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rec.pets.dogs: Juvenile Renal Disease
Last-modified: 07 Nov 1997
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Juvenile Renal Disease
Susan L. Fleisher, . Copyright 1996, all rights
Table of Contents
* Recognizing the Problem
* Eliminating JRD
In January of 1990, I had my twenty one month old Standard Poodle
puppy put down. She was one of three puppies in a litter of eleven to
die of Juvenile Renal Disease. All three of the puppies with the
disease appeared healthy and grew normally until clinical signs
appeared at ten months in one, and twenty months in the other two. She
died two weeks after being diagnosed. The disease is devastating. The
prognosis is dismal. Nobody expects to lose a puppy of that age. I
have been collecting information since her death on the disease that
Despite the fact that several articles on Juvenile Renal Disease and
Familial Renal Disease were published in veterinary journals in the
1970s, and many others have been published since that time on JRD in
Dobermans Pinchers, Alaskan Malamutes, Norwegian Elkhounds and
Samoyeds as well as in Standard Poodles, most individual cases of JRD
are treated by owners and veterinarians as isolated occurrences rather
than as the manifestation of a genetic disease. The disease is also
well known in Rottweilers, Shiz Tsus and Lhasa Apsos, and is seen in
Soft Coated Wheaten Terriers, Portuguese Water Dogs, Shar Peis,
Miniature Schnauzers, and Cocker Spaniels, among others. It is now
being seen in Golden Retrievers, a breed in which it had not before
Early symptoms of Juvenile Renal Disease include drinking copious
amounts of water, something that might not be readily apparent in a
house with more than one dog, frequent urination, and dilute urine
which has little color or odor. Some affected puppies will leak urine,
others won't. As the disease progresses, vomiting, weight loss,
anorexia, lethargy, and muscle weakness are seen. There is often a
chemical odor to the breath, and teeth are sometimes discolored. Some
puppies grow normally until they are diagnosed, and some appear as
failures to thrive.
Treatment for JRD consists of a low protein prescription diet, Hill's
K/D, and, in addition, IV fluids can be given to act as a kind of
dialysis. Epogen, an expensive drug which needs to be carefully
monitored, can be also be given to treat the hypoproliferative anemia
of chronic renal failure. Some Veterinary schools are experimenting
with kidney transplants, but transplanted kidneys in dogs are commonly
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 do know of several dogs who have JRD with less severe kidney
involvement, and who are being well maintained on low protein diets.
These dogs are both more than three years old, and were diagnosed
before they were symptomatic. One because his litter was decimated by
the disease, and one because his vet was giving free BUN tests to
Recognizing the Problem
If a breeder is informed about a medical problem in a puppy she has
sold, and often she is not, or, if just the owner of the dam is
informed, and it is only one puppy in a litter about whom she is
informed, it is usually treated as an isolated incident. Unless there
are multiples in a litter, and the breeder is informed about each, the
fact that the illness from which a puppy is suffering is a genetic
disease is not recognized, and no recognition is made nor thought
given to those littermates who are carriers. Without an understanding
of the genetics involved, and most veterinarians treat isolated
incidences as being from an unknown cause rather than as Juvenile
Renal Disease, veterinarians are unable to offer counseling to
breeders, and more and more carriers are unknowingly bred. In the
breeds in which JRD is known to occur many of the puppies who fall
into the "fading puppy syndrome" and die at a young age may well have
died of JRD. Many stillborn puppies are victims of this disease.
Often, however, an affected puppy will grow normally until it is
between ten and twenty four months of age before it is symptomatic,
diagnosed and dies.
George Padgett, D.V.M., a geneticist and professor of pathology at
Michigan State University, told me that JRD affects about 20 breeds.
In most of the breeds in which it has been studied it is a simple (one
gene), autosomal (not sex linked), recessive (both parents have to
carry the gene) disease. Both parents of an affected puppy are
therefore defined carriers. The presence of just one affected puppy
determines that both parents are carriers. Littermates of an affected
puppy have a 66% chance of being carriers. Aunts and uncles of an
affected puppy have a 50% chance of being carriers, as do
grandparents. According to Dr. Padgett, if a sire has produced an
affected puppy, and is therefore a defined carrier, he has also proven
bitches who are probably clear: those who when bred to him have
produced sizeable litters in which there were no affected puppies.
"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' book
Genetics of The Dog. If the disease is caused by a simple autosomal
recessive gene, both parents must be carriers of the gene to produce
an affected puppy. However, even if only the sire or only the dam is a
carrier, the other parent being clear, 50% of all the puppies born are
carriers themselves. If the cause of JRD is polygenic, several genes
would be necessary collectively in order for the disease to occur. In
Samoyeds the mode of inheritance is now known to be x-linked
recessive. In that breed, only males are affected with the disease,
but females pass it on through the x chromosome.
Among the pedigrees I have collected are those of twenty five litters
of an American Champion sire. There are a large number of American
Champions among his offspring. In two of these litters there was one
puppy with JRD. The sire is therefore a carrier, and half of the
puppies in every one of his litters are carriers. This is just one
si the arithmetic is stunning. The possibility that this will not
eventually touch every breeder in the breeds in which it is known is
unlikely, and, by the time it does, it will be difficult if not
impossible to eliminate.
In order for Juvenile Renal Disease, sometimes called Familial Renal
Disease, Renal Dysplasia, or Congenital Hypoplasia to be studied in
any breed, several things have to occur. Breeders of breeds affected
by this disease should have any stillborn pups and all pups who die
before being sold, autopsied, if only to look for this one disease. If
the puppy is seen to have JRD, (the kidney cells actually have to be
studied under a microscope, since occasionally the kidneys appear
normal to the naked eye), the rest of the litter can be tested.
Bloodwork should be done to look for an elevated BUN, and urine tested
to establish a urine protein creatinine ratio. Unaffected litter mates
should all be considered carriers, since there is no way to
distinguish a carrier from a non carrier puppy. The only positive
outcome of having an affected litter that I can think of is that it
enables the breeder to identify carriers and potential carriers. Every
affected litter has the potential to stop carriers from producing more
carriers. If an autopsy shows that a puppy did not die of JRD, that is
also useful information. I realize that post mortem examinations are
expensive, though a restricted exam to look for one specific finding
would be much less expensive. I can assure anyone that is infinitely
more expensive on an emotional as well as a financial basis not to
have an autopsy done to look for this disease. Once carriers and dogs
who are clear have been identified, concerned and careful breeders can
work to systematically breed the disease out.
George Lees, DVM of Texas A & M University is currently doing
reasearch on Juvenile Renal Disease in Cocker Spaniels. The Soft
Coated Wheaten Terrier Club of America is sponsoring research by Dr.
Shelley Vaden at the North Carolina State University College of
Veterinary Medicine. Dr Vaden is collecting health records on SCWT,
and she has established a breeding colony.
The Department of Human Genetics at Michigan State University has a
large grant to be used in gene marker research. 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 the meantime, since the funding is sufficient only
to develop the probe system and not to study any particular disease,
funding will have to be provider by breeders themselves or by other
outside sources for the study of specific disease gene projects. For
the first few individual studies, the estimate is that the cost will
run from $25,000 to $50,000 to screen through the 400 probes to
establish a close linkage. 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. Blood samples from at least two affected puppies and
two unaffected puppies in each litter, as well as from both parents
have to be available for study. Puppies from a repeat breeding are
considered littermates for this purpose. The blood samples can, of
course, be stored for future use. Several other universities, such as
Texas A & M and the University of California at Berkeley are involved
in DNA research also.
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. In some
instances, careful breeders have succeeded in largely eradicating some
genetic disorders from their breeds. Success depends on a number of
factors. Every puppy buyer must be encouraged to report any major
illness back to the breeder. Breeders must have a clear understanding
of the modes of transmission of genetic disorders that affect their
breeds. Known carriers as well as possible carriers, (littermates and
offspring of those discovered to be carriers) must be conscientiously
kept out of the gene pool. A method of communication among breeders
must be established. Clearly, an open registry such as the open
registry begun in July, l992 for Sebaceous Adenitis in Standard
Poodles (this disease also occurs in other breeds) is an important
step forward and an invaluable resource. Registries in many canine
diseases are being established at the GDC (Genetic Disease Control) in
Davis, California. In Europe, open registries have made it possible
for careful breeders to greatly reduce the number of cases of some
An open registry would include the names of carriers of the disease as
well as the names of dogs who are clear, those who when bred to a
carrier did not produce any cases of the disease in a litter of
significant size. Obviously, the early onset of Juvenile Renal Disease
allows carriers to be identified much sooner than does a disease which
manifests itself later in life.
Malcolm B. Willis wrote in his introduction to Genetics of The Dog,
"We are the custodians of our chosen breeds during the relatively
short period of our dog breeding lives. It behoves us to hand over the
material we breed with in a better state than when we received it or
we have achieved nothing and the breeds we profess to love will be the
Contributed by Maria Unson,
* Thomas DA.
+ Juvenile renal disease in a dobermann [letter].
+ Veterinary Record, 1984 Oct 27, 115(17):446-7.
* DiBartola SP; Chew DJ; Boyce JT.
+ Juvenile renal disease in related Standard Poodles.
+ Journal of the American Veterinary Medical Association, 1983
Sep 15, 183(6):693-6.
+ Abstract: Chronic renal failure was diagnosed in 6 young
Standard Poodles from 2 related litters. Clinically, the
disease was characterized by polydipsia, polyuria, anorexia,
lethargy, vomiting, and bony deformities suggestive of
fibrous osteodystrophy. Laboratory evaluation revealed
azotemia and hypercholesterolemia in all 6 dogs and
nonregenerative anemia in 3 dogs. Two dogs had
hyperphosphatemia and another 2 were hypercalcemic.
Isosthenuria and proteinuria were found in both dogs for
which urinalyses were available. The kidneys were
characterized pathologically by interstitial fibrosis,
variable interstitial infiltrates of lymphocytes and plasma
cells, tubular atrophy, tubular dilatation, tubular basement
membrane mineralization, cystic glomerular atrophy, and
immaturity of glomeruli, with inconspicuous capillary lumens.
* Chew DJ; DiBartola SP; Boyce JT; Hayes HM Jr; Brace JJ.
+ Juvenile renal disease in Doberman Pinscher dogs. Journal of
the American Veterinary Medical Association, 1983 Mar 1,
+ Abstract: Renal failure was diagnosed in 22 young Doberman
Pinscher dogs. The clinical findings were anorexia, weight
loss, vomiting, lethargy, polydipsia, polyuria, and
dehydration. Laboratory findings were azotemia,
hyperphosphatemia, lymphopenia, nonregenerative anemia,
hypercholesterolemia, and proteinuria. The kidneys were
characterized pathologically by glomerular sclerosis, cystic
glomerular atrophy, tubular dilatation, tubular atrophy,
mononuclear interstitial inflammation, interstitial fibrosis,
interstitial mineralization, and hyperplasia of the
collecting duct epithelium.
* Picut CA; Lewis RM.
+ Juvenile renal disease in the Doberman Pinscher:
ultrastructural changes of the glomerular basement membrane.
Journal of Comparative Pathology, 1987 Sep, 97(5):587-96.
+ Abstract: Ten cases of juvenile renal disease in Doberman
Pinschers were examined by light microscopy and 8 of them
additionally by electron microscopy. Two distinct basic
ultrastructural lesions of the glomerular basement membrane
(GBM) were observed. One is characterized by lamellation of
the lamina densa with intramembranous focal areas of lucency
containing electron-dense particles, the second by diffuse
attenuation of the lamina densa with intramembranous and/or
subendothelial deposition of matrix entrapping cross-banded
fibres (collagen). Based on similar ultrastructural changes
in other hereditary nephropathies in man and dogs, a
metabolic or biochemical basis for the structural lesions is
* Rosenbruch M., [Pathomorphology of so-called juvenile renal
disease in the dog].
+ Zentralblatt fur Veterinarmedizin. Reihe A, 1986 Mar,
33(3):193-207. Language: German.
* Morton LD; Sanecki RK; Gordon DE; Sopiarz RL; Bell JS; Sakas PS.
+ Juvenile renal disease in miniature schnauzer dogs.
Veterinary Pathology, 1990 Nov, 27(6):455-8.
Juvenile Renal Disease
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