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Diagnostic approach to hypoalbuminemia | VETgirl Veterinary Continuing Education Podcasts

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In this VETgirl online veterinary continuing education podcast, Dr. Garret Pachtinger, board certified emergency and critical care specialist and co-founder of VETgirl, reviews the diagnostic approach to hypoalbuminemia in dogs and cats. Hypoalbuminemia is a common problem seen by the small animal veterinarian. It is important to understand that albumin is the major determinant of oncotic pressure (i.e., otherwise known as colloidal osmotic pressure or “COP”). This pressure is the main force that holds fluid within the vascular space.

Without oncotic pressure, important osmotically-active particles in the bloodstream (e.g., sodium, urea and glucose) would pass freely between the vascular and interstitial compartments. Albumin is much larger than these molecules, and cannot pass freely through the vascular endothelium; as a result, it remains within the bloodstream to provide this oncotic pressure. When hypoalbuminemia is present, there is a decreased plasma oncotic pressure and ultimately results in leakage of fluid out from the vascular compartment.

In dogs, normal albumin ranges from 2.6 to 3.5 g/dL. Cats are similar at 2.8 to 3.9 g/dL. While you can subcategorize a decrease in albumin to be mild, moderate, or severe, once you get lower than 2.0 g/dL or certainly less than 1.5 g/dL, that is when we classify this as severe hypoalbuminemia and worry about third spacing of fluids including interstitial edema and even effusions such as pleural or peritoneal effusion.

Once a patient is identified as being hypoalbuminemic on bloodwork, the clinician’s next general thought is the WHY? Why do they have such a low albumin? Provided it is not lab error, common causes for hypoalbuminemia include the following below (NOTE: This list is not an exhaustive list):

– Liver failure (as this liver is the primary organ responsible for making albumin)
– Gastrointestinal disease (e.g., protein-losing enteropathy, as seen commonly in Yorkshire terriers)
– Renal protein loss (e.g., protein-losing nephropathy)
– Hypoadrenocorticism
– External losses including hemorrhage
– Hyperglobulinemia resulting in a compensatory decrease in albumin production
– Starvation, malnutrition, or chronic illness where the body is focused on production of other factors

The list continues, but those are the more common differentials to consider.

While this list of differentials can be overwhelming, fortunately the diagnostic approach to hypoalbuminemia is straightforward.

Considering some of the causes we discussed above, external protein loss causes including third spacing (e.g., as seen in cases such as sepsis, pyometra, or severe skin burns) are often evident on history or physical examination. Other specific causes that would also fall into that category include an open pyometra, pyothorax or peritonitis.

Typical hypoadrenocorticism would have notable electrolyte changes, specifically hyponatremia and hyperkalemia. Atypical hypoadrenocorticism may require further testing such as a baseline cortisol or ACTH stimlation test.

Once these causes are ruled out (or ruled “in” if you are lucky), we essentially leave ourselves with 3 remaining causes for hypoalbuminemia.

1. Liver failure
2. Protein-losing enteropathy (PLE)
3. Protein-losing nephropathy (PLN)

Aside from a CBC and biochemistry panel, what other diagnostics should be considered?

The first test I would consider would be a complete urinalysis including a urine sediment evaluation. Normal patients have little to no protein in their urine. If there is little to no protein in the urine, a PLN can be ruled out. With that said, proteinuria should be considered in light of the urine specific gravity. For example, trace to 1+ of protein may be normal in well-concentrated urine (e.g., greater than 1.035 USG). Conversely, this level of proteinuria in dilute urine may be significant. If there is an active urine sediment, this may indicate lower urinary tract disease, and proteinuria should be re-evaluated after appropriate therapy. If there is a concerning amount of protein within the urine, the next step is to consider a urine protein: creatinine ratio (UPC). This is a good predictor of 24-hour urine protein excretion and is much easier to obtain to confirm the diagnosis of PLN.

Another differential for hypoalbuminemia is liver failure, which may be apparent on blood work. Common changes on bloodwork seen with severe liver disease include:

– Hypoalbuminemia
– Hyperglobulinemia
– Low blood urine nitrogen
– Hypoglycemia
– Hyperbilirubinemia
– Elevated liver values such as the ALT and ALKP

If you are concerned there is liver disease, abdominal imaging such as ultrasonography would be a next step to consider. Abdominal radiographs would also help to assess liver size and structure, but they would be less helpful as compared to ultrasound. Additional liver tests to consider would be liver function testing such as a resting ammonia or serum bile acids test.

Last but not least, let’s then talk about gastrointestinal disease such as protein-losing enteropathy (PLE). If the patient has gastrointestinal illness signs with normal renal and liver function, this would suggest PLE, particularly if hypoglobulinemia is also present. With that said, I personally have diagnosed patients with PLE that had little to no gastrointestinal history of vomiting or diarrhea. How do we diagnose PLE? Aside from finding hypoalbuminemia as well as ruling out the previous causes, this is confirmed by intestinal biopsies. Since biopsies are often both costly and invasive, this is why we try to rule out other causes such as PLN and liver failure first. Other testing to consider includes fecal parasitology, serum TLI, folate and B12 levels.

Ultimately, while hypoalbuminemia can be a challenging process to diagnose, I hope this was a systematic and clear approach to not only understnading what can cause hypoalbuminemia, but a clear approach on how to work through these cases.

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