Hypothyroidism
Hypothyroidism is the result of inadequate output of hormone from the
thyroid gland in the neck. Thyroid deficiency causes the coat to become
scanty. The hair is coarse and brittle and falls out easily. The skin gets
thick, tough and dark in color. The neck and body are most often involved.
Since control of metabolism is under the influence of the thyroid, a deficiency
of hormone slows down the production of energy. In the dog, the signs of
thyroid deficiency are lethargy, obesity, drooping of the eyelids, mental
dullness and irregular heat cycles. These signs develop gradually and may
take months to become evident. A dog with a mild thyroid deficiency may
show little or no signs of it. You might begin to suspect this only in connection
with an infertility problem. Diagnosis requires a thyroid blood test.
Treatment: Hypothyroidism is easy to treat with daily thyroid replacement.
It usually is permanent and requires lifetime treatment. For more information
on Hypothyroidism, check out:
Thyroid
Disease by Jean Dodds
Hypothyroidism
Hypothyroidism and
Dogs
Cherry Eye
Cherry Eye is a condition which results when the tear gland on the inner
surface of the third eyelid enlarges because of infection. As it swells
it is forced out from behind the lid, exposing a red cherry like growth
at the nasal corner of the eye. Usual treatment is corrective surgery, which
has a very high success rate. Some sources of information on Cherry Eye
can be found at:
Cherry Eye... Third Eyelid
Eversion In The Dog
Prolapsed Gland of the Third Eyelid
Cherry
Eye
Epilepsy
Epilepsy is a recurrent seizure disorder that may be acquired or congenital.
Three to four months after a brain concussion, some dogs acquire seizures
as a result of scars on the brain.
Post-encephalitic seizures occur three to four weeks after the onset of
encephalitis. Distemper, in particular, is characterized by typical attacks
that begin with champing, tongue chewing, foaming at the mouth, shaking
of the head and blinking of the eyes-then a dazed look, and a return to
normal.
To establish a diagnosis of epilepsy, the attacks must be recurrent and
similar. A typical epileptic seizure has three phases. The first is called
the aura. It is recognized by the onset of sudden apprehension and restlessness.
There may be bizarre behavior, such as sniffing in the corner or snapping
the air.
Most grand mal seizures start with champing, chewing, foaming at the mouth,
head shaking and eye flickering. During the rigid phase the dog collapses,
the head is thrown back, and the dog slobbers and twitches at the face.
Pupils dilate. As the rigid phase begins to pass, the dog makes running
movements with all four legs (paddling) and may lose control of bowels or
bladder.
During the post seizure phase the dog recovers but remains confused and
wobbly. If overstimulated by a loud noise or rough handling, a second seizure
can occur. The first two phases pass quickly (in about three minutes). The
post seizure state can persist for several hours. This might give the impression
that the seizure was of long duration. However, a true epileptic seizure
is over in less than five minutes.
Stimuli that can trigger a seizure are fatigue, excitement, anxiety, bright
lights, loud noises, fever, overbreathing and estrus.
Not all epileptic seizures are typical. To help make the diagnosis, your
veterinarian probably will ask for a description of the attack, and will
want to know if other attacks follow the same pattern.
Treatment: When a seizure starts, stand aside until your dog quiets down,
or cover the dog with a blanket. (Don't put your fingers in the mouth or
try to wedge something between the teeth.) Then call your veterinarian.
As most seizures will be over in a few minutes, it is unlikely that your
veterinarian will need to stop it with medications. Your vet may want to
examine the dog to determine the cause of the seizure.
Seizures lasting over five minutes (continuous seizures) are dangerous.
They must be stopped to prevent permanent brain damage. Valium is given
intravenously to stop a continuous seizure.
The complete elimination of seizure activity is not always a realistic goal
in treating dogs with recurrent seizure disorders. Dosages and rates of
action of anticonvulsant drugs are quite variable. Many drugs, such as Dilantin,
used for treating epilepsy in people, are rapidly metabolized in dogs when
given in like dosage. Only phenobarbital and primidone (which metabolizes
to phenobarbital) have been found to be both safe and efficacious for controlling
seizures in dogs. In general, seizures will worsen if not controlled, although
young dogs are less likely to have progressive disease than dogs that acquire
seizures later in life. The most common causes of treatment failure are
inadequate levels of medication and failure to administer the drug as directed.
It is important to work closely with your veterinarian. For more information
on epilepsy check out:
Canine
Epilepsy Rescource Center
Canine Epilepsy
Canine Epilepsy Research
Addison's Disease
Every Newf begins life with two adrenal glands. The adrenal glands
sit directly in front of each kidney within the abdominal cavity and they
are responsible for producing several important hormones including adrenaline,
estrogen and testosterone (most of these two hormones are actually produced
within the testicles and ovaries), cortisone, and aldosterone. Addison's
disease is defined as a substantial decrease in the production of cortisone
and aldosterone. The adrenal glands are the primary source of these two
hormones and neither man nor beast can live without adequate levels of both
of them. Cortisone has an effect on virtually every tissue in the body.
It is essential for the normal function of every organ within the body and
is responsible for a normal appetite and sense of well-being. Aldosterone's
main function is the regulation of sodium and potassium levels within the
body. In the absence of aldosterone, the blood potassium level increases
and the blood sodium level decreases, both of which may be life threatening
abnormalities. The adrenal glands need to be told to make cortisone and
aldosterone. Hormones produced in two areas of the brain (the pituitary
gland and the hypothalamus) stimulate the adrenal glands to manufacture
these hormones. So, Addison's Disease can be caused by a problem within
the adrenal glands themselves or within specific areas of the brain. For
more information on Addison's Disease, check out:
Addison Dogs
Canine Addisons Disease
Addison's Disease (Hypoadrenocorticism)
Cataracts
A Cataract is a loss of normal transparency of the eye lens. Any spot
on the lens that is opaque, regardless of it's size, is technically a cataract.
Cataracts affect dogs of all ages, but the majority occur in dogs under
five years of age. It is impossible to differentiate hereditary and nonhereditary
cataracts solely from the appearance of the lens. Breed predisposition and
line history are more suggestive. Cataracts can develop in diabetic dogs.
It is important to recognize the possibility of diabetes before considering
cataract extraction. If the diabetes is controlled, the operation is more
likely to be successful. To find out more on cataracts, please check out:
Cataracts
in Dogs
Inheritance
of Cataracts in Dogs
CERF
Glomerulophy
(renal disease)
Juvenile Renal Disease in Standard Poodles
I. Definition and Description
Juvenile renal disease (JRD) and other congenital or familial forms of renal
dysplasia are seen in about twenty breeds of dogs. According to Kenneth
Bovee, DVM, (Professor of Medicine at the University of Pennsylvania), the
clinical entity has considerable variation from breed to breed and has completely
different prevalence rates. A table which lists all of the congenital and
familial renal diseases of dogs by breed can be found in Veterinary Pediatrics
Dogs & Cats from Birth to Six Months. (1) In affected standard poodles,
histological findings include "cystic glomerular atrophy and large
numbers of immature ("fetal") glomeruli are observed, especially
in dogs at 3 to 4 months of age. Secondary tubular changes consist of focal
to diffuse tubular dilatation and atrophy as well as basement membrane mineralization.
The cortical interstitium contains segmental areas of fibrosis, whereas
more diffuse lesions occur in the medulla. Interstitial infiltrates of mononuclear
cells are minimal in younger dogs and more severe in older dogs." (2)
"Hypoplastic kidneys appear as miniature replicas of normal kidneys
composed of reduced numbers of histologically normal nephrons". (1)
There are a number of hereditary nephropathies that cause renal failure
in young dogs. The genetic nature of these diseases makes accurate diagnosis
imperative so that affected animals are not bred. Usually, in standard poodles
the disease is discovered before breeding age, but diagnosing a puppy affected
with JRD could prevent both the sire and dam from being bred again.
In standard poodles with JRD, symptoms can be noted as early as a few weeks
after birth; and affected puppies are almost without exception symptomatic
before two years of age. Some puppies are seen because of a failure to thrive:
most grow normally until symptoms appear. Puppies with renal dysplasia may
appear clinically normal for extended periods of time before developing
signs of chronic renal failure. The rate at which renal dysplasia progresses
to overt renal failure depends on the severity of initial renal lesions
and factors resulting in progressive loss of renal functional mass. (1)
Larry Cowgill, DVM, (University of California, Davis), told me that many
puppies born with renal dysplasia do better than dogs who acquire kidney
disease later in life. He said that these puppies are able to plateau until
a small insult occurs, and then they decompensate.
Early symptoms of juvenile renal disease include polydipsia, polyuria, and
dilute urine which has little color or odor. Some affected puppies leak
urine, many do not. Often a puppy owner's earliest complaint is about the
difficulty of housebreaking a puppy later discovered to have JRD. The volume
of water consumed, and, in some puppies, leakage of urine can make housebreaking
a formidable task. As the disease progresses, vomiting, weight loss, anorexia,
lethargy, and muscle weakness are seen. There is sometimes a chemical odor
to the breath as a result of metabolic waste not being excreted by the kidneys.
If the reduction in renal function is identified early, when only polydipsia
and polyuria are evident, medical management can be instituted immediately.
Although the renal damage is not reversible, the quality and length of the
patient's life may be improved by early treatment. (3)
Blood urea nitrogen (BUN) and creatinine are the two most commonly utilized
measurements of renal function, with creatinine being the more accurate
measurement. They are approximations of the glomerular filtration rate (GFR),
and when the GFR is reduced to 25% of its normal rate, they become elevated
above the accepted reference ranges . BUN and creatinine test for renal
failure and will not indicate renal disease prior to failure. BUN and creatinine
values begin to rise slightly as renal function is lost, but do not exceed
the reference range until only 25% of renal function remains.
Although a BUN can be elevated by non renal causes, BUN values seldom exceed
50mg/dl as a result of non-renal causes. If the elevation is not the result
of primary renal failure, then the patient should be able to concentrate
his/her urine to a specific gravity (SG) above 1.030, except in instances
of renal medullary washout. The inability to concentrate urine occurs when
two thirds of the renal function is lost. (3)
Serum phosphorus levels are often not elevated in cases of juvenile renal
disease. Where the reduction in renal function progresses slowly, the puppy
compensates and the serum phosphorus levels can remain normal. About 75%
of renal function must be lost before this elevation is detectable. (3)
In the cases I have followed, although BUN and creatinine levels were often
greatly elevated, serum phosphorus levels were increased in only about 50%
of cases.
If a standard poodle under two years of age is found to have an elevated
BUN and creatinine and significant proteinuria, as indicated by an increased
urine protein:creatinine ratio, JRD should be strongly suspected. Abdominal
palpation may reveal small irregularly shaped kidneys. An ultrasound can
be a useful diagnostic tool, since the kidneys are usually atrophied and
underdeveloped. It must be kept in mind, however, that kidneys from affected
dogs may be normal size.
The most accurate method for diagnosing JRD is a wedge biopsy from one kidney
taken any time after the second month of life, or a histopathologic exam
at necropsy. The histopathology of these puppies should be examined by an
experienced pathologist. There are a number of pathologists who have a considerable
interest in this disease. (4) A biopsy or autopsy of a puppy less than 2
months of age would not be fruitful, since the normally immature kidneys
could not be distinguished from those affected by JRD. It would not be reasonable
to expect the owner of a JRD puppy to consent to a wedge biopsy, since the
findings would not change the treatment or prognosis of the disease.
Treatments for the symptoms of JRD include a low protein prescription diet,
such as Hill's K/D. The predominant effect of the low protein diet is to
minimize production of uremic toxins so that the patient feels better. Low
protein diets may help extend life in dogs. Phosphorus is more important
in this regard, since high phosphorus accelerates renal failure, and restricted
phosphorus slows it down. K/D is low in phosphorus, so it remains a good
food for dogs in this condition. Low phosphorus diets allow management of
secondary hyperparathyroidism by restricting phosphorus intake and reducing
phosphorus absorption from the gastrointestinal tract.( 5, 6) In addition
to diet, IV fluids can be administered to correct disturbances created by
the retention of uremic toxins, extracellular fluid volume, hyperkalemia,
and acid-base imbalances. Epogen can be prescribed to treat the hypoproliferative
anemia of chronic renal failure, resulting in improving the quality, and
probably the length of life. Some veterinary schools are performing organ
transplants, but transplanted kidneys in dogs are commonly rejected, and
involve an extraordinary expense and commitment.
These treatments are palliative at best, and the prognosis for JRD is grim.
Puppies usually die within several months of being diagnosed, almost always
before age two I am, however, following the progress of two dogs who have
JRD with what appears to be less severe kidney involvement, and who are
being well maintained on low protein and low phosphorus diets. These dogs
are now both more than three years old, and both were diagnosed before they
were symptomatic. One was tested because five of his littermates died of
JRD, and one because his veterinarian was giving free BUN tests to her clients
along with heartworm checks. These two dogs are an exception in my experience
with JRD in this breed. Although they are doing well, ultrasound has revealed
that their renal disease is bilateral. Unilateral renal dysplasia may be
clinically silent, and the dog may live a fairly normal lifetime.
Because no effective treatment for JRD exists, the most promising approach
for dealing with it is for clinical veterinarians, owners and breeders to
understand its genetic basis. Veterinarians can play an important role in
research by being aware of genetic diseases in specific breeds, of ongoing
research in these genetic diseases in specific breeds, and by directing
breeders and owners of dogs affected by these diseases to the people researching
them. Every puppy who comes to our attention, adds to the JRD data in our
research database. If the mode of inheritance can be determined using litter
data from puppies already born, it may not be necessary to breed test litters,
or it may be possible to breed fewer test litters.
II Background of my involvement
In January of 1990, I had my 21 month old standard poodle puppy put down.
She was one of three puppies in a litter of 11 to die of JRD. All three
of the puppies with the disease appeared healthy and grew normally until
clinical signs appeared at 10 months in one, and at 20 months in the other
two. The disease is devastating. Nobody expects to lose a puppy of that
age. As a first time dog owner, I was not aware that her prodigious water
consumption was abnormal, or that her urine, which had very little color
or odor was evidence of pathology. Veterinarians who ask questions of new
pet owners to elicit information about water consumption and the concentration
of urine increase a client's awareness of these variables.
After her death, I began searching the literature to discover what was known
about JRD in standard poodles, including what, if any, research was being
done in order to establish the mode of inheritance of this disease in this
breed. After finding that no one was working on this problem, I began a
collaboration with George Padgett, DVM, geneticist and Professor of Pathology
at Michigan State University. Our objective is to establish the mode of
inheritance of JRD in standard poodles, and an eventual open registry at
the Institute for Genetic Disease Control in Animals (GDC), in Davis, California.
Using an open registry, breeders who wish to can reduce the incidence of
this disease, if not breed it out entirely.
III What is known about the genetic basis of JRD
Dr. Padgett told me that in most of the breeds in which JRD has been studied,
it is a simple (one gene), autosomal (not sex linked), recessive (both parents
have to carry the gene) disease. The presence of just one affected puppy
determines that both parents are carriers. Littermates of an affected puppy
have a 67% chance of being carriers. Aunts, uncles, and grandparents of
an affected puppy have a 50% chance of being carriers.
A sire who has produced an affected puppy is a defined carrier. If the same
sire has been bred to bitches who produced sizable litters with no affected
puppies, those bitches have proven themselves to be probably clear. This
is referred to as Retrospective Test Mating. "Proven" is used
rather loosely here, since statistically a dog mated to a carrier and producing
six normal offspring would still have a 17.8% chance of being a carrier.
Twelve normal offspring would reduce that chance to 3.17%. The preceding
figures which refer to simple autosomal recessive anomalies are from Malcolm
B. Willis's book, Genetics of The Dog. (7) Even if only the sire or dam
of a litter is a carrier, the other parent being clear, an average of 50%
of all their puppies are carriers themselves.
I have been tracking a large number of affected litters, and the number
of JRD puppies within them. Dr. Padgett informed me in March, 1996, that
using the Chi-square statistical test on the data I have collected, the
data is consistent with JRD in standard poodles being a simple autosomal
recessive disease at the 97.5% level of significance. (6) It is possible
that as more data is collected, the conclusion about the specific mode of
inheritance may change.
Dr. Padgett noted that with perhaps as few as six additional accurately
diagnosed litters which are already in existence or with one or two test
matings of proven carriers, the data will become sufficiently robust to
be publishable in any of a number of scientific journals. (8)
IV What clinical veterinarians can do to help
In order for JRD to be further studied in standard poodles several things
have to occur. Veterinarians need to become aware that JRD is a problem
in this breed. Clients with affected puppies should be informed that this
disease is genetic, and should be encouraged to inform the breeder and the
owner of the sire of the puppy's illness. If the puppy is determined to
have JRD, the rest of the litter can be tested.
Most individual cases of JRD are treated by owners and veterinarians as
isolated occurrences rather than as the manifestation of a genetic disease.
Often breeders are not informed about a medical problem in a puppy they
have sold. When owners do inform breeders, it is usually just the owner
of the dam who is contacted. Unless there are multiples in a litter, it
goes largely unrecognized, and no thought is given to those littermates
who are carriers.
When a puppy suspected of having JRD is diagnosed, or dies, the client should
be referred to researchers by the veterinarian involved in his/her care.
If that does not occur, the affected puppy will have died without it's death
having contributed to the valuable fund of information. In these cases,
the puppy and the entire litter is wasted and lost to us for research purposes.
Unless veterinarians are aware of the ongoing research and the need for
referral of these puppies, we will not be successful in obtaining the data
that is necessary to understand JRD.
Veterinarians can also encourage owners to have limited autopsies performed,
so that the kidney tissue can be examined under a microscope. If the cost
of a limited autopsy to examine the kidneys is a great financial burden
for a client, it is possible that we could find some financial assistance.
The mode of inheritance of JRD can be established from information about
the number of puppies born in a large number of affected litters and the
number of puppies in those litters who are affected by JRD. In addition
to the litter data, obtainable from the owner and breeder, we need data
from the veterinarian to confirm the diagnosis of JRD. Lab reports, ultrasound
reports, biopsy results and autopsy reports are all useful.
Several of the most heavily used standard poodle sires have been carriers
of JRD, and there is a high probability that a veterinarian with standard
poodle breeders or owners among his/her clients, will encounter this disease.
V Ongoing Research
The Department of Human Genetics at Michigan State University has a large
grant to be used in gene marker research on dogs. The initial effort will
be to develop 400 DNA probes in order to saturate the dogs' chromosomes
with the probes. After the probes have been established, screening can begin
for linkage of any dog disease gene of interest. Eventually, the benefits
will be that dogs will be able to be screened for the carrier state of the
gene. This research will not be completed for many years.
In order to carry out screening for linkage for this or any other genetic
disease, pedigrees of 15-20 litters in which there are at least two affected
and two unaffected puppies must be identified. Cheek swabs (buckle smears)
from at least two affected puppies and two unaffected puppies in each litter,
as well as from both parents have to be made available for study. Puppies
from a repeat breeding are considered littermates for this purpose.
Several other universities, Texas A & M, and the University of California
at Berkeley (The Dog Genome Project) with the University of Oregon, are
involved in canine DNA research, as is Cornell University. If the mode of
inheritance of a disease is known, screening for the DNA marker(s) becomes
easier and less expensive.
George Lees, DVM, Professor of Medicine at Texas A & M University, has
a grant to study JRD in English cocker spaniels. The JRD in cockers is a
form of hereditary nephritis, and is not the same disease as that seen in
standard poodles. He and his researchers are using electron microscopy,
and intend to search for the genetic basis of that disease in English cocker
spaniels when more funds become available. Their research will include other
breeds as well, but they are only investigating hereditary nephritis. (9)
Waiting for DNA testing to become readily available is not a feasible solution
to the problems of genetic diseases. Selectively breeding away from carriers
now is the only responsible action.
Registries for many canine diseases are being established at the The Institute
for Genetic Disease Control In Animals. (10) Clearly, an open registry such
as the one established at the GDC in July, l992, for sebaceous adenitis
in standard poodles (this disease also occurs in about 30 breeds) is an
important step forward and an invaluable resource. In Europe, open registries
have made it possible for breeders to greatly reduce the number of cases
of some genetic disorders.
I have collected pedigrees of 75 litters of an American Champion sire. There
are a large number of Champions among his offspring. In at least two of
these litters there was one puppy with JRD. The sire is therefore a carrier,
and, on average, half of the puppies in every one of his litters are carriers.
The possibility that JRD will touch every standard poodle breeder eventually
is likely. By the time it does, it will be difficult if not impossible to
eliminate from the breed.
VI Prior Research
Several articles on JRD and familial renal disease were published in veterinary
journals in the 1970s, and others have been published since that time on
juvenile or familial renal diseases in Doberman pinschers, Alaskan malamutes,
Norwegian elkhounds, bull terriers, Airedale terriers, bedlington terriers,
boxers, King Charles spaniels, keeshunden, Yorkshire terriers, Newfoundlands,
and samoyeds. (1) These diseases have also been reported in rottweilers,
chow chows, miniature schnauzers, shih tzus, Lhasa apsos, soft coated wheaten
terriers, Portuguese water dogs, Chinese shar- peis, and cocker spaniels,
among others. (2,11 ) There was a recent report in the Veterinary News section
of the AKC Gazette, that it is being seen in golden retrievers, as well,
a breed in which it had not before been recognized. An article written by
Stephen DiBartola, et al., JRD in related standard poodles, appeared in
JAVMA in September, 1983, and provides references to the literature prior
to that date. (12) Dr. DiBartola also lists more recent references in his
chapter, Familial Renal disease in Dogs and Cats, Textbook of Veterinary
Internal Medicine. (2)
Acknowledgements: I thank the following people for their generosity and
time in providing me with a greater understanding of this disease, in conversation,
in letters, and on-line: Kenneth Bovee, DVM, University of Pennsylvania;
George Brewer, MD, University of Michigan; Larry Cowgill, DVM, University
of California, Davis; Stephen P. DiBartola DVM, Ohio State University; George
Lees, DVM, Texas A & M University; Barbara Licht, PhD, Florida State
University, Tallahassee; George Padgett, DVM, Michigan State University;
Dianne Sequoia, DVM, Berkeley, California; Sue Tornquist, DVM, Washington
State University; and the wonderful veterinarians on VETMED-L. Any errors
are my own, and not those of the veterinarians with whom I spoke or corresponded.
Susan Fleisher
I can be reached at:
74723.1637@compuserve.com
fax 510 549-1381
phone 510 527-0793
2112 Eunice Street, Berkeley, CA 94709-1417
(c) Copywrite 1996. This article may be reprinted without permission
only in its entirety. I would appreciate being sent a copy of any publication
in which it appears.
A "Problem Specific Data Base for Renal Failure in Immature Dogs"
is included in the chapter on renal disease in Veterinary Pediatrics, Dogs
& Cats from Birth to Six Months, 2nd edition, as is a table on "Medical
Management of Chronic Renal Failure". (1)
1. Kruger, J.M., Osborne, C.A., et al. : Congenital and Hereditary Disorders
of the Kidney. Veterinary Pediatrics Dogs & Cats from Birth to Six Months.,
2nd edition. (J.D. Hoskins, ed.) W.B.Saunders, Philadelphia, Pa, 1995: pp
401-406.
2. DiBartola Stephen P. et al: Familial Renal disease in Dogs and Cats.
Textbook of Veterinary Internal Medicine. (S.J. Ettinger, & E.C. Feldman,
ed) W.B. Saunders, Philadelphia, Pa. 1995:pp 1796-1801.
3. McMaw, D.l; Fleming, E.J.; Mikiciuk, M.G. : Chronic renal failure in
dogs: Managing an irreversible condition. Symposium on Renal disease. Veterinary
Medicine; March 1989; p 297-303.
4. Kenneth Bovee, DVM (University of Pennsylvania); Stephen DiBartola, DVM
(Ohio State University); and George Padgett, DVM (Michigan State University
may be contacted for referrals.
5.. Polzin, D.J.; Osborne, C.A.: Update - Conservative Medical Management
of Chronic Renal Failure. Current Therapy IX (R.W. Kirk, ed.) W. B. Saunders,
Philadelphia, PA., 1986 pp 1167-1173.
6. Finco, D.R.: The Role of Phosphorus Restriction in the Management of
Chronic Renal Failure of the Dog and Cat; Proc. 7th Kal Kan Sypm. . Veterinary
Learning Systems, Lawrenceville, NJ 1983; pp 131-133
7. Willis, Malcolm B: Genetics of the Dog. Howell Book House, New York,
NY, 1989;p 356
8. Poodle Variety, Santa Barbara, CA, February-March 1996, pp 88-89
9. personal correspondence September 5,1995.
10. GDC, P.O. Box 222, Davis CA 95617. telephone or fax 916 756-6773
11. Crawford, M.A.:The Kidneys, Congenital and Inherited Disorders.Veterinary
Pediatrics Dogs & Cats from Birth to Six Months. (J.D. Hoskins, ed.)
W.B. Saunders, Philadelphia, Pa, 1990: pp 272-276.
12. DiBartola S.P., Chew D.J., et al: Juvenile Renal Disease in related
Standard Poodles. JAVMA:183:693-696.
Bovee, K.C.: Overview of the Uremic Syndrome. Current Veterinary Therapy
VII (R.W. Kirk, ed.) W.B. Saunders. Philadelphia, Pa., 1980. pp 1079-1080.
Chew, D.J.; DiBartola, S.P.: Manual of Small Animal Nephrology and Urology.
Churchill Livingston. New York, NY. 1986; pp 1-78.
Krawiec, D.R.: Renal Failure in Immature Dogs. JAAHA 23:101-107; 1987.
McMaw, D.l; Fleming, E.J.; Mikiciuk, M.G.. : Selecting the right diagnostic
tests for renal disease. Symposium on Renal disease. Veterinary Medicine;
March 1989; pp 297-303.
McMaw, D.l; Fleming, E.J.; Mikiciuk, M.G. : Interpreting the results of
urinalysis: A key to diagnosing renal disorders. Symposium on Renal Disease.Veterinary
Medicine; March 1989; p 281-286.
Picut, G.A.; Lewis. R.M.: Comparative Pathology of Canine Hereditary Neuropathies:
An Interpretive Review. Vet. Res. Comm. 11:561-581; 1987.
Picut, G.A.; Lewis, R.M.: Microscopic Features of Canine Dysplasia. Vet.
Path. 24:158-163; 1987.
For information specifically on glomerulophy in Newfs see:
"Veterinary Pediatrics: Dogs and Cats from Birth to Six Months",
page 402, second edition, WB Saunders Co., 1996, ed. John D. Hoskins DVM.
Also check out the information at these sites:
