On-the-spot blood kidney panel: creatinine, urea, and uric acid.

Why does kidney panel testing matter in a point-of-care setting?

Chronic kidney disease affects over 10% of the global population and is one of the most consistently underdiagnosed conditions in primary care. The majority of people with early-stage CKD have no symptoms and are unaware of their condition. For point-of-care businesses, that represents a significant and actionable opportunity.

Many adults with metabolic risk factors such as hypertension, type 2 diabetes, or obesity have never had their kidney function checked despite being at substantially elevated risk. Because kidney dysfunction frequently co-occurs with cardiovascular and metabolic conditions, adding a kidney panel alongside a lipid panel or HbA1c creates a more complete preventive health picture in a single appointment, without additional complexity for the customer or the point-of-care team. Periodic kidney function monitoring is also particularly relevant for customers on long-term medications with known nephrotoxic potential, making the pharmacy an ideal setting for routine follow-up.

Why pharmacies and other point-of-care businesses should offer kidney panel testing:

• Identify customers with early or undiagnosed kidney dysfunction, including those with known metabolic risk factors such as hypertension, type 2 diabetes, and obesity.
• Monitor customers on medications with known or potential nephrotoxic effects with a convenient on-site check.
• Provide a rapid renal screening option as part of a broader health check, for example, alongside cardiometabolic markers.
• Support timely referral to clinical care when results indicate impaired kidney function.

What does each marker in a kidney panel mean? 

Creatinine 

Creatinine is a waste product generated continuously by muscle metabolism, specifically from the breakdown of creatine and phosphocreatine. Because it is produced at a relatively constant rate and is eliminated almost entirely by glomerular filtration in the kidneys, creatinine is the most widely used and clinically established marker of kidney function.

When the kidneys are functioning normally, creatinine is filtered efficiently, and blood levels remain stable. When glomerular filtration is impaired, due to acute kidney injury, chronic kidney disease, or obstruction, creatinine accumulates in the blood, resulting in elevated blood or serum creatinine levels. Blood or serum creatinine is also the basis for calculating estimated glomerular filtration rate (eGFR), the standard metric used for CKD staging and monitoring.

An important limitation of creatinine as a marker is its dependence on factors beyond kidney function. Individuals with high muscle mass may have elevated creatinine without any kidney impairment, while those with reduced muscle mass, for example, older adults, individuals with limb loss, or those with muscle-wasting conditions, may have normal creatinine despite significantly reduced kidney function. A diet high in cooked meat, dehydration, strenuous physical exercise, and certain medications can also raise blood and serum creatinine independently of renal function. This means creatinine should always be interpreted in context and alongside other markers.

Creatinine values are normally higher in males than in females, reflecting differences in average muscle mass.

Urea

Urea is the end product of protein metabolism. Amino acids from dietary protein and tissue turnover are broken down to ammonia, which the liver then converts to urea via the urea cycle. Urea is then excreted by the kidneys. When kidney function declines, urea clearance is reduced, and blood urea levels rise.

Urea is a useful complementary marker to creatinine because it is influenced by different factors. While creatinine primarily reflects muscle metabolism, urea reflects protein intake and liver function as well as kidney excretion. A high-protein diet, dehydration, certain bleedings, or increased tissue breakdown can all raise urea independently of kidney function. This means that an elevated urea in isolation requires careful contextual interpretation and should always be considered alongside creatinine and uric acid.

It is also worth noting that urea level can be low in certain liver diseases, since a damaged liver produces less urea from ammonia. A low urea result in the context of known or suspected liver disease therefore requires clinical attention.

Uric acid

Uric acid is the final breakdown product of purine metabolism. Purines are found in many foods and are also released during normal cell turnover. In humans, uric acid is excreted primarily by the kidneys. When kidney function declines, uric acid excretion is impaired, and blood uric acid levels rise, making elevated uric acid a recognized consequence of reduced renal function.

Uric acid is the least kidney-specific of the three markers in this panel. Elevated uric acid is most prominently associated with gout. Gout is a painful form of inflammatory arthritis caused by uric acid crystal deposition in joints. It is also associated with hypertension, cardiovascular disease, metabolic syndrome, and kidney stones. The relationship between hyperuricemia and CKD progression is an active area of research; epidemiological evidence shows a consistent association between elevated uric acid and CKD incidence and progression, though whether this relationship is causal or primarily reflects impaired renal clearance remains a subject of ongoing debate.

Beyond kidney function, uric acid levels are influenced by a range of non-renal factors. A diet rich in purines, including red meat, organ meats, shellfish, and alcohol, can raise uric acid independently of kidney function. Dehydration reduces renal uric acid excretion and can transiently elevate blood uric acid levels. Certain medications are also well-established contributors that reduce renal uric acid excretion and can raise blood uric acid levels. This means an elevated uric acid result should always be interpreted in the context of other markers, diet, hydration, diseases, and medication use.

For a pharmacy customer, an elevated uric acid result is clinically meaningful. It suggest the need for further evaluation regardless of whether kidney disease or gout is the primary concern.

How is the kidney panel measured?

• Sample: Small capillary whole blood sample (finger prick)

• Markers measured: creatinine, urea, uric acid

• Units: urea in mmol/L, creatinine and uric acid in µmol/L.

• Result time: Minutes

Interpretation: Kidney panel results are most informative when all three markers are considered together rather than in isolation. Always follow the instructions for use (IFU) provided with your testing device and kit to ensure accurate results in your point-of-care setting. Results should be interpreted using local reference ranges and in the personal context of each individual customer.

Kidney panel testing with Igloo Reader Pro

Creatinine, urea, and uric acid are all measurable from a single fingerprick whole blood sample using Igloo Reader Pro. No laboratory referral or venous blood draw is required. Results are available within minutes, making it a practical addition to any pharmacy or other point-of-care setting.

Benefits of kidney panel testing with Igloo Reader Pro in pharmacies:

• Deliver objective, quantitative kidney function results on-site, with no laboratory referral needed.
• Reach customers with metabolic risk factors who may never have had their kidney function assessed.
• Monitor customers on long-term medications with known nephrotoxic potential as part of a routine medication review.
• Build out a broader preventive health offering and act as a first point of contact for timely clinical referral.

Best practices for kidney panel testing

• Hydration: Dehydration concentrates creatinine, urea, and uric acid in the blood and can produce falsely elevated results independent of kidney function. Customers should be normally hydrated before testing by drinking adequate water beforehand and avoiding diuretics such as excessive tea or coffee on the day of the test for a representative result.

• Diet: A high-protein meal in the hours before testing can transiently raise urea and creatinine. A diet high in purine-rich foods, including red meat, organ meats, shellfish, and alcohol, can raise blood uric acid level. Customers should eat normally and avoid unusually high protein or purine intake immediately before testing.

• Exercise: Strenuous physical activity raises creatinine through increased muscle breakdown and creatine phosphate turnover. Customers should avoid intense exercise for at least 24-48 hours before testing for a representative result.

• Medications and supplements: Several commonly used medications affect kidney markers. Creatine supplementation can also raise creatinine independently of kidney function. Always note a customer's medication and supplement history when interpreting results.

• Repeat testing: A single kidney panel result is informative, but trends over time are more meaningful. Customers with borderline values benefit from follow-up monitoring under consistent pre-test conditions.

Learn more about the kidney panel >

Why should pharmacies offer kidney panel testing?

Chronic kidney disease affects approximately 1 in 7 adults globally, yet the majority of those in early stages have no symptoms and remain undiagnosed. For pharmacies, creatinine, urea, and uric acid are fast, quantitative markers that can change that.

Many adults with hypertension, type 2 diabetes, or obesity  have never had their kidney function assessed despite being at substantially elevated risk. Customers on long-term medications with known nephrotoxic potential benefit from periodic renal monitoring as part of a routine medication review. And because kidney dysfunction frequently co-occurs with cardiovascular and metabolic conditions, adding a kidney panel alongside a lipid panel or HbA1c creates a more complete preventive health picture in a single appointment.

Literature

• Kovesdy CP. Epidemiology of chronic kidney disease: an update 2022. Kidney Int Suppl (2011). 2022 Apr;12(1):7-11. https://pmc.ncbi.nlm.nih.gov/articles/PMC9073222/
• Gounden V, Bhatt H, Jialal I. Renal Function Tests. In: StatPearls. Last Update: July 27, 2024. https://www.ncbi.nlm.nih.gov/books/NBK507821/
• Hosten AO. BUN and Creatinine. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 193. https://www.ncbi.nlm.nih.gov/books/NBK305/
• Higgins С, Urea and the clinical value of measuring blood urea concentration, 2016, https://acutecaretesting.org/en/articles/urea-and-the-clinical-value-of-measuring-blood-urea-concentration
• Buddhi Prakash Jain, Shyamal K. Goswami, Shweta Pandey, Chapter 9 - Clinical Biochemistry, Protocols in Biochemistry and Clinical Biochemistry,
• Academic Press, 2021, Pages 101-118, https://doi.org/10.1016/B978-0-12-822007-8.00001-5 and https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/uric-acid-blood-level
• Arthritis Foundation. High & Low Uric Acid Symptoms: How to Stay in a Safe Range. https://www.arthritis.org/diseases/more-about/high-low-uric-acid-symptoms-how-stay-in-safe-range
• Acute Renal Injury During High Intensity Training (HIFRT-KH), ClinicalTrials.gov ID NCT03678285, Sponsor University of Wyoming, Last Update Posted 2021-07-16, https://clinicaltrials.gov/study/NCT03678285

Disclaimer

This information is educational and does not constitute medical advice. Always use local reference ranges and consult a healthcare professional for diagnosis and treatment.