Equis ISSN 2398-2977

Protein-losing conditions

Synonym(s): Protein-losing enteropathy, protein-losing nephropathy, cutaneous plasma loss

Contributor(s): Prof Derek Knottenbelt, Ruth Morgan, Jamie Prutton

Introduction

  • Protein-losing conditions result in hypoproteinemia (likely hypoalbuminemia), debilitation, weight loss or inability to gain weight and generalized edema.
  • Cause: nephropathy, enteropathy, bacterial or helminth infections, vasculitis, hepatopathy, burns and disease with a marked metabolic demand.
  • Signs: debilitation, edema, diarrhea, weight loss or lack of weight gain in the face of adequate nutrition, signs associated with hepatopathies.
  • Diagnosis: biochemical analysis of proteins followed by identification of the source and cause of protein loss.
  • Treatment: supportive therapy, depending on severity, includes administration of plasma or synthetic colloids; specific treatment will depend on cause and can include cessation of drugs (NSAIDs).
  • Prognosis: depends on cause and severity.

Pathogenesis

Etiology

Protein loss in feces

Protein loss in urine

Other sources of protein loss

  • Vascular or lymphatic hypertension.
  • Blood loss, eg parasitism, wounds.
  • Wound exudation/burns. The skin uses 25-30% of daily protein intake for maintenance of hair and the epidermis but this can increase 5-fold in skin disease.
  • Vasculitis Vasculitis.
  • Severe inflammatory disease.
  • Hepatopathy.

Predisposing factors

General

  • Young horse for parasitic disease, older horses for neoplastic processes.

Specific

  • Bacterial infection.
  • Parasitic infestation.
  • Toxic damage to kidneys secondary to drug administration.

Pathophysiology

  • The protein-losing state (see below) will lead to loss of albumin most frequently (in severe cases this can be globulins) thus causing a generalized hypoproteinemia Hypoproteinemia.
  • The loss can be in urine, feces, serum or due to consumption. This loss then leads to a reduction in the colloidal osmotic potential and subsequent edema and associated clinical signs.
  • Malabsorptive diseases (inflammatory bowel disease Chronic inflammatory bowel disease, lymphoma Lymphoproliferative disorders, etc) can lead to a reduction in intake of nutrient essential for protein synthesis.

Protein loss into feces

  • Usually associated with large-intestinal diarrhea, eg Salmonellosis Intestine: salmonellosis/Clostridiosis Gastrointestinal: clostridiosis.
  • May co-exist with malabsorption syndromes, eg inflammatory bowel disease → changes in mucosal and submucosal morphology and function → villous atrophy, cellular infiltrates, lymphangiectasia.
  • Can be seen in anterior enteritis without evidence of diarrhea.
  • In younger (and PPID cases Pituitary: adenoma) this can be seen with parasitism due to the mass emergence of encysted cyathostomins.
  • Right dorsal colitis Colon: colitis secondary to NSAID therapy Therapeutics: anti-inflammatory drugs will see large amounts of protein loss and diarrhea.

Protein loss into urine

  • Usually associated with tubular nephrosis, eg toxic → obstruction to tubular flow and reabsorption.
  • More rarely associated with glomerulonephritis → increased permeability of basement membrane → protein loss into tubular fluid → nephrotic syndrome.
  • Reagent strip analysis can give a false positive protein result if the urine is alkaline so care should be taken in the interpretation.
  • Mares are reported to excrete urine at 1.6-11.2 g/day which equates to 100 mg/dL on analysis.
  • Pre-renal failure can be associated with congestive heart failure Heart: failure – overview thus leading to proteinuria.
  • NSAID toxicity Toxicity: non-steroidal anti-inflammatory (NSAID) is a relatively frequent cause of renal pathology. NSAIDs cause medullary crest or papillary necrosis due to the reduced blood flow seen in the renal cortex and therefore increased susceptibility.
  • Aminoglycoside Therapeutics: aminoglycosides use can lead to acute tubular necrosis.
  • 86% of chronic renal failure horses (irrespective of etiology) have hypoalbuminemia.

Protein metabolism

  • In disease states with high metabolic demands, a subsequent hypoalbuminemia can be seen (often seen with respiratory disease such as equine multinodular pulmonary fibrosis Lung: multinodular fibrosis).

Hepatopathy

  • Multiple etiologies can lead to hepatic insufficiency, and as the liver synthesizes 90% of plasma proteins there can be subsequent hypoproteinemia.

Timecourse

  • Depends on etiology: acute colitis is rapid and often fatal, whereas Lawsonia intracellularis infection is chronic lasting several months.
  • Renal disease can also have an acute insult but often the clinical signs will be insidious in nature.

Epidemiology

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • McGorum B C & Pirie R S (2010) Antimicrobial associated diarrhoea in the horse. Part 2: Which antimicrobials are associated with AAD in the horse? Equine Vet Educ 22, 43-50 VetMedResource.
  • Johns I et al (2009) Blood culture status in mature horses with diarrhoea: A possible association with survival. Equine Vet J 41, 160-164 PubMed.
  • McGorum B C & Pirie R S (2009) Antimicrobial associated diarrhoea in the horse. Part 1: Overview, pathogenesis and risk factors. Equine Vet Educ 21, 610-616 VetMedResource.
  • Naylor R J & Dunkel B (2009) The treatment of diarrhoea in the adult horse. Equine Vet Educ 21, 494-504 VetMedResource.
  • Frazer M L (2008) Lawsonia intracellularis infection in horses: 2005-2007. J Vet Intern Med 22, 1243-1248 VetMedResource.
  • Klei T R & French D D (1998) Special workshop presentation - Small strongyles, an emerging parasite problem for horses. Equine Pract 20 (3), 26-30 VetMedResource.
  • Goetz T E & Coffman J R (1984) Ulcerative colitis and protein-losing enteropathy associated with intestinal salmonellosis in histoplasmosis in a horse. Eq Vet J 16 (5), 439-441 VetMedResource.
  • Roberts M C (1983) Protein-losing enteropathy in the horse. Comp Contin Educ Pract Vet (10), 550-556 VetMedResource.

Other sources of information

  • Reed S, Bayly W & Sellon D (2010) Equine Internal Medicine. 3rd edn. Elsevier.


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