Understanding Proteinuria in Dogs and Cats

Proteinuria, the presence of protein in the urine, is a finding of growing importance in small‐animal practice. For both dogs and cats, persistent proteinuria can be a red flag for underlying renal disease or systemic disorders and may adversely impact prognosis. In this blog post we’ll explore what proteinuria is, how to interpret and test for it, what causes it, and what treatment strategies exist.

Definition & physiology

In healthy dogs and cats, the glomerular filtration barrier (glomerular endothelium + basement membrane + podocytes) prevents the bulk of plasma proteins (especially large and negatively-charged ones) from entering the filtrate; any that do pass are reabsorbed by the renal tubules. Proteinuria occurs when there is increased leakage of protein into the urine (via glomerular damage or overload) or failure of tubular reabsorption, or when proteins are introduced post-glomerularly (e.g., from the urinary tract).

Why it matters

• Persistent renal proteinuria is associated with progression of chronic kidney disease (CKD) in both dogs and cats.
• In dogs, overt proteinuria (UPC > ~0.5) is associated with increased risk of uremic crisis and death.
• In cats with CKD, a UPC > 0.4 is linked with a ~4-fold increased risk of death or euthanasia compared with UPC < 0.2.
• For the pet owner, protein in the urine may indicate something more than “just a urinary tract infection” — monitoring and early intervention can improve outcomes.

Basic classification

From consensus and guideline sources:

• Non-proteinuric: UPC < 0.2 (dogs and cats)
• Borderline proteinuric: Dogs ~0.2-0.5; Cats ~0.2-0.4
• Proteinuric: Dogs > 0.5; Cats > 0.4

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Causes of Proteinuria (Dogs & Cats)

Broad categories

1. Prerenal proteinuria – excess circulating low-molecular-weight proteins (e.g., hemoglobinuria, myoglobinuria, immunoglobulin light chains) that overwhelm the tubular reabsorptive capacity.
2. Renal proteinuria – due to glomerular (most severe) or tubular/interstitial disease:
   • Glomerular: Loss of selective filtration barrier → large proteins in urine. Common in dogs; less common in cats.
   • Tubular: Failure to reabsorb smaller proteins due to tubular damage.
3. Postrenal proteinuria – proteins entering urine from the urinary tract distal to kidneys: e.g., urinary tract infection (UTI), urolithiasis, neoplasia, haemorrhage.

Specific disease/condition examples

• Urinary tract inflammation or bleeding – quite common in both species; must rule out before assuming renal origin.
• Systemic hypertension – contributes to glomerular damage by increasing glomerular capillary pressure.
• Tick-borne/infectious diseases (dogs) – e.g., Lyme, Anaplasma, Ehrlichia, Leishmania can trigger immune complex glomerulonephritis.
• Endocrine diseases (dogs/cats) – e.g., hyperadrenocorticism (Cushing’s) can be associated with proteinuria.
• Breed‐associated/hereditary glomerular diseases – some dog breeds (e.g., Samoyed with hereditary nephropathy) have early glomerular proteinuria.
• Primary renal disease/CKD – cats and dogs with intrinsic renal disease often manifest persistent proteinuria.

If your pet has proteinuria, the origin might not always be kidney disease. It could be a urinary infection, stones, or inflammation. But because persistent proteinuria especially in the absence of obvious urinary tract disease may indicate kidney damage, further investigation is important.

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Testing & Diagnostics

Stepwise approach

1. Screening urinalysis – Perform dipstick for protein, urine specific gravity (USG), sediment exam (look for red blood cells, white blood cells, bacteria, casts). If there is significant haematuria, pyuria, or bacteriuria, a postrenal cause is likely.
2. Confirm elimination of prerenal & postrenal causes – For example: rule out UTIs (culture if indicated), bleeding, inflammation, strenuous exercise, sample collection issues.
3. Quantify proteinuria with urine protein:creatinine ratio (UPC or UPCR) – This is the gold standard. Because urine concentration (USG) varies, UPC gives a normalized measure of protein loss over time.
   • In dogs: UPC < 0.2 = non-proteinuric; 0.2-0.5 borderline; > 0.5 significant.
   • In cats: UPC < 0.2 non-proteinuric; 0.2-0.4 borderline; > 0.4 significant.
4. Assess for underlying disease – Minimum database: CBC, chemistry panel (including SDMA if available), urine culture, blood pressure measurement, imaging (renal ultrasound) as indicated. Infectious disease panel, endocrine tests (e.g., thyroxine in cats, adrenal tests in dogs) depending on signalment and risk.
5. Monitor – After therapy initiation, recheck UPC (typically 2-4 weeks after starting therapy, then every 3-6 months once stable) and monitor for progression or response.

Key practical points & tech-tips

• Collect urine when the pet hasn’t just been exercising hard or stressed, as these can cause transient proteinuria.
• Ensure the sediment is inactive (i.e., no significant cellular or bacterial contamination) before interpreting UPC. If active sediment, treat underlying process and re-evaluate.
• Use cystocentesis where feasible to avoid contamination; ensure proper storage and timely submission.
• Educate clients: repeated UPCs (often 2-3 separated by ≥2 weeks) help define persistence rather than a single “snapshot.”

Explaining to pet owners

When we say your pet’s urine has ‘too much protein,’ we’re looking for protein that shouldn’t normally leak out of the kidneys. We’ll first check that it’s not coming from a urinary bladder infection or inflammation. If it’s persistent and coming from the kidneys, it may tell us about early kidney damage or a systemic disease, and we’ll treat accordingly.

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Treatment & Management

Once persistent renal proteinuria is confirmed (i.e., prerenal/postrenal causes excluded, UPC elevated on multiple occasions), then the treatment goal is to slow renal disease progression and reduce proteinuria.

Key components of treatment

1. Dietary management:
   • Prescription renal diets (moderately protein-restricted, often with added omega-3 fatty acids) can reduce proteinuria and have been shown to improve outcomes.
   • For cats or dogs in earlier stages, dietary modification remains important in conjunction with medical therapy.
2. Blood pressure control:
   • Hypertension exacerbates glomerular damage; therefore control of systemic blood pressure is essential.
3. Renin–angiotensin-aldosterone system (RAAS) inhibition:
   • Angiotensin-converting enzyme (ACE) inhibitors (e.g., enalapril, benazepril) reduce glomerular capillary pressure (via efferent arteriole dilation) and decrease proteinuria. Evidence shows improved survival in dogs.
   • Angiotensin receptor blockers (ARBs) like telmisartan have been shown in cats (and dogs) to be effective for renal proteinuria.
   • Monitoring of GFR/creatinine and potassium is required when initiating these therapies (since they may reduce GFR or cause hyperkalemia).
4. Therapy of underlying disease:
   • If infectious disease (e.g., tick-borne disease) or endocrine disease (e.g., Cushing’s) is identified, appropriate treatment is essential.
   • In dogs with confirmed immune‐complex glomerulonephritis (via biopsy), immunosuppressive therapy may be indicated.
5. Antithrombotic therapy:
   • Dogs with significant glomerular disease and hypoalbuminaemia may be hypercoagulable; thromboprophylaxis (e.g., low-dose aspirin or clopidogrel) may be considered.
6. Monitoring & reassessment:
   • After initiating therapy: recheck UPC in 2-4 weeks.
   • Goal: reach UPC < 0.5 in dogs and < 0.4 in cats (or reduce by > 50% compared with baseline) ŏin many cases.
   • In stable patients: recheck every 3-6 months; more frequently if adjustment or progression.

For pet owners

• If your pet has proteinuria, we’ll often recommend:
  1. A diet designed for kidney support (you’ll receive details from your vet).
  2. Medication(s) that protect the kidneys and reduce protein loss.
  3. Monitoring: repeated urine tests, blood pressure checks, possibly ultrasounds.
  4. Treat any underlying disease (for example infections, high blood pressure, endocrine disorders).
• Encourage compliance: feeding the right diet, giving medications consistently, and returning for rechecks is critical.
• Emphasize that early detection + intervention often means a better quality of life and longer survival.

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Key Takeaways & Practical Pearls

For veterinary professionals

• Screen at-risk patients: pets with CKD, hypertension, protein-losing nephropathy (PLN), infectious disease exposure, or breeds predisposed to glomerular disease.
• Do not ignore isolated proteinuria: even in non-azotemic pets, persistent proteinuria may indicate early disease.
• Always assess the urine sediment + dipstick before UPC: an active sediment suggests postrenal cause, and UPC interpretation will be confounded.
• Set measurable goals: aim for target UPC reduction and monitor response.
• Communicate clearly with owners: explain why proteinuria matters, what the follow-up will look like, and foster adherence.

For pet owners

• Protein in your pet’s urine isn’t a diagnosis; it’s a finding that prompts further investigation.
• Some causes are treatable (bladder infections, stones), while others (kidney‐related) require long-term management.
• Treatment often means diet + medications + regular monitoring — these are not optional add-ons; they make a real difference.
• Ask your veterinarian what the urine protein:creatinine ratio is, what target they’re aiming for, and when you’ll recheck.

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In summary, proteinuria in dogs and cats is more than just a lab abnormality. It can be a harbinger of significant kidney or systemic disease. For primary care veterinarians, technicians, and tertiary care specialists alike, recognizing, quantifying, investigating, and managing proteinuria proactively can influence outcomes. And for owners, understanding the significance of proteinuria means being a partner in your pet’s care. By integrating screening protocols, standardized testing (UPC), therapeutic strategies (diet, RAAS inhibitors, blood pressure control), and clear client communication, we can shift proteinuria from a silent prognostic marker to a manageable component of patient care.