Lab Results

A guide to the blood chemistry panel for cats with CKD, covering BUN, creatinine, SDMA, electrolytes, and other values.

Quick Answer: The blood chemistry panel is the backbone of diagnosing and monitoring feline CKD. The core kidney values are BUN (or urea), creatinine, and SDMA, and the panel also checks electrolytes like potassium and sodium, proteins like albumin, and other readings such as cholesterol and glucose that can be affected by kidney disease or point to something else going on entirely.

Measures of Kidney Function

BUN (Blood Urea Nitrogen) or Urea

BUN, called urea in most countries outside the USA, is produced by the liver as a byproduct of protein digestion and is normally filtered out by the kidneys. When the kidneys are not working well, BUN builds up in the blood.

BUN is easy to measure and widely available, but it is not a perfect indicator on its own. It rises with high protein diets, dehydration, gastrointestinal bleeding, and stress, so a high BUN with a normal or only mildly elevated creatinine often points to one of these other causes rather than to worsening kidney disease. A sudden sharp rise in BUN alongside creatinine can signal an acute injury layered on top of existing CKD, sometimes caused by an infection, dehydration, or a blockage from kidney stones, and is worth flagging to your vet promptly.

Creatinine

Creatinine is a waste product from muscle breakdown, and it is generally considered a more reliable measure of kidney function than BUN because diet and hydration affect it less. Creatinine is used to confirm and stage CKD (see our post on IRIS staging for more detail), but it comes with an important caveat: since it is produced by muscle, a large muscular cat may show a mildly elevated creatinine without having CKD, while a cat who has lost a lot of muscle mass may show a falsely low creatinine even with meaningful kidney damage. This matters most in cats who have lost significant weight, where declining creatinine should not automatically be read as improving kidney function.

Creatinine is also not a straight-line measurement. A rise from a low starting point represents a much bigger loss of function than the same numerical rise from an already elevated starting point, so try not to panic over small increases at higher creatinine levels while still taking early, small increases seriously.

SDMA

SDMA (symmetric dimethylarginine) is a newer blood marker, first offered commercially in 2015, that can flag reduced kidney function well before creatinine rises. Research suggests SDMA levels increase around 17 months on average before creatinine starts to climb, meaning it can potentially detect CKD when only about 40 percent of kidney function has been lost, compared to the 60 to 70 percent typically required before creatinine becomes elevated.

Unlike creatinine, SDMA is not significantly affected by muscle mass, which makes it a useful cross check in cats who are very muscular or who have lost a lot of weight. It should not be interpreted in isolation, though. It is best read alongside creatinine and urinalysis, particularly when either value sits near the upper end of normal.

Azotemia: Where the Problem Sits

When BUN and creatinine are both elevated, this is called azotemia, and it is worth understanding that azotemia has three possible sources, because they call for very different responses.

Pre-renal azotemia happens before blood even reaches the kidneys, caused by things like dehydration, low blood pressure, heart problems, or a high protein diet reducing blood flow through the kidneys. If the underlying cause is treated promptly, there may be no lasting kidney damage at all.

Renal (intrinsic) azotemia originates in the kidney itself, and this is what CKD and acute kidney injury represent.

Post-renal azotemia happens after the kidneys, usually due to a blockage somewhere further down the urinary tract, such as kidney stones preventing urine from leaving the body.

Urine specific gravity is the main tool used to help distinguish between these, since pre-renal azotemia with otherwise healthy kidneys typically comes with well-concentrated urine, while renal azotemia usually does not.

Early Detection Markers

Beyond SDMA, a few other markers are being explored specifically for catching CKD earlier, though most are not yet in routine use.

FGF-23 is a hormone involved in regulating phosphorus, and research suggests it can rise even before phosphorus and PTH levels move out of range. It is not currently used as a primary diagnostic tool, but rather as a way to flag the need for earlier dietary phosphorus management, even in cats whose phosphorus still looks normal on paper. We cover this in more depth in our post on phosphorus and calcium.

RenalTech is an AI-based predictive tool that uses a cat’s existing routine bloodwork and urine values, along with age, to estimate the likelihood of developing CKD within the next two years. It requires no new sample types, just the tests most CKD-prone cats are already having run, and is available through certain reference laboratories in the USA.

The fAIM saliva test is a newer development announced in 2025, using a cheek swab to detect a protein linked to kidney repair and damage. It is a promising area to watch, though as with any new diagnostic, it is worth waiting to see how it performs across a wider population of cats before treating it as a replacement for established testing.

Glomerular filtration rate (GFR) is considered the most direct and sensitive measure of kidney function, but it requires specialized equipment and multiple precisely timed blood draws, so it is rarely available outside of veterinary schools and is unlikely to be part of your cat’s routine care.

Electrolytes

Potassium

Potassium is essential for muscle function, including the heart. CKD cats more commonly run low on potassium than high, and low potassium can cause weakness or, in severe cases, more serious muscle and heart problems. Some CKD cats, particularly those with more advanced disease, run the opposite way and develop elevated potassium instead. Since potassium imbalance is so common in CKD, it is often checked alongside every kidney recheck.

Sodium

Sodium levels can rise in CKD cats because damaged kidneys are slower to adjust to changes in sodium intake, and vomiting or diarrhea can also play a role. There is some ongoing debate about whether elevated sodium might worsen high blood pressure in CKD cats, so it is one more reason blood pressure and sodium are worth tracking together.

Magnesium

Magnesium is not part of every routine panel, but it is worth requesting periodically, since both high and low magnesium can occur in CKD cats and each carries its own risks. Low magnesium in particular has been associated with worse outcomes in some studies and often occurs alongside low potassium, so if potassium stays low despite supplementation, magnesium is worth checking. High magnesium is more common in advanced CKD and matters practically too, since phosphorus binders and fluids containing magnesium should generally be avoided in cats who already run high.

Proteins in the Blood

Albumin

Albumin is the main protein in blood and can run either high or low. High albumin often simply reflects dehydration. Low albumin is more concerning and can point to poor nutrition, gastrointestinal bleeding, chronic inflammation, or liver disease, and a persistently falling albumin alongside falling body weight is generally a sign that a cat’s nutrition needs closer attention.

Globulin and the Albumin to Globulin Ratio

Globulins contain antibodies, so elevated levels often reflect infection or inflammation somewhere in the body. The ratio between albumin and globulin is normally close to even, and a low ratio combined with very high globulins can be a flag for feline infectious peritonitis, though this needs to be interpreted alongside other findings rather than on its own.

Other Readings Worth Knowing

A handful of other values on a standard panel are commonly seen out of range in CKD cats, usually without being a primary concern in themselves.

Cholesterol often runs a bit high in CKD cats and does not carry the same cardiovascular significance it does in humans.

Glucose can spike from stress alone at the vet, sometimes quite dramatically, so a single elevated reading should prompt a urine glucose check rather than an immediate diabetes diagnosis.

ALT is a liver-associated enzyme that can also rise mildly with hyperthyroidism or with certain medications, and mild, stable elevations are often not a cause for concern.

Amylase is excreted by the kidneys, so it is fairly common for CKD cats to run somewhat elevated here without pancreatitis being the cause. It is worth investigating further mainly when the level is very high and other pancreatitis symptoms are also present.

Creatine kinase (CK) is a muscle enzyme that can rise simply from the stress of a difficult blood draw or from prolonged inactivity, and mild elevations are common and usually not significant in an otherwise stable cat.

Frequently Asked Questions

My cat’s BUN is high but creatinine looks normal. Does that mean no kidney disease? Not necessarily, but it is a useful clue. A high BUN with a largely normal creatinine often points toward dehydration, a high protein diet, or gastrointestinal bleeding rather than CKD itself, and is worth discussing with your vet rather than assuming the worst.

Is SDMA a replacement for creatinine? No, they work best together. SDMA can flag a problem earlier and is not thrown off by muscle mass the way creatinine is, but creatinine remains central to staging and monitoring once CKD is confirmed.

Should I ask for FGF-23 or RenalTech even if my vet hasn’t mentioned them? It is a reasonable question to raise, particularly if your cat is in early stage CKD or if you want the earliest possible warning of phosphorus problems. Availability and cost vary, so this is worth a direct conversation with your vet about whether it fits your cat’s situation.

Why did my cat’s creatinine go down after losing weight? Isn’t that good news? Not always. Because creatinine comes from muscle, significant muscle loss can lower creatinine even if kidney function has not actually improved. A falling creatinine alongside falling body weight is worth flagging to your vet rather than treated as a straightforward improvement.

Sources

  • Comparison of serum concentrations of symmetric dimethylarginine and creatinine as kidney function biomarkers in cats with chronic kidney disease (2014) Hall JA, Yerramilli M, Obare E, Yerramilli M & Jewell DE Journal of Veterinary Internal Medicine 28 pp1676-1683
  • Early diagnosis of chronic kidney disease in dogs and cats: use of serum creatinine and symmetric dimethylarginine (2016) Grauer GF Today’s Veterinary Practice Mar/Apr 2016
  • Effects of dietary protein content on renal parameters in normal cats (2011) Backlund B, Zoran DL, Nabity MB, Norby B & Bauer JE Journal of Feline Medicine and Surgery 13(10) pp698-704
  • Relationship between plasma fibroblast growth factor-23 concentration and survival times in cats with chronic kidney disease (2015) Geddes RF, Elliot J & Syme HM Journal of Veterinary Internal Medicine 29(6) pp1494-1501
  • Predicting early risk of chronic kidney disease in cats using routine clinical laboratory tests and machine learning (2019) Bradley R, Tagkopoulos I, Kim M, Kokkinos Y, Panagiotakos T, Kennedy J, De Meyer G, Watson P & Elliott J Journal of Veterinary Internal Medicine 33(6) pp2644-2656
  • Apoptosis inhibitor of macrophages in cats: A potential link between an Exon 3 variant allele and progression of naturally occurring chronic kidney disease (2025) Evangelista GCL, Hwang JK, Broughton-Neiswanger LE, Carlo Reis EC, Court MH, Mealey KA & Villarino NF Journal of Veterinary Internal Medicine 39(4)
  • Prognostic importance of plasma total magnesium in a cohort of cats with azotemic chronic kidney disease (2018) Van den Broek DHN, Chang YM, Elliott J & Jepson RE Journal of Veterinary Internal Medicine 32(4) pp1359-1371
  • Symmetric dimethylarginine in cats with hypertrophic cardiomyopathy and diabetes (2018) Langhorn R, Kieler IN, Koch J, Christiansen LB & Jessen LR Journal of Veterinary Internal Medicine 32(1) pp57-63