kidney disease (PKD) is a
genetic disorder characterized by
the growth of numerous cysts in the
kidneys. The cysts are filled with
fluid. PKD cysts can slowly replace
much of the mass of the kidneys, reducing
kidney function and leading to kidney
kidneys are two organs, each about the size
of a fist, located in the upper part of
a person's abdomen, toward the back. The
kidneys filter wastes from the blood to
form urine. They also regulate amounts of
certain vital substances in the body.When
PKD causes kidneys to fail—which usually
happens after many years—the patient
requires dialysis or kidney transplantation.
About one-half of people with the major
type of PKD progress to kidney failure,
also called end-stage renal disease (ESRD).
can cause cysts in the liver and problems
in other organs, such as the heart and blood
vessels in the brain. These complications
help doctors distinguish PKD from the usually
harmless "simple" cysts that often
form in the kidneys in later years of life.
the United States, about 500,000 people
have PKD, and it is the fourth leading cause
of kidney failure. Medical professionals
describe two major inherited forms of PKD
and a noninherited form:
is autosomal dominant PKD?
dominant PKD is one of the most common
inherited disorders. The phrase "autosomal
dominant" means that if one parent
has the disease, there is a 50-percent
chance that the disease will pass to a
child (see Genetic Diseases). At least
one parent must have the disease for a
child to inherit it. Either the mother
or father can pass it along, but new mutations
may account for one-fourth of new cases.
In some rare cases, the cause of autosomal
dominant PKD occurs spontaneously in the
child soon after conception—in these
cases the parents are not the source of
people with autosomal dominant PKD live
for decades without developing symptoms.
For this reason, autosomal dominant PKD
is often called "adult polycystic
kidney disease." Yet, in some cases,
cysts may form earlier, even in the first
years of life.
disease is thought to occur equally in
men and women and equally in people of
all races. However, some studies suggest
that it occurs more often in whites than
in blacks and more often in females than
cysts grow out of nephrons, the tiny filtering
units inside the kidneys. The cysts eventually
separate from the nephrons and continue
to enlarge. The kidneys enlarge along
with the cysts (which can number in the
thousands), while retaining roughly their
kidney shape. In fully developed PKD,
a cyst-filled kidney can weigh as much
as 22 pounds. High blood pressure occurs
early in the disease, often before cysts
are the symptoms of autosomal dominant
most common symptoms are pain in the back
and the sides (between the ribs and hips),
and headaches. The dull pain can be temporary
or persistent, mild or severe. People
with autosomal dominant PKD also can experience
- urinary tract
- hematuria (blood
in the urine)
- liver and pancreatic
- abnormal heart
- high blood
- kidney stones
- aneurysms (bulges
in the walls of blood vessels) in the
(small sacs on the colon)
is autosomal dominant PKD diagnosed?
To diagnose autosomal dominant PKD, a
doctor typically observes three or more
kidney cysts using ultrasound imaging.
The diagnosis is strengthened by a family
history of autosomal dominant PKD and
the presence of cysts in other organs.
- How is
autosomal dominant PKD treated?
a cure for autosomal dominant PKD is not
available, treatment can ease the symptoms
and prolong life.
A doctor will first suggest over-the-counter
pain medications, such as aspirin
or Tylenol. For most but not all cases
of severe pain, surgery to shrink
cysts can relieve pain in the back
and flanks. However, surgery provides
only temporary relief and usually
does not slow the disease's progression
toward kidney failure.
that are severe or that seem to feel
different from other headaches might
be caused by aneurysms, or swollen
blood vessels, in the brain. Headaches
also can be caused by high blood pressure.
People with autosomal dominant PKD
should see a doctor if they have severe
or recurring headaches—even
before considering over-the-counter
tract infections. Patients
with autosomal dominant PKD tend to
have frequent urinary tract infections,
which can be treated with antibiotics.
People with the disease should seek
treatment for urinary tract infections
immediately, because infection can
spread from the urinary tract to the
cysts in the kidneys. Cyst infections
are difficult to treat because many
antibiotics do not penetrate into
the cysts. However, some antibiotics
blood pressure. Keeping blood
pressure under control can slow the
effects of autosomal dominant PKD.
Lifestyle changes and various medications
can lower high blood pressure. Patients
should ask their doctors about such
treatments. Sometimes proper diet
and exercise are enough to keep blood
renal disease. Because kidneys
are essential for life, people with
ESRD must seek one of two options
for replacing kidney functions: dialysis
or transplantation. In hemodialysis,
blood is circulated into an external
machine, where it is cleaned before
reentering the body; in peritoneal
dialysis, a fluid is introduced into
the abdomen, where it absorbs wastes,
and it is then removed. Transplantation
of healthy kidneys into ESRD patients
has become a common and successful
procedure. Healthy (non-PKD) kidneys
transplanted into PKD patients do
not develop cysts
recessive PKD is caused by a particular
genetic flaw that is different from
the genetic flaw that causes autosomal
dominant PKD. Parents who do not have
PKD can have a child with the disease
if both parents carry the abnormal gene
and both pass the gene to their baby.
The chance of this happening (when both
parents carry the abnormal gene) is
one in four. If only one parent carries
the abnormal gene, the baby cannot get
the disease. The
symptoms of autosomal recessive PKD
can begin before birth, so it is often
called "infantile PKD." Children
born with autosomal recessive PKD usually
develop kidney failure within a few
years. Severity of the disease varies.
Babies with the worst cases die hours
or days after birth. Children with an
infantile version may have sufficient
renal function for normal activities
for a few years. People with the juvenile
version may live into their teens and
twenties and usually will have liver
problems as well.
are the symptoms of autosomal recessive
Children with autosomal recessive PKD
experience high blood pressure, urinary
tract infections, and frequent urination.
The disease usually affects the liver,
spleen, and pancreas, resulting in low
blood-cell counts, varicose veins, and
hemorrhoids. Because kidney function is
crucial for early physical development,
children with autosomal recessive PKD
are usually smaller than average size.
is autosomal recessive PKD diagnosed?
imaging of the fetus or newborn baby
reveals cysts in the kidneys but does
not distinguish between the cysts of
autosomal recessive and autosomal dominant
PKD. Ultrasound examination of kidneys
of relatives can be helpful; for example,
a parent or grandparent with autosomal
dominant PKD cysts could help confirm
diagnosis of autosomal dominant PKD
in a fetus or child. (It is extremely
rare, although not impossible, for a
person with autosomal recessive PKD
to become a parent.) Because autosomal
recessive PKD tends to scar the liver,
ultrasound imaging of the liver also
aids in diagnosis.
- How is
autosomal recessive PKD treated?
Medicines can control high blood pressure
in autosomal recessive PKD, and antibiotics
can control urinary tract infections.
Eating increased amounts of nutritious
food improves growth in children with
autosomal recessive PKD. In some cases,
growth hormones are used. In response
to kidney failure, autosomal recessive
PKD patients must receive dialysis or
transplantation (see End-stage renal
Cystic Kidney Disease
- What is
develops in kidneys with long-term damage
and bad scarring, so it often is associated
with dialysis and end-stage renal disease.
About 90 percent of people on dialysis
for 5 years develop ACKD. People with
ACKD can have any underlying kidney
disease, such as glomerulonephritis
or kidney disease of diabetes. The cysts
of ACKD may bleed. Kidney tumors, including
kidney (renal) cancer, can develop in
people with ACKD. Renal cancer is rare
yet occurs at least twice as often in
ACKD patients as in the general population.
- How is
with ACKD usually seek help because
they notice blood in their urine (hematuria).
The cysts bleed into the urinary system,
which discolors urine. Diagnosis is
confirmed using ultrasound, CT scan,
or MRI of the kidneys.
- How is
ACKD patients are already receiving
treatment for kidney problems. In rare
cases, surgery is used to stop bleeding
of cysts and to remove tumors or suspected
have begun to identify the processes that
trigger formation of PKD cysts. Advances
in the field of genetics have increased
our understanding of the abnormal genes
responsible for autosomal dominant and autosomal
recessive PKD. Scientists have located two
genes associated with autosomal dominant
PKD. The first was located in 1985 on chromosome
16 and labeled PKD1. PKD2 was localized
to chromosome 4 in 1993. Within 3 years,
the scientists had isolated the proteins
these two genes produce—polycystin-1
both of these genes are normal, the proteins
they produce work together to foster normal
kidney development and inhibit cyst formation.
A mutation in either PKD1 or PKD2 can lead
to cyst formation, but evidence suggests
that the disease development also requires
other factors, in addition to the mutation
in one of the PKD genes.
analyses of most families with PKD confirm
mutations in either the PKD1 or PKD2 gene.
In rare cases, however, families with PKD
have been found to have normal PKD1 and
PKD2 genes. As a result, researchers theorize
that a PKD3 gene exists, but that gene has
not been mapped or identified.
recently identified the autosomal recessive
PKD gene (called PKHD1) on chromosome 6.
No genetic test kit is yet available to
detect mutations in PKHD1.
have bred mice with a genetic disease that
parallels both inherited forms of human
PKD. Studying these mice will lead to greater
understanding of the genetic and nongenetic
mechanisms involved in cyst formation. In
2000, scientists reported that a cancer
drug was successful in inhibiting cyst formation
in mice with the PKD gene. In 2003, scientists
also demonstrated that another compound,
one that blocks function of a kidney receptor,
inhibits cyst formation in mice with the
ADPKD or ARPKD gene. The scientists hope
that further testing will lead to safe and
effective treatments for humans.
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