Your dog’s body produces a number of extremely important proteins, called enzymes. One group of these are the digestive enzymes that participate in
the breakdown and digestion of food.
In humans, digestion begins in the mouth where saliva contains digestive enzymes. Dogs, however, don’t chew their food they gulp it down in chunks. Dog saliva serves
in digestion only to moisten and lubricate the mouth and food as it is pushed back into the oesophagus for its journey to the stomach.
The gastro intestinal tract has to perform many functions in order to absorb food then excrete the waste products. The mucosal layer lines the inner surface of the tube and is responsible for secretion
and absorption of nutrients to the body. The surface area of the mucosa contains villi. Damage to the villi can cause villous atrophy which leads to malabsorption and
The major digestive and absorption processes occur in the small intestine. Several digestive enzymes are mixed into the food along with bile. These secretions are used to break down carbohydrates,
proteins and fats into smaller molecules, which are then absorbed by special cells while the mixture is churned and pushed along by intestinal muscle contractions.
Dogs intestines are relatively short (about five times their body length) so complex foods have a short time to be broken down and absorbed.
By the time this mixture reaches the large intestine, the final leg of its journey, there should be little of nutritional value left. The large intestine completes the absorption of water and electrolytes
and the remaining undigested food is then filtered and stored for elimination in the colon.
When a dog suffers from malabsorption, as in the case of PLE, digestive enzymes fail to absorb protein into the body and it passes through the large intestine into the faeces. A forerunner to PLE
can be inflammatory bowel disease (IBD).
PLE is characterised as a loss of protein from the intestines due to intestinal disease. There can be many causes of PLE, but it's important to note that there maybe a hereditary component in Wheatens, predisposing them to IBD and/or intestinal Lymphangiectasia.
PLE is a condition in which protein is lost excessively into the intestine and can represent a number of abnormalities, which result in the loss of plasma proteins from the gastrointestinal tract.
The loss of the healthy mucosal layer allows the leakage of vital protein-rich fluids. This is a hallmark of Protein Losing Enteropathy (PLE).
The liver and other cleansing systems are unable to compensate for the loss.
Mechanisms for gastrointestinal protein loss include lymphatic obstruction, mucosal disease with erosions, or ulcerations.
PLE is probably related to immunological defence of the intestinal tract.
The average age of onset is 4.5 years (range 0.5 to 11 years ).
A PLE dog may exhibit diarrhoea, vomiting, edema/ascites, picky appetite and weght loss. Since these are symptoms of many types of illness, serious and minor, proper diagnosis is important. Left untreated, PLE can become serious and fatal.
Treatment is with medication and diet and can result in extended life.
Tests necessary to detect the presence of PLE are blood, urine and, if necessary, endoscope biopsy and Faecal investigation.
Please refer to the Comparison Chart of Hereditary Diseases for signs and symptoms of this disease.
Learn more about PLE here
Learn more about IBD here
Please note that links given to articles that are general in nature on external websites are not a substitute for your own Veterinarian's advice.
The Testing Protocols page has information about tests available for PLE.
North America only - there is the FecalAPI test. Further information avalable on SCWTCA Endowment Inc. Web site.
The mode of inheritance for PLE is not known.
At the present time there is no test available to show if dogs are carrying the deleterious (bad) mutations which cause this disease.
For one owner's account of dealing with PLE, go to the link 'Megan - My Angel Eyes'
The kidneys filter waste and extra fluid from the blood. The filtering process takes place in the nephron where microscopic blood vessel filters called glomeruli,
are attached to fluid-collecting tubules. A number of different disease processes can damage the glomeruli, thereby causing kidney failure.
Glomerulonephritis and glomerulosclerosis are broad terms that include many forms of damage to the glomeruli.
PLN is also known as glomerular disease. It causes protein loss through the glomerulus, a structure of the kidneys.
While PLN can have several causes, it's important to note that Wheatens can have familial PLN due to podocytopathy causing glomerulosclerosis. Note that PLN is not "old age" kidney disease and is different to Renal Dyspasia. PLN can be associated with systemic hypertension, thromboembolic events, edema/ascites and eventually chronic renal failure.
Some forms of kidney failure can be slowed down but scarred glomeruli can never be repaired. This is what makes early detection so vital. Treatment given in the early stages of kidney failure depends
on the disease causing the damage.
Kidney failure may be ‘silent’ for many years. Approximately 70% of the kidney can be damaged before any physical signs show themselves.
The glomeruli are the filters of the kidneys (imagine a water filter in a jug), they filter the blood and make urine. Normally, large molecules such as proteins,
and cells such as red blood cells or white blood cells, do not pass through the filters and are retained within the blood because they are so important for health.
Small molecules pass completely through the filters. Some of these are completely reabsorbed back into the blood since they are so important in maintaining the right chemical balance of the body e.g. glucose, salt etc. Other
molecules, which are not required for body functions are passed freely into the urine, for example Urea, Uric Acid and Creatinine.
There are two main effects of damage to the glomeruli. Substances, which are normally retained in the circulation escape into the urine through the filtration
mechanism, one of these is Albumin. As a consequence, protein and red cells appear in the urine and can be detected by a dipstick urine test.
Protein in the urine is called proteinuria. Normally there is very little protein in the urine. If the damage gets worse, the filter shuts down and that function of the kidney is lost.
If sufficient damage occurs to enough glomeruli kidney failure may occur.
Glomerulonephritis is the inflammation of the membrane tissue in the kidney that serves as a filter, separating wastes and extra fluid from the blood. Glomerulosclerosis
describes the scarring or hardening of the tiny blood vessels within the kidney.
The average age of onset is is years (range 2 to 11 years).
Dogs will not usually exhibit symptoms until the disease is very advanced.
Left untreated, PLN is usually fatal.
Treatment is with medication and diet. Early intervention can result in a longer lifespan.
PLN is a condition in which plasma protein is lost to excess in the kidney.
In the SCWT the most common disease causing PLN syndrome is glomerulonephritis.
The term “glomerulonephritis” defines a group of inflammatory diseases of the kidneys affecting the most important functional components of renal tissue, the glomeruli
and adjacent structures.
There are several immune mechanisms involved in this inflammatory disease.
SCWT's affected with PLN have damaged glomeruli because the ‘holes’ in the basement membrane are too large and allow more than waste to pass through.
One of the larger molecules that pass through the faulty membane is protein. That is why excess protein (Albumin) is found in the urine of SCWTs who have one of the diseases that causes
A Urinalysis test is one of the key factors to show protein loss associated with PLN far earlier than in a blood test.
Tests necessary to detect the presence of PLN are blood, urine and if necessary, a wedge biopsy. Go to the Testing Protocols page for further
The mode of inheritance for PLN is not known, but in 2012, Dr Paula Henthorn and Dr Meryl Littman at the University of Pennsylvania School of Veterinary Medicine (Penn Vet - details click
here) identified mutations in two genes associated with PLN.
Learn more about PLN here.
Some useful links for your Veterinarian: : International Renal Interest Society (“IRIS”) Consensus Clinical Practice Guidelines for Glomerular Disease in Dogs
It is important when testing for the PLN-Variant gene that this includes both NPHS1 and KIRREL2 genes in the test. Further details on this link. (pdf - opens on new page)
For the PLN-Variant Genes Test it is preferred that Penn Laboratory (PennGen) is used, as this enables
continuity of research. In Europe and Scandinavia Laboklin Laboratories also offer the test but the result does not directly aid this research.
PennGen Laboratories, at the University of Pennsylvania School of Veterinary Medicine are, from April 2020, offering individual and combination genetic testing for PLN (and Microphthalmia and Degenerative Myelopathy) in Soft Coated Wheaten Terriers. Select this link for further details of costs. (pdf - opens on new page)
Test Results definitions (updated August 2017)
This table clarifies the reporting formats between PennGen and Laboklin tests results.
A dog without any of the variant alleles
A dog that has no copies of the variant alleles is at the least risk of developing PLN
A dog with one copy of the variant alleles
A dog with one copy of the variant allele is at medium risk of developing PLN
A dog with two copies of the variant alleles
A dog with two copies of the variant alleles is at the highest risk of developing PLN, but this does not mean it will develop PLN
Homozygous for the PLN causative mutation
Affected refers to both copies of the allele,
it does not mean the dog is currently, or will be affected with PLN
Further reading - Differentiating Renal Dysplasia (Juvenile Renal Disease) from Protein Losing Nephropathy (PLN) in our Wheatens. Meryl Littman 2006 click
here for pdf file