for PaO2 is generally thought to be greater than 80 mmHg.

High PaO2: Usually due to over-oxygenation from supplemental O2 (Think non-rebreather or too high FIO2). This may be better than low PaO2, but don’t forget that too much oxygen can be deleterious as well. Oxygen toxicity can produce reactive oxygen species and cause cellular injury, inflammation, and cell death. It can also accentuate hypercapnia (i.e. COPD).

Low PaO2: Hypoexmia from respiratory disease or anemia

Peripheral Oxygenation (SaO2)

The SaO2 is the peripheral oxygenation, which is equivalent to the Pulse Ox reading.

Normal levels are >96%, whereas levels <92% indicate hypoxia.ABG Interpretation Infographic

The 4 Acid-Base Disturbances

The following 4 categories are the 4 acid-base disturbances that can occur in someone who is sick. The above information will tell you which acid-base disturbance you may be dealing with. The below information is for you to understand what could possibly be causing the underlying disturbance. Don’t forget someone can have multiple acid-base disturbances going on at one time, and this makes clinical interpretation difficult – everything is not black and white in medicine, but this should give you a pretty good idea of what may be causing your patient’s acid-base disturbance.

Respiratory Acidosis

Respiratory acidosis is due to alveolar hypoventilation. The lungs are NOT able to remove enough carbon dioxide quickly enough, so it builds up in the blood. It also decreases Bicarbonate levels, which decreases pH and causes acidosis.

Hypercapnia tends to occur late in the lung disease or when respiratory muscles are fatigued – this is usually seen in severe respiratory failure. The acidosis can be acute or chronic.

Acute: Could be from CNS disease (think stroke, traumatic brain injury), drug-induced respiratory depression (Opioid or Benzo overdose), Neuromuscular disease (Myasthenia Gravis, ALS, Guillan Barre), or most commonly airway obstruction (asthma/COPD).

Chronic: Chronic respiratory acidosis may occur when the PaCO2 is elevated, but the pH remains normal secondary to renal compensation and elevated serum Bicarb levels. Causes of chronic respiratory acidosis may be Obesity-Hypoventilation syndrome (Pickwickian syndrome), ALS, interstitial fibrosis, and thoracic skeletal deformities.

COPD: Patients with COPD have less responsiveness to hypoxia and hypercapnia. There is also increased dead-space ventilation and decreased diaphragmatic function due to fatigue and hyperinflation.

Respiratory Alkalosis

This acid-base disturbance is due to alveolar hyperventilation. The lungs remove too much carbon dioxide too quickly, so hypocapnia (low PaCO2) and alkalosis occur.

It is commonly found in those who are critically ill including those who are mechanically ventilated, early-intermediate pulmonary disorders (PNA, PTX, aspiration, PE, Asthma, bronchitis), pain, panic/anxiety, psychosis, fevers, high-altitude, sepsis, severe anemia, hepatic failure, CHF

Electrolyte disturbances:

Acute hypocapnia causes a reduction in serum K+ levels (intracellular shifts) and phosphorus, as well as ionized calcium (it increases binding to albumin so there is less calcium in its ionized active form). This explains the common symptoms of numbness/tingling that people having a panic attack may experience.

Metabolic Acidosis

This acid-base disturbance is due to increased plasma acidity. Metabolic Acidosis is further broken down into whether or not the Anion Gap is normal (termed hyperchloremic metabolic acidosis) or elevated (Elevated gap metabolic acidosis).

Severe HCO3 levels <12 are almost always caused by some degree of metabolic acidosis, instead of just compensation for respiratory alkalosis.

Normal Gap: characterized by hyperchloremia, Bicarb is lost via the GI tract or kidneys. This usually occurs from diarrhea, chronic renal failure, or renal tubular acidosis.

Elevated Gap: Can be from multiple underlying pathologies, but usually caused by Lactic acidosis as in the case of sepsis, ketoacidosis in the case of DKA, acute kidney injury (acute renal failure), and ingestion of certain poisons.

Metabolic Alkalosis

This acid-base disturbance is caused by increased serum bicarb and decreased acidity. The acidity or hydrogen ions (H+) is usually lost in some manner. You know when you throw up and you taste the acid in your throat? This is one way the body loses its acidity – through vomiting. This can also occur in the setting of prolonged NG tube suction. The kidneys can also lose bicarb with the use of diuretics. Sometimes too many alkalotic agents are given and the kidneys aren’t able to excrete them fast enough – this can rarely occur from massive over-consumption of milk products or antacids.

Bicarb (HCO3) levels >35 almost always is caused by some degree of metabolic alkalosis instead of compensation for respiratory acidosis.

And That’s about it for Acid-Base Disturbances. I know – it’s long and hard and I probably lost many of you along the way. Half the battle is remembering which terms have which meanings. Once you establish that – it gets easier understanding the balance that is acid-base homeostasis.

If you have any questions or notice an error (because let’s be real), drop a comment and I’ll be sure to respond/fix it! Otherwise, sign up below for free nursing organization sheets!

Urinalysis (UA) Interpretation

Urinalysis (UA) Interpretation

Urinalysis or UA is a lab test frequently ordered in all types of medical settings: hospitals (ER, ICU, Inpatient floors), urgent cares, and outpatient offices. In many cases, the correct evaluation of the urinalysis is imperative to making an accurate diagnosis. To provide additional data, many labs perform urine microscopy, giving you exact details on the contents within the urine and quantifying the results. Read all about how to interpret the Urinalysis dipstick, as well as the urine microscopy in this article!

Urinalysis UA Interpretation: featured image


Before you even run the urinalysis, you can tell quite a bit about the patient just by using your God-given senses.


The color of the urine is the easiest way to determine someone’s hydration status. Surprisingly, it can indicate other aspects of health as well.

Amber Urine

Normal urine varies from very clear yellow to a darker amber color. Generally speaking, the less hydrated you are – the more concentrated your urine is with nitrogenous waste and electrolytes – thus darker urine. The more hydrated you are, the more dilute the urine, leading to clear yellow urine.

The first void of the morning is typically darker and more concentrated – this is normal. However, darker urine throughout the day should prompt an increased need to drink water. I think ALL nurses have realized that after a busy shift, their urine is much too dark.

Red Urine

When we see red urine – we typically think of blood. Medical conditions such as kidney stones (nephrolithiasis), UTIs, glomerular damage, or even malignancy. As little as 1mL of blood can cause a color-change, and the presence of red urine does not automatically mean large amounts of blood.

Rhabdomyolysis can cause myoglobin in the urine which has a red-brown appearance as well. It will also cause the Heme to react on the dipstick, but we will dive into that deeper in a bit. There are also various other factors that can cause red urine including certain foods such as Beets, Blackberries, and rhubarb; as well as different medications such as Propofol, Chlorpromazine, or Ex-Lax.

Orange-Red Urine

You may see a neon orange-red from the antibiotic Rifampin used in the treatment of TB, or phenazopyridine (Pyridium) used to treat bladder burning and discomfort during a UTI. Patient’s with a UTI will often take OTC Azo which will often cause this color or urine.

Other crazy Urinalysis colors:

Other foods, drugs, and disease processes can turn urine every color of the rainbow. Certain UTIs can cause Green or purple urine, Fava beans can cause brown urine, amitriptyline or IV promethazine can cause blue urine. While these are very interesting, they are also super uncommon and you probably don’t need to commit them to memory.


Urine turbidity is how clear the urine is. Cloudy urine is very turbid, and clear urine is, well… clear. When we see cloudy urine, our first thought should be infection which may be accurate. However, other causes of cloudy urine are casts, protein, and/or cellular debris from damaged kidneys. We will dive deeper into that later on.


Yes, sniffing urine can tell you more than you realize! Urine has somewhat of an aromatic smell, and stronger-smelling urine tends to indicate dehydration (concentrated urine). Infections tend to have a very distinct foul-smell of bacteria which is difficult to describe but does smell like ammonia as the bacteria often splits urea to form ammonia.

Sweet-smelling urine may mean spilling of glucose into urine from hyperglycemia. Lastly, If the urine smells like feces, a fistula might have formed somewhere between the GI tract and the Urinary tract.


Nah I’m just kidding – but did you know they used to taste urine to detect glucose in the urine?…. GROSS!


Once you’ve assessed the urine with your own senses, its time to send the urine off to the lab for urinalysis

Specific Gravity

The specific gravity indicates how dilute or concentrated the urine is. The normal range for this is 1.005 (being very dilute) to 1.030 (very concentrated). This can give the interpreter a pretty good idea of hydration status when looking at the urinalysis.

Test Considerations:

  • Protein, ketones, and glucose, as well as recent IV contrast dye, can falsely elevate the specific gravity.

Clinical Significance:

  • Levels within the normal range indicate hydration status, 1.005 being very hydrated and 1.030 being very dehydrated.
  • Levels below the normal range may indicate diabetes insipidus, renal failure, pyelonephritis, glomerulonephritis, psychogenic polydipsia, or malignant hypertension
  • Levels above the normal range may indicate severe dehydration, hepatorenal syndrome, heart failure, renal artery stenosis, shock, or SIADH.


pH of urine stands for potential of hydrogen. The more hydrogen ions there are, the more acidic something is. The pH scale runs of 0-14, with lower numbers being more acidic, and higher numbers being more basic. Normal urinary pH tends to be about 6 but runs as low as 4.5 and as high as 8. Because the kidneys regulate your acid/base balance, any change within the body should show up in your urine. However, various different disease processes can interfere with your kidney’s ability to do this effectively.

Test Considerations:

  • Diet: Cranberries and high-protein diets can cause acidic urine, whereas citrus fruits and low-carb diets can cause alkaline urine
  • Medications: Sodium bicarbonate and thiazide diuretics can cause more basic urine

Clinical Significance:

  • Metabolic acidosis: Any excess hydrogen ions (acidity) should be secreted by the kidneys into the urine, causing a lower pH (<5.3).
  • Kidney Stones:
    • Alkaline urine typically is typically associated with Calcium oxalate, Calcium phosphate, Magnesium-ammonium phosphate, and staghorn calculi.
    • Acidic urine typically is associated with uric acid and cystine calculi.
  • UTIs: Urea-splitting bacteria such as Proteus and Klebsiella cause more alkaline urine (between 7.0-7.5).
  • Renal Tubular Acidosis: Differentiating renal tubular acidosis is beyond the scope of this post, but pH can be used in the diagnosis and differentiation of RTA.

Related Article: “Arterial Blood Gas (ABG) Interpretation”


The urine normally has <150mg/day of protein and should be undetectable on a dipstick, but when this level exceeds 300mg/day, high protein in urine will show up on a dipstick. The urine protein dipstick is specific for albumin (a type of protein). Any damage to the glomerular basement membrane will let albumin and other larger particles pass through the membrane and into the urine.

Protein in urine typically used to evaluate kidney damage in diabetics, people with Congestive Heart Failure (CHF), or other causes of kidney damage. When there is high protein in urine, sometimes it is transient which means temporary and often benign. Benign causes of high protein in urine include dehydration, emotional stress, fever, heat injury, inflammation, intense activity, acute illness, or an orthostatic disorder.

All other causes of proteinuria involve the kidney – specifically the glomerulus or the renal tubules. Some common causes of glomerular proteinuria include Diabetic nephropathy, lupus nephritis, preeclampsia, various infections (HIV, hepatitis B, post-streptococcal glomerulonephritis), certain cancers, and certain drugs like Heroin, NSAIDs, and Lithium. Some causes of tubular proteinuria include interstitial cystitis, Sickle-cell, and nephrotoxicity from NSAIDs or antibiotics like aminoglycosides.

Test Considerations:

  • Urinary concentration will impact the results, so correlate with the Specific Gravity. Very dilute urine can lead to underestimation of protein, and very concentrated urine can lead to overestimation.

Clinical Significance:

  • In general, the dipstick is a crude estimate, and evaluation by 24-hr urine specimen is the standard of care for ongoing proteinuria. Once renal cause is found, a Nephrology consult is warranted.
  • In the acute setting, the dipstick for protein isn’t too informative as acute illness, inflammation, stress, and dehydration are common presentations and can cause a temporary elevation in urinary protein. 

Heme (Blood)

Blood in urine is detected with the use of Heme on the dipstick. The test for heme is very sensitive and can detect down to 1-2 RBCs/HPF. Thus, a negative dipstick theoretically excludes hematuria (blood in the urine). There are many potential causes of hematuria including UTIs, STDs, contamination, trauma/irritation, glomerular damage, coagulopathies, kidney stones, and malignancy.

Test Considerations:

  • False-Negatives: Urinary ascorbic acid has been shown to cause false-negatives in some cases. Ascorbic acid is also known as Vitamin C – so the intake of dietary vitamin C or supplements can potentially cause false-negatives to occur. Some dipsticks do add a chemical to neutralize this effect. Overall, false-negatives are unlikely.
  • False-Positives: Myoglobin (as during rhabdomyolysis), semen (recent ejaculation), alkaline urine >9.0, contamination from hemorrhoids, vaginal blood, or oxidizing compounds used to clean the perineum can all cause false-positive heme to occur in the urinalysis.
  • A positive Heme requires urine microscopy for confirmation.

Clinical Significance:

  • If the patient is >50 years old and has persistent hematuria, they should be evaluated for malignancy.
  • If hematuria also presents with casts and proteinuria – glomerular damage is likely.
  • If hematuria presents with leukocyte esterase, WBCs, and nitrites – consider hemorrhagic cystitis

Leukocyte Esterase

Leukocyte esterase is a component of WBCs that is released when these white blood cells are lysed. The presence of leukocyte esterase supports the diagnosis of a Urinary Tract Infection (UTI). However, the presence can also indicate various autoimmune disorders, STDs, kidney stones, or intra-abdominal infections.

Test Considerations:

  • False-Negatives: Proteinuria, glucosuria, excessively concentrated urine, or tetracycline.
  • False-Positives: Contamination with vaginal discharge, certain medications (ampicillin), salicylate toxicity, and strenuous exercise.

Clinical Significance:

  • Presence supports the diagnosis of UTI, whereas its absence means infection is unlikely.


Nitrates are present in the urine at baseline. Some species of bacteria, specifically of the Enterobacteriaceae species (E. coli, Klebsiella, Proteus, Enterobacter, Citrobacter, and Pseudomonas), release an enzyme called nitrate reductase which converts urinary nitrate to nitrite, causing nitrites in urine.

Test Considerations:

  • Certain bacteria produce low levels of nitrate reductase such as enterococcus, and many bacteria do not produce any.
  • This reaction requires dwelling time within the bladder to occur. Urinary frequency or the presence of a Foley catheter can make this impossible. It can take up to 4 hours of dwelling before nitrites are detected.
  • A person might not intake a sufficient amount of nitrates in their diet.
  • False-Positives: Azo dye metabolites and bilirubin, as well as letting the urine sit for too long can produce false-positives. Higher specific gravity reduces the sensitivity.
  • False-Negatives: Ascorbic acid can produce false-negative.

Clinical Significance:

  • If negative, it really doesn’t mean much. If positive, then it is highly likely an infection is present.


When serum glucose spills into the urine – this is termed glucosuria. Typically, glucose in urine does not occur until the kidney glucose threshold is reached – which is around 180mg/dL. As you can tell, this can be useful for evaluating hyperglycemia in the setting of diabetes. However, periods of stress or fever have been known to cause small amounts of glucose within the urine as well, so glucose in urine does not automatically mean diabetes.

Test Considerations:

  • Ascorbic Acid (vitamin C) has been known to cause false-negatives.

Clinical Significance:

  • Glucosuria can indicate hyperglycemia in undiagnosed diabetics when blood-work is not obtained.


Ketones are released from fat cells when fat metabolism is increased. Most notably this occurs with Diabetic Ketoacidosis (DKA). However, ketones may also be present in low-carb ketogenic diets when dietary carbohydrates are kept below 50 grams per day, as well as with starvation such as during acute illness with decreased intake or nausea/vomiting. I see this all the time in the ER.


Urinary bilirubin may be present in low amounts, but increased levels are due to abnormalities of bilirubin metabolism or liver function. Other causes include hepatitis, hepatobiliary obstruction (gallstones), hemolysis, liver parenchymal disease, constipation, or intestinal bacterial overgrowth. The urinalysis must be sent immediately as bilirubin is unstable, especially when exposed to light.  Clinical Significance:

  • Urinalysis Clinical Significance: The presence of bilirubin may indicate elevated LFTs, but overall does not seem to add significant information toward diagnosis.



Crystals, as the name implies, are crystallizations within the urine. Crystals in urine can be normal as long as they are composed of substances normally found within the urine.

Clinical Significance:

  • Ethylene glycol ingestion: Typically presents with calcium oxalate crystals (“envelope-shaped”) and acute kidney injury
  • Tumor Lysis Syndrome: Presents with large amounts of uric acid crystals (“diamond” or “barrel” shaped) and acute kidney injury
  • Gout: May see uric acid crystals
  • Cystinuria: Present with cystine crystals (“hexagonal”)
  • UTIs: Magnesium ammonium phosphate and triple phosphate crystals (struvite) are “coffin-lid” shaped and seen with UTIs caused by urea-splitting organisms such as Proteus and Klebsiella.


Bacteria are NOT normally found in the urine as it should be a sterile environment. If found, it usually indicates infection or contamination.

Test Considerations:

  • Bacteria multiply rapidly if the urine specimen is left standing for too long at room temperature.

Clinical Significance:

  • If there are leukocyte esterase +/- nitrites present with <15-20 epithelial cells/HPF, then infection is highly likely. Consider starting empiric antibiotics if symptomatic and obtain a culture and sensitivity for confirmation.


RBC: Normally there are less than 2 RBCs/hpf. Microscopic hematuria is defined as the presence of at least 3 RBCs/HPF. Microscopic hematuria confirms a heme+ dipstick.

WBC: 2-5 WBCs/HPF or less is normal within the urine. If higher, this indicates possible infection, inflammation, or contamination. Most of the WBCs found in the case of infection are neutrophils.

Epithelial: Squamous epithelial cells are the skin cell of the external urethra. >15-20 epithelial cells/HPF indicates contamination.


Casts are tube-like protein structures made of various cells. Low urine pH, low urine flow rate, and high urinary salt concentration promote cast formation by favoring protein denaturation and precipitation. The presence of casts, other than hyaline casts, represents pathology within the kidney itself.

Hyaline casts: These can be present in normal healthy adults and are nonspecific. They can be found after strenuous exercise or dehydration, as well as with diuretic use.

RBC casts: Likely indicates glomerulonephritis or vasculitis.

WBC casts: Uncommon, but when present is usually seen with tubulointerstitial nephritis and acute pyelonephritis, but also seen with renal tuberculosis and vaginal infections.

“Muddy-brown” granular casts: are diagnostic of acute tubular necrosis, the leading cause of Acute Kidney Injury.

Waxy casts: Consistent with acute or chronic renal failure.

Broad casts: Consistent with advanced renal failure.

Fatty casts and lipiduria: Indicates Nephrotic syndrome

Renal tubular epithelial casts: seen in acute tubular necrosis, acute interstitial nephritis, and proliferative glomerulonephritis


Hopefully, this gives you a pretty good idea of how to interpret a urinalysis. Whether you are a nurse, an advanced practice provider, or a physician, this skill is important to have. If there are any other diagnostic interpretations you would like to see, please leave a comment below!

Related Articles:


  1. Carroll, M. F., & Temte, J. L. (2000). Proteinuria in adults: A diagnostic approach. American Family Physician, 62(6), 1333-1340. Retrieved April 1, 2018, from
  2. Fischbach, F. T., & Dunning, M. B., III. (2009). Manual of laboratory and diagnostic tests (8th ed.). Wolters Kluwer Health.
  3. Lerma, E. V. (2015). Urinalysis. Medscape. Retrieved April 1, 2018, from
  4. Meyreir, A. (2020). Sampling and evaluation of voided urine in the diagnosis of urinary tract infection in adults. In T.W. Post (Ed.), UpToDate. From
  5. Tintinalli, J. E., Stapczynski, J. S., Ma, O. J., Cline, D., Meckler, G. D., & Yealy, D. M. (2016). Tintinallis emergency medicine: A comprehensive study guide (8th ed.). New York: McGraw-Hill Education.
  6. Walk, R. W. (2018). Urinalysis in the diagnosis of kidney disease. In T.W. Post (Ed.), UpToDate. Retrieved April 1, 2018, from

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