Welcome To Lava Kennels Chinese Shar-Pei
Written by Dr.Jeff Vidt
1. The underlying basis of amyloidosis in Shar-Pei is Familial Shar-Pei Fever (FSF). It is quite possible that FSF has variable age of onset and variable degrees of severity in terms of the inflammatory disease it causes. This may result in a variable rate of progression in the development of amyloidosis in different individuals. For example, the response of the liver to FSF and the synthesis and release of the acute phase proteins, especially SAA, may be more acute in some dogs resulting in a more rapid deposition of amyloid. In other individuals, the response to FSF may be more chromic and result in slower deposition of amyloid. In effect, there may be milder forms and more severe forms of the same disease.
2. The exact mechanism of amyloid deposition may be different in different individuals.
3. There may be other effects of FSF on the body which are additive with the amyloidosis. As an example, we know Shar-Pei are more susceptible to disseminated intravascular coagulation (internal blood clotting) during an episode of FSF and blood clots in the kidneys may cause more kidney damage than just amyloid deposition itself.
4. Some dogs may have other disease processes going on which can be additive with the effects of amyloidosis.
These are just some ideas on why we see different presentations of the same disease. One fact remains - any amyloid deposits found in a Shar-Pei have to be regarded as related to FSF and genetic until proven otherwise. It really doesn't matter whether a little or a large amount of amyloid is found. Another point to keep in mind is that the mechanisms initiating amyloid deposition are normal protective responses seen in any breed of dog. It appears in our breed that the mechanisms, which regulate the inflammatory response, don't work properly allowing this normal response to go out of control and cause disease.
Action for Amyloidosis
1. Monitor weight - This involves weighing your dog at regular intervals using a scale. Do not rely on eyeball judgements. Too often I see dogs in an advanced state of weight loss which the owner has just noticed, but which has been going on for several weeks. Remember, we are trying to uncover this condition at its earliest point - minor weight loss can indicate early renal amyloidosis.
2. Monitor appetite - Daily fluctuations in appetite do occur, but a change in what is normal for your dog may indicate early kidney problems.
3. Monitor water consumption - A normal dog consumes approximately 1 oz. of water per pound of body weight per day. This varies with activity level, season of the year, type of food being fed (canned vs. dry), etc. I advise measuring water intake periodically by measuring how much water is put down in the morning and measuring it again at night. Obviously this will involve a little more ingenuity on the owner's part when multiple dogs are involved. Increased water consumption may indicate early kidney failure
addition to the above home monitoring program, I also advise having your
veterinarian check a urine sample every three months on any Shar-Pei over two
years of age. The main parameters I watch in the urine are the urine specific
gravity and the urine protein reading. Urine specific gravity is a measure of
the concentration of the urine. If the kidneys were not functioning at all this
reading would be 1.008 - 1.012 (a dilute urine). Normal concentration should be
above 1.025 and usually is greater that 1.045 (a concentrated urine). Ideally
the urine sample should be a morning sample collected after the dog's water bowl
has been removed overnight (remember to close the toilet lid!). By depriving the
dog of water overnight we force the kidneys to concentrate the urine, if they
are able to do so. Inability to concentrate urine indicates that approximately
75% of the kidneys are non-functional - this is still compatible with life, but
treatment needs to be started quickly to preserve the remaining kidney function.
A. Glomerular - If the amyloid deposits occur primarily in the glomerulus, we see increased protein levels in the urine.
B. Tubular - If the amyloid deposits occur in the tubular part of the kidney we see loss of concentrating ability which manifests as a dilute urine.
C. Combination - This occurs when amyloid is deposited in both the glomeruli and the kidney tubules and we see increased protein levels in the urine and dilute urine.
The clinical signs and the routine urine check constitute the first level of diagnostics. If the urine sample is abnormal and one or more clinical signs are present, then we immediately proceed to the second level of diagnostics. This level incorporates the following tests:
1. A complete blood count - This includes a packed cell volume, a white blood cell count, red blood cell count, platelet count, and a white blood cell differential count.
2. A health panel - This includes at least a BUN, creatinine, sodium, potassium, calcium, phosphorous, cholesterol, total protein, albumin, globulin and, glucose. It often includes liver tests and thyroid hormone levels.
3. An immune panel - This should consist of a direct Coomb's test, an anti-nuclear antibody test (ANA), a Rheumatoid arthritis factor test (RA), and an LE prep for systemic lupus.
4. A urine protein/creatinine ratio - A value above 1.0 is considered abnormal and indicates excessive urine protein loss.
5. Abdominal radiographs - Used to evaluate kidney size and shape.
Based on the results of the first and second level diagnostics the following steps are taken to manage the patient:
1. Diet - A low protein diet is initiated using Hill's Prescription Diet K/D® or its home-made counterpart. I'm also using the Iams Eukanuba Veterinary Kidney Diets - Early Stages® and Advanced Stages®.
2. Vitamin-mineral supplementation.
3. Ascriptin® - 1/4 tablet once a day.
4. 1 cooked egg per day - used in cases where albumin is being lost in the urine.
Additional medical therapy may be instituted using either colchicine
tablets or DMSO via injection or orally. The effectiveness of both these drugs
in the prevention and treatment of renal amyloidosis in the dog has yet to be
substantiated, but their use is justified given the grave prognosis of this
condition in the Shar-Pei. Colchicine is a human anti-gout medication whose mode
of action is largely unknown. It appears to prevent the formation of amyloid in
the laboratory, but whether this occurs in the living animal is not known.
Dimethyl sulfoxide (DMSO) is another drug whose mode of action is unknown, but
has demonstrated the property of dissolving amyloid in the laboratory. Again,
whether this action occurs in the living animal is unknown.
A. Colchicine - this dose can be obtained from Dr. Linda Tintle or myself (see the July/August 1992 issue of The Barker).
B. DMSO - numerous dosages are in the veterinary literature. Your veterinarian should refer to an excellent article on renal amyloidosis by DiBartola in Current Veterinary Therapy XI.
6. Equally important is the avoidance of further kidney damage. -
A. Avoid dehydration- provide plenty of fresh water daily.
B. Avoid kidney-damaging drugs such as aminoglycoside antibiotics, methoxyflurane anesthesia, various chemotherapeutic agents, sulfonamide antibiotics, etc.
C. Avoid stress- boarding, traveling, showing, etc.
level diagnostics may be done depending on your veterinarian or the availability
of specialists in your area.
1. Coagulation panel - Increased levels of fibrinogen may indicate impending thromboembolism (throwing of blood clots) associated with DIC (Disseminated Intravascular Coagulation) especially if associated with increased cholesterol and decreased albumin levels (nephrotic syndrome). This panel should include a platelet count and a measurement of FDP's (Fibrin Degradation Products).
2. Fractional clearances of various eletrolytes.
3. 24-hour urine protein excretion.
4. Creatinine clearance testing to evaluate kidney function.
5. Kidney ultrasound.
6. Kidney biopsy.
The kidney biopsy is the definitive diagnosis of renal amyloidosis and the decision to biopsy should be made early in the course of the disease for a number of reasons:
1. Early on, the animal is a much better surgical candidate and many complications of renal amyloidosis such as bleeding tendencies and uremia are not present.
2. There is a real danger in the Shar-Pei to blame every kidney problem on renal amyloidosis and fail to pursue other causes of kidney disease such as kidney infection, heartworm disease, and immune-mediated diseases like systemic lupus and immune-mediated glomerulonephritis.
3. The information from an early kidney biopsy can guide the medical and dietary management of the case and provide valuable prognostic information.
important as the early diagnosis of renal amyloidosis is the continued
monitoring of the patient while on therapy. This allows us not only to monitor
and watch for the progression of the disease, but also to evaluate the various
therapeutic modalities and determine which are effective and which are not.
Monitoring at one to two week intervals initially and then at monthly intervals
thereafter is recommended. I usually repeat a kidney panel and cholesterol
level, a CBC, and a urinalysis including a urine protein/creatinine ratio.
1. Nephrotic syndrome - characterized by decreased serum albumin, increased serum cholesterol and increased protein loss in the urine. A serious complication of this syndrome is thromboembolism ("throwing blood clots"). Your veterinarian may do a blood fibrinogen level and coagulation panel to evaluate the blood clotting system. If the fibrinogen level is >300 mg/dl, aspirin therapy is strongly indicated. Another serious complication of this condition is the development of edema or fluid accumulation in the abdomen or chest and in the limbs. In this case, the use of diuretics such as Lasix may be necessary.
2. Uremia - or the accumulation of body waste products which are normally filtered by the kidneys into the urine. The build-up of these wastes causes clinical signs such as appetite loss, weight loss, vomiting, diarrhea, depression and lethargy. More serious effects include anemia (decreased red blood cell production) and gastrointestinal ulceration. Treatment here may include intravenous fluid therapy, dietary therapy such as Hill's Science Diet U/Dā, Iams Eukanuba Veterinary Kidney Diet - Advanced Stagesā, phosphate binders such as Amphojelā, ulcer medication such as Carafateā and other therapy as deemed necessary by your veterinarian. Eventually, uremia will progress and lead to the death of the animal. As an aside, current nutritional research indicates that there is no advantage to instituting dietary protein restriction prior to the onset of kidney failure. This means that feeding protein-restricted diets prior to developing laboratory or clinical signs of kidney failure will not prevent kidney failure.
3. Hypertension - The kidneys are very important in the regulation of blood pressure. It is speculated that up to 80% of the dogs in kidney failure have significant hypertension as a consequence. The use of indirect blood pressure monitoring in animals has recently become available to the veterinarian and hopefully will lead to more advances in this area. Your veterinarian may wish to institute therapy using vasodilators and/ or diuretic medication.
4. Disseminated Intravascular Coagulation (DIC)- The body's coagulation system is in a fine state of balance between forming blood clots and dissolving them. When this balance is disrupted coagulation factors are used up before they can be replaced and out of control bleeding is the result. This condition is associated with high mortality and is a poor prognostic factor. Treatment is not very effective.
Streptococcal Toxic Shock Syndrome (STSS) -This is an unusual complication which
results in areas of skin death leading to skin sloughing almost like a burn. The
condition seems to be caused by toxins produced by Streptococcus canis and is
rapidly fatal sometimes in spite of treatment.
Lynn & Michael Olds