Basic Information about Dense Deposit Disease (one of the rarest of the rare diseases . . . )

Introducing Jamie Sue

Jamie Sue Turner of Runnells, Iowa is 8 years old and in the second grade. She’s somewhat of a girly-girl favoring the color pink, singing and dancing, and Disney TV fare such as “Hannah Montana.” Her beauty is certainly more than skin deep, yet her wide smile and large, expressive eyes  no doubt added to the "total package" that won her a tiara in a children's beauty pageant at the Iowa State Fair in 2009. But little girls are made of sugar AND spice, are they not? In addition to hobbies like scrapbooking, Jamie Sue is a tough cookie who plays on a youth softball team in the summer.

Until recently, Jamie Sue has enjoyed the kind of idyllic childhood that we all cherish. Her life has revolved around her large family, many friends, pet dogs, hobbies, school and social activities. Due to circumstances beyond her control, Jamie has spent much more of her time at the University of Iowa Hospital in Iowa City than she has at home over the past 10 weeks. You could say Jamie has added another dimension to her active life, and she’s proving that in addition to everything else, she is a tenacious fighter.

Jamie Sue was the picture of robust health until something alarming occurred on December 15, 2009. That evening her ankles were unaccountably swollen. The next day Jamie Sue was at her doctor's office where it was revealed that her kidneys were responsible for the fluid retention.  Early treatment and intervention didn't resolve the symptoms, and her journey within the medical system was well underway . . .  A kidney biopsy early in the course of her illness established a diagnosis of Dense Deposit Disease, a rare autoimmune condition that affects the kidneys.

Dense Deposit Disease (DDD) is the second, and more serious, type of Membranoproliferative Glomerulonephritis. DDD usually leads to chronic kidney failure and the need for regular kidney dialysis. Typically there is a window of time (8-10 years) before the disease damages the kidneys to that extent. Unfortunately, Jamie Sue is an exception to the rule. Her experience with DDD has been rapid and unrelenting so that she is already battling imminent chronic kidney failure as physicians strive to slow the progression of the disease. At the moment, Jamie Sue is receiving a combination of plasmapheresis and occasional renal dialysis for two purposes: to prevent her immune system from continually damaging her kidneys by removing the certain "bad" proteins from her blood, and to cleanse her blood of toxic waste products and excess fluids. Soon Jamie expects to begin clinical trials to determine whether a hopeful new medication may better spare her kidneys from continued damage by her immune system.

About Dense Deposit Disease

 

It’s been written that Dense Deposit Disease (DDD) is rare even among rare diseases.  DDD makes its appearance in childhood, usually between the ages of 5 and 15 years of age.  Experts have estimated that DDD occurs in only two to three people out of 1 million. We can do the math to demonstrate how DDD is “rare among rare” diseases. Taking a rough estimate of 304 million U.S. citizens and expecting to find 2 to 3 cases of DDD per 1 million, we can estimate that significantly less than 1,000 Americans would be afflicted with Dense Deposit Disease. To gain even more perspective, keep in mind that in the U.S. diseases are officially designated as “rare” when less than 200,000 Americans are affected. (So even if there were 200 times more cases of DDD in the U.S., this condition would still fall into the “rare” category.)

 

Basic Information about Dense Deposit Disease

 

A lot of great scientific articles have been written about Dense Deposit Disease. This blog entry doesn’t pretend to be one of them. Instead, this piece intends to take a complicated disease and break some of the key features into understandable concepts in order to help parents, family, and friends be better informed about this condition. When a serious illness affects a child that we love, we want to learn as much as we can in order to be helpful and supportive. As parents we want to know as much as possible in order to advocate for our children. Scientific literature is written in a language all its own and often with explanations that may include unfamiliar and confusing terms. (It’s always best to jot down specific questions as you think of them to ask your child’s physicians). For a great website written by experts who manage and study Dense Deposit Disease, visit the University of Iowa’s website devoted to DDD, it's called Kidneeds, and if you are affected by DDD in some way, you will want to check it out.

What’s in a Name . . . ?

In medical jargon, many diseases and conditions have more than one name. When you are looking for information about Dense Deposit Disease, you will also see it referred to as Membranoproliferative Glomerulonephritis Type II (or MPGN II). Scientists originally felt that Dense Deposit Disease was a variation of two similar types of kidney diseases, therefore it was differentiated by calling it “MPGN Type II.” However, in recent years scientific research has discovered that the unique features of this particular variation makes the name Dense Deposit Disease more appropriate. So although MPGN II is an “older” term, you will still see it in literature about this condition.

What are Dense Deposits?

Physical signs and symptoms are present when the kidneys are functioning poorly.  Nephrotic Syndrome, is a term that refers to the combined signs and symptoms that occur when the kidneys are unhealthy.  More information and test results may be necessary before the physician is able to pinpoint a specific reason for the kidney dysfunction.

A kidney biopsy is necessary to diagnose DDD. This procedure gathers evidence of the underlying reason for kidney damage and allows the physician to make a definite diagnosis. When the tissue from the biopsy is examined with an electron microscope, the unique features of Dense Deposit Disease are clear to the trained eye. As the body’s immune system has malfunctioned, certain proteins have "gone crazy" and started to attack an important membrane deep within the kidneys; bits and pieces of the rogue proteins end up "stuck" to the kidney’s membrane in thick ("dense") ribbon-like patches ("deposits").

An Autoimmune Disease

Dense Deposit Disease is an autoimmune disease.  This means that the patient with DDD is suffering an attack  from within; their kidneys are damaged by their own immune system.

In theory our immune system protects our bodies from outside invaders such as viruses and bacteria.  Sometimes, for reasons that are not well understood, a “glitch” in the immune system causes it to go out of sync.  The out-of-sync immune system triggers proteins that usually protect us to, instead, attack healthy tissues within our bodies by mistake. There are more than 80 different types of autoimmune disorders; each one has resulted from a glitch that is aimed at a specific organ or tissue type. Some well-known examples of autoimmune diseases and their specific targets include Multiple Sclerosis in which nerve sheaths are damaged; Lupus, which affects connective tissue throughout the body; Type 1 Diabetes in which insulin-producing cells of the pancreas are destroyed; and Crohn’s Disease and Ulcerative Colitis which both affect the lining of the digestive tract. Autoimmune disorders are chronic in nature meaning they are not reversible, but there are specific treatments for most autoimmune illnesses that can control or manage the condition.

Why an autoimmune illness affects one person and not another is still a mystery. Roughly 5% of the population is afflicted by some type of autoimmune condition. A number of theories have been introduced to try to explain what goes wrong.  Heredity, environmental factors, viruses and certain drugs have been suggested. It may be that a combination of just the “right” factors is all it takes for the immune system to make a mistake that will spiral out of control and direct damage towards a specific tissue in our body. Much research is directed towards unlocking the secrets behind what really triggers an autoimmune disease. It’s intriguing (and frustrating) that over the years evidence shows that even with identical twins, one twin may be afflicted by an autoimmune disease while the other stays completely healthy.

Glomerular Basement Membrane

An anatomy and physiology reference is the best source for an in-depth understanding of the intricate and complex means in which the complement proteins of the immune system attack and damage the glomerular basement membrane (GB Membrane) in Dense Deposit Disease. However, I can give you a few key points in layman’s terms to provide a very basic understanding of what this illness entails.

The glomerular basement membrane is the part of the kidney that filters extra fluid and waste products out of the blood. On one side of the GB Membrane is the bloodstream, on the other side of the GB Membrane is urine. The fluid and waste that are filtered out of the blood cross the GB Membrane to become components in urine and are ultimately eliminated from the body in the usual way. 

When the immune system damages the GB Membrane, it no longer filters properly. Proteins that circulate in our blood have various important "jobs" to perform within the body so we certainly don't want to lose them. When our kidneys are healthy, there is very little chance of that happening.  Proteins are simply too large to go across a healthy GB Membrane. Unfortunately, a damaged GB Membrane does allow those large proteins to be filtered through, and with terrible consequences. When these useful proteins cross the GB Membrane, they are eliminated with the urine.  Because they are gone from the bloodstream, the specific jobs they are supposed to perform in the body are jeopardized.

(If you are having trouble visualizing this concept, imagine a trampoline--when the fabric is tight we can hit the surface and bounce back off without fear, but if we happen to bounce on a patch of fabric that is loose and frayed we may fall right through and hit the ground instead.  Instead of "bouncing off" the GB Membrane as they normally would, the large proteins go right on through the weakened membrane and are lost to the body when they are expelled by urination.)

With kidney disease the loss of proteins in urine results in a “Catch 22 scenario.” The same proteins that leave the body when the kidneys are damaged have functions that include absorbing unneeded fluids in the bloodstream. Without these proteins to soak them up, the extra fluid in the blood seeps back into the tissues and causes swelling (edema). Importantly, in addition to fluid, dangerous waste products such as creatinine and urea are also retained in the bloodstream.  These waste products eventually become toxic to tissue.  If the kidneys become too diseased to handle removal of these substances, kidney dialysis is essential.

High Blood Pressure, too . . .

 

Along with fluid retention from poor kidney function comes sodium retention.  Damage to the kidneys also causes an increase in a hormone the kidneys produce (called renin).  These three factors combine to cause dangerously elevated blood pressure which must be treated by medication. 

Signs and Symptoms of DDD

The early signs and symptoms of poor kidney function may be subtle.  When the kidneys are unhealthy enough to allow protein to enter the urine, the urine that is voided is often fizzy or frothy looking.  Red and white blood cells may also leak into the urine.  White blood cells tend to make the urine cloudy, while red blood cells may cause a red or pinkish hue (or they may only be detected by a lab test and not visible to the naked eye.)

More dramatic and obvious signs of kidney problems include:

• “Puffiness” or swelling (called edema) around the eyes, feet and ankles, hands, and abdomen.
• A general inability to concentrate and mental confusion.
• Dark, "tea-colored" urine. Dark urine is a symptom of glomerular problems and it is related to the inability of the kidneys to properly filter the waste products from the blood.(But dark urine can also be caused by other conditions and can even result from eating certain foods.) 

Treatment

Plasmapheresis is one way in which DDD is treated. Plasma is the “watery” part of our blood.  Among other things, plasma carries the components of the immune system that cause damage to the "good cells” in people with autoimmune illnesses. In DDD the object is to preserve kidney function for as long as possible, removing the damaging immune components has proven to be a helpful means of doing so.  This is done by plasmapheresis in which the patient’s blood is filtered through a machine that removes their plasma and replaces it with plasma from a donor. The donor plasma doesn’t contain the damaging autoimmune components, so the kidneys get a temporary break. With DDD, the patient's body will eventually produce more of the "bad" immune system proteins which will again be circulated in the bloodstream.  

Over time the damaging effects of DDD leads to chronic renal failure (abbreviated as CRF and also simply called "kidney failure").  About 50% of all individuals diagnosed with DDD will require regular dialysis within 8 to 10 years of diagnosis in order to stay alive. 

Kidney transplants have been performed on patients with DDD, but the nature of the disease makes this only a temporary benefit. The body attacks the donor kidney in the same manner that it attacked the original and the donated organ eventually fails. For patients with DDD and their potential kidney donors, the risk of transplant versus the limited benefit to the recipient makes it difficult for the medical establishment to easily recommend this option. 

Back to Jamie Sue . . .

Lately, as Jamie Sue ponders the future she envisions a career in medicine.  She wants to be a doctor.  She can do that.  She can do anything she wants to do.  Individuals with autoimmune conditions learn to adapt and live life to the fullest while managing their illness and undergoing whatever specific treatments that their disease requires.  Jamie Sue will do this . . . 

How Can You Help?

Support research that aims at finding a cure for DDD.  Participate in Fundraising via the Universtiy of Iowa's Kidneeds program which supports DDD research.

Donate Blood or Plasma.  Plasma donation is a great way to contribute and it costs only your time.  Learn more about the process in the article "Plasma Donation" from LifeShare Blood Centers.  

To learn more about blood donation opportunities and find a location near you:

• Visit American Red Cross website  or call them at 1-800-GIVE-LIFE (1-800-448-3543)
• Visit America's Blood Centers website or call 1-888-USBLOOD

All rights reserved for written content, Carolyn Cooper, MPH, RN, March 2010.

Photos of Jamie Sue Turner used by permission of Misty Turner; photos copyright of Misty Turner.

For Additional Reading:

National Kidney and Urologic Diseases Clearinghouse, "The Kidneys and How They Work"

National Organization for Rare Diseases, Membranoproliferative Glomerulonephritis Type II

Smith, R.J.H.; Sethi, S.; Zipfel, P.F. (2007). Dense Deposit Disease, Membranoproliferative Glomerulonephritis Type II, Accessed online.

Ferrario, F. & Rastaldi, M. P. (undated), Renal Pathology Learning, Type II Membranoproliferative Glomerulonephritis; Accessed online Mar. 3, 2010.

Appel, G.B.; Cook, H.T.; Hagerman, G.; Jeannette, J.C.; Kashgarian, M., Kirschfink, M.; et al. (2005 May; Epub 2005 Mar 30). Membranoproliferative glomerulonephritis type II (dense deposit disease): an update.  Journal of the American Society of  Nephrology, 16(5):1392-403.

Plasmapheresis, The free dictionary online, medical dictionary. 

. .. .

 

Another Black Box: Aranesp, Epogen, Procrit, What you should know about drugs that tell your body to make more red blood cells

Erythropoiesis Stimulating Agents (ESAs) tell your body to make more red blood cells. Drugs in this class include:

• Aranesp (darbopoetin alfa)
• Epogen (epoetin alfa)
• Procrit (epoetin alfa)
• There are other brand names & epoetin variants marketed worldwide

The Good News First . . .

Twenty years ago we didn’t have synthetic medications to treat anemia. Depending on the cause anemia was often treated through diet, by administering supplementary iron or vitamin B12, and frequently, by blood transfusions. The 1980's was a decade of concern over the safety of our blood supply due to blood borne pathogens such as Hepatitis B and C and the HIV virus. New technologies in recombinant DNA allowed science to explore and develop innovative alternative therapies.

In 1989, Epogen (epoetin alfa), the first of a class of drugs called erythropoiesis stimulating agents (abbreviated as “ESAs”), was approved by the FDA in the United States to treat patients suffering from anemia due to chronic kidney disease. Epogen was eventually joined by similar ESAs called Aranesp and Procrit and treatment was eventually broadened to include patients suffering from anemia related to chemotherapy.

The benefit to both groups was that they no longer needed to rely on frequent blood transfusions to treat their anemia. ESAs directly influence the body to speed up the production of its own red blood cells by introducing a synthetic version of the hormone erythropoietin. Erythropoietin is a chemical messenger of sorts with the specific mission of instructing our bone marrow to produce more red blood cells. Epogen, Aransep, and Procrit are easily given by a simple injection under the skin from one to three times per week.

So what exactly is anemia? Anemia results when we don’t have enough healthy red blood cells called erythrocytes circulating in our bloodstream. Healthy red blood cells are vital; they carry a protein called hemoglobin which picks up molecules of oxygen from our lungs and delivers it to the tissues throughout our body. We don’t store oxygen in our body but we use it continuously, and our body’s demand for oxygen is constant as oxygen molecules literally fuel every basic function that each cell in our body must perform.

Symptoms of Anemia. Moderate to severe anemia can cause symptoms of weakness, fatigue, shortness of breath, rapid/irregular heartbeat and pale skin. Milder or chronic anemia may cause subtle symptoms or no symptoms at all.

Erythropoietin. This hormone is a chemical messenger with several functions relating to the manufacture of red blood cells, preserving their lifespan in the body, and enhancing the growth of blood vessels. As we develop before birth, erythropoietin is active within our livers. After we are born, erythropoietin is manufactured and released by cells in the kidney.

Kidneys and Anemia. People often don’t think of a relationship between the kidneys and anemia, but when you carefully consider it, it makes sense for the kidney to have this function. Like a waste-water treatment plant adds chemicals based on the scientific observations of the plant technicians, the kidneys have specialized cells that detect decreased oxygen levels in the blood circulating through them, and as a result, these specialized cells release erythropoietin to enhance red blood cell formation and longevity. If the kidneys become diseased and fail, this system of checks and balances is impaired or lost. When ESAs, or synthetic erythropoietin, was first introduced in 1989, the drug was intended specifically for the benefit of patients in kidney failure.

Chemotherapy and Anemia. Cancer cells are bizarre mutant cells that divide rapidly. therefore, malignant tumors can grow large very quickly. The goal of chemotherapy is to target those rapidly-dividing bizarre cells and kill them. Other “good” rapidly-dividing cells in our body get caught in the cross-fire and are also damaged by chemo drugs. Hair is lost when rapidly-dividing cells in the roots are targeted by the chemo drugs. Other fast-growing cells affected by chemotherapy are in the digestive tract; that’s why mouth sores, nausea, and vomiting are a common consequence of chemo. The body’s rapidly dividing blood cells (red cells, white cells, and platelets) are also among the good cells that fall prey to chemotherapy. The anemia that results from chemotherapy is not caused by a lack of erythropoietin, but ESAs were approved by the FDA in 1993 to treat anemia to reduce the amount of blood transfusions necessary for patients suffering from chemotherapy-induced anemia.

Sobering News about ESAs . . .

All medications have both benefits and risks. In the U.S. the FDA places "black box warnings" on the medication labels and inserts of drugs when research suggests there is a risk of serious adverse effects. The first black box warning for ESAs appeared in March of 2007. Eight months later in November 2007, the black box warning was emphatically strengthened by the FDA.

Both the chronic renal failure and chemotherapy patients were found to have some increased risks when using ESAs. Patients with certain types of cancer were found to be at risks of tumor progression and decreased survival when taking ESAs to increase red blood cell production. Chronic renal failure patients were found to be at increased risk of developing heart attack, stroke, blood clots, heart failure and death if their ESA dose was high enough to cause them to make more than recommended number of red blood cells.

The FDA’s guidance to physicians was very specific on the recommended dosage to achieve good results without increasing patients’ risks for a bad outcome. Further, their guidance suggested that physicians specifically discuss the risks and benefits of these medications with their patients.

What’s Inside the Black Box . . . guidance for physicians about prescribing:

For patients with cancer: ESAs should only be used to treat anemia caused by chemotherapy—not to treat anemia from any other cause. After chemotherapy is finished, ESAs should no longer be used. Risks of tumor progression and decreased survival were noted in some clinical trials. The FDA strongly recommends that healthcare professionals discuss these risks with their patients before this therapy is started.

For anemic patients with chronic renal failure: Treat with the lowest level of the drug which will maintain hemoglobin levels within the target range of less than 12 g/dL. The established goal for this group is to maintain hemoglobin between 10-12 g/dL, because the risk for death and serious cardiovascular events increases when higher hemoglobin levels are achieved on ESA therapy. Further, it’s recommended that ESA therapy be discontinued if the patient’s hemoglobin levels remain so low that blood transfusions are still required.

What the FDA recommends for physicians and other healthcare professionals to discuss with their patients:

1. The primary goal of treatment with erythropoiesis stimulating agents (ESA) is to increase the number of red blood cells in order to avoid receiving blood transfusions.
2. These medications require at least two weeks of treatment before there is an increase in the number of red blood cells, and the dose may be adjusted periodically, but not more often than every four weeks.
3. ESAs increase the patient’s chance of blood clots and the risk of dying may be greater in certain circumstances.
4. Patients should keep appointments for blood tests so hemoglobin levels can be monitored.
5. Patients should monitor their blood pressure and call their healthcare provider for changes outside of the range that has been established for them.
6. Call the healthcare provider if they experience any of the following symptoms:

• Pain and/or swelling in the legs
• Worsening in shortness of breath
• Increases in blood pressure
• Dizziness or loss of consciousness
• Extreme tiredness
• Blood clots in hemodialysis vascular access ports

What the FDA wants patients to know about treatment with Aranesp, Epogen and Procrit . . .

Patients with cancer who are currently using or considering the use of an ESA should know the following:
• ESAs may shorten your survival time or may cause your tumors to grow faster.
• ESAs should only be used to treat anemia caused by chemotherapy and not other anemia from other causes in patients with cancer
• ESAs should not be used to treat the symptoms of anemia, such as fatigue or improve the quality of life in patients with cancer. The goal of treatment with ESAs is to avoid blood transfusions
• Treatment with an ESA should be stopped after you complete your course of chemotherapy.

Patients with chronic kidney failure (this includes both patients on dialysis and those not on dialysis) who are currently using an ESA should know the following:
• Your hemoglobin level should be checked regularly to make sure it stays between 10 and 12 g/dL.
• ESAs can increase your chance of heart attack, stroke, blood clots, heart failure, and death when they are given to maintain higher hemoglobin levels.
• If you are not responding to treatment with an ESA (your hemoglobin levels are not increasing) ask your doctor if you need to be checked for other causes of anemia.

Report Adverse Reactions to the FDA: Healthcare professionals are to report adverse and unexpected reactions with these meds to the FDA MedWatch reporting program online or by phone: 1-800-332-1088.

Links to more information about ESAs:

• Comprehensive information about ESAs from the U.S. Centers for Medicaid and Medicare Services: www.cms.hhs.gov/determinationprocess/downloads/id203d.pdf
• Kidney Disease and Anemia: http://kidney.niddk.nih.gov/kudiseases/pubs/anemia/
• Anemia and Kidney Disease: http://www.aakp.org/aakp-library/Anemia-in-Chronic-Kidney-Disease/
• A plus: Anemia and Kidney Disease from Anemia.org: http://www.anemia.org/patients/information-handouts/kidney-disease/
• ESA use for anemia in cancer patients: http://www.medscape.com/viewarticle/571464




.(All rights reserved, Carolyn Cooper, MPH, RN, 2009)  .. . .

24 Hour Urine Collection: How to do it and Why it's done

See my highlighted links at the bottom for links to instructions for this test in Spanish and other foreign languages.


What's the Purpose of Urine Testing?


An incredible amount of information can be obtained from examining a urine sample. In fact, over 100 different tests can be performed on a single specimen. Most of the time a simple "quick catch" specimen of urine (voided into a cup) is sufficient for a basic urine test. Urinalysis results may reveal problems with the body's electrolytes or hormones, the presence of infection, dehydration, evidence of microscopic blood (that can't be seen with the naked eye), drug levels, or problems with kidney function.


Why a 24-Hour Urine Collection?


A small sample of urine isn't always sufficient. In addition to blood tests, physicians will order a 24-hour urine collection if they have reason to be concerned about overall kidney function. This test typically focuses on creatinine clearance, sodium, protein, and urine osmolality. Other substances may be examined in a 24-hour collection; for example, hormone levels, urea nitrogen, or copper. The volume of urine that is voided during the 24-hour period also yields important information.  The laboratory will make calculations based on your 24-hour (or 12-hour) urine collection that will help determine how well your body is clearing waste products via the urine.  This finding will be compared to a blood test that measures how much of the waste products are circulating in your blood.

If your physician hasn't explained WHY he or she is requesting the 24-hour urine collection, ask for details. As a patient, being informed is one of your fundamental rights.

Tips for Collecting Your 24-Hour Urine Specimen


A 24-hour urine collection is easy to mess up, and that can be very frustrating. Just one moment of accidentally forgetting to collect and save the urine during the 24-hours ruins the test, and the collection might have to start all over again . . .

Before the test: Your doctor's office will provide you with one or two brown plastic collection jugs and written instructions. Certain tests may require that urine be placed in a "double container" or that a preservative be added to the collected urine; you'll be given the supplies and containers appropriate for your test.


What you need from your lab or doctor's office:

• Special instructions for the test and a lab sticker with your patient information to attach to the collection container(s).
• Collection container(s)--depending on the size of container the lab stocks--you may receive one or two of these jugs. They are made of heavy brown plastic, not just any container will do for this collection, so be sure to use the container(s) provided.
• Nice to have items--I'd ask for these if they don't offer them to you. For men: A plastic urinal to void into. For women: a plastic "nun's hat" to set in the toilet to collect the voided urine. If you don't have these items, it's okay to void into a bedpan, large plastic cup or bowl, etc. You will pour the collected urine into the brown collection container after each void, so it's nice to have something that pours easily.
• You'll also need: a way to keep the collected urine cool during the collection period. One of the most common ways to do this is to set the brown urine collection jug in larger container filled with icy water (an ice bath). An ice chest (cooler) is another option. It's also possible to place the collection jug in the refrigerator, although there are many reasons to make this impractical.

When to begin? Find out in advance when and where to return your 24-hour urine collection. This information will help you decide when to begin, because if the lab or physician's office isn't going to be open when you finish the collection, you'll have to keep the sample in a refrigerator, cooler, or in an ice bath until you can turn in your specimen. It's often suggested that you begin a 24-hour collection first thing in the morning--but that is certainly not required. However, it is essential that you make note of the date and time that the specimen collection was started and stopped. This information will need to be recorded on the specimen container (and/or label).


Ready to start? Completely empty your bladder by voiding into the toilet and flushing--DO NOT save this first urine sample. The first time you empty your bladder you are flushing away urine that has been building up in your bladder for several hours or more.  That hours-old urine will yield incorrect results if we collect it for our 24-hour specimen.  We want to start with an empty bladder to collect only the urine our body makes during the 24-hour-period. 


Record the start time and determine your stop time. All other urine during the 24-hours will need to be saved and poured into the collection jug. It's helpful to use the same bathroom all day long and post a note with the start/stop time to help remind you to collect all of your samples. Replenish the ice in the basin surrounding your collection jug from time-to-time in order to keep the specimen cool.


Ending the collection: When the 24-hour-collection period is ending, make a last effort to urinate--even if you don't have the urge to "go," you will still be able to produce an ounce or two of urine. Make sure your collecton jugs are tightly capped and labelled with your name, date of birth, collection date and start/stop times.   (Note: If you weren't given a label for your specimen jug, make one and tape it securely to your jug.) Keep the specimen in the ice bath, cooler, or refrigerator until you are ready to return it to the lab or doctor's office. Place your specimen jug(s) in a sturdy plastic bag for easy carrying. (Your specimen will be just fine without being on ice while you return it to the lab or doctor's office---as long as you are not exposing it to heat for a prolonged period of time.)

What If . . . ? Special circumstances . . .

• You filled up the container the lab provided, but your 24-hour-collection is not yet complete. Use a very clean glass or plastic container to continue collecting your urine.  Your brown jug protects the collected urine from light--so if you have to use a transparent collection bottle, be sure to guard it from the light along with keeping it chilled. Using an ice chest would be a good strategy for you in this case--if that's not possible, cover the transparent container with a brown paper bag to protect it from the light.  When you return your sample to the lab, keep the transparent container in a brown paper bag, or some similar technique to keep it protected from the light.
• You have started the 24-hour-collection, but find you need to leave the house for several hours.  Take a backpack with you, a plastic bottle with a secure lid, and a large ziplock bag full of ice.  This will allow you to carry your collection items discreetly.  For ladies, a wide mouthed plastic container will allow you to urinate and pour the sample into your capped bottle.  Your ziplock bag of ice will help keep your sample cool while you are on the go. I know this is a rather bulky idea, but the best I can come up with at the moment.
• For patients with urinary catheters. It would be preferable to start your collection with a fresh catheter bag in place--if that's not possible, it would be nice to clean the existing bag--at least remove the bag from the catheter and give it a good rinse out.. Begin your collection by completely emptying the current catheter bag and flushing the accumulated urine. Record this as your start time. During the remainder of the 24-hour-collection period, empty the foley bag into the brown collection jugs at regular intervals and keep the collection jugs in the refrigerator on in an ice bath just as anyone else would do. At the designated stop time, empty your collection bag for the last time.
• Urine becomes mixed with feces or blood. Do not empty any urine that has been contaminated by feces or menstrual blood into your collection jug. Make note of the time and stop the collection. Contact your lab or physician's office to inform them. In some cases, if enough time has elapsed (12 hours or more), your physician may give the go-ahead to stop the test early. Possibly, you may be asked to start all over again.
• Patients who are incontinent (cannot hold their urine).  Certainly your physician may not realize (or remember) that a particular patient struggles with complete or partial incontinence.  Do let your doctor know about incontinence issues.  Perhaps the 24-hour-test will be impossible because of complete incontinence; perhaps they might recommend a bladder catheter for the test, or perhaps they might allow a shorter period of time (12-hours or thereabouts) for the urine collection. 
• "Oops! I didn't collect every void during the 24 hours!" If you forget to collect all of your urine, the test results may be inaccurate. Talk to your lab or doctor's office before disposing of all that you've collected. If you have already completed at least 12 hours of the urine collection, mark down the time of the last urination and keep your container on ice or in the refrigerator as discussed later in this article.  Talk to your physician's office or lab to let them know what you have been able to collect.  They should be able to use your sample and calculate the important information based on the number of hours you have collected--but it's important that they know the correct number of hours when you turn in the sample.  It's possible that you'll be asked to start all over again, but there's a good chance that they can use what you've collected and make adjustments to correctly calculate the results.
• Why keep the urine specimen on ice?  The ice bath is just a technique for keeping the urine cool enough so that bacterial growth doesn't overwhelm your specimen.  The ice bath should keep your specimen in the 40-45 degree Farenheit range as would your refrigerator.  Keeping a 24-hour-specimen in the refrigerator is really awkward and inconvenient.  Having your specimen container right there in the bathroom "on ice" is so much easier.
• Other questions? Call your physician's office or lab. If you'd like to suggest anything to make this entry more helpful or accurate--please let me know. I'll gladly tweak this entry to make the information more user-friendly.

For further reading, check out these links:

• Procedures and Diagnostic Tests (From the National Institute's of Health)
• Instructions for a 24-Hour Urine Collection (in English) (648 KB) (in Spanish) (32 KB) (also from NIH) 
• Health Info Translations:  Get instructions for this test in Spanish, Korean, Japanese, Chinese, French, Somali, Russian and Ukranian. 
• St. Clare Hospital Health Service: Patient Education Brochure, 24-hour urine collection: These comprehensive instructions allow the doctor ordering the test to also provide specific dietary instructions to follow depending on what element of the urine is being tested. 
• A 2008 Renal/Urology article that discusses how 12-hour-urine samples can be substituted in place of 24-hour-samples:  24-hour-urine collection may be avoidable.

• Please do try your level best to complete the 24-hour-collection for best results.  If you run into a problem with your collection after 12 hours or more, ask your doctor or lab if they can calculate your results using what you have collected.

. . . http://docs.google.com/gview?a=v&q=cache:Yi0raZ73PAEJ:www.ssmhc.com/internet/home/stclare.nsf/0/F8DF7DDC6ED0F94E862574BE004EF645/%24FILE/24-hr%2520urine%2520collection.pdf%3Fopenelement+how+to+do+24+hour+urine&hl=en&gl=us