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National Kidney Month Kicks Off

The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), which makes up part of the National Institutes of Health (NIH), has issued a press release recognizing World Kidney Day on March 11.  The awareness-raising day occurs during National Kidney Month. 

According to NIDDK, “Chronic kidney disease affects approximately 23 million adults in the U.S. and is a major public health challenge. In 2007, almost 111,000 people in the U.S. began treatment for the most advanced stage of the disease, kidney failure. That year, treatment costs paid by Medicare totaled $23.9 billion — 5.8 percent of the Medicare budget.”

Kidney Health and Food Safety–HUS and E. coli O157:H7

There is a close connection between kidney health and food safety.  Hemolytic uremic syndrome (HUS), a potentially fatal complication of E. coli O157:H7 infection, is the most common cause of kidney failure in children.[1]  HUS is a frequent cause of long-term kidney injury in both children and adults.

Hemolytic uremic syndrome develops when the toxins from bacteria such as E. coli O157:H7, known as Shiga-like toxins (SLT), enter the bloodstream through the inflamed bowel wall.[2] SLT attach to receptors on the inside surface of blood vessel cells and initiate a chemical cascade that results in the formation of tiny thrombi (blood clots) within these vessels.[3] Several organs appear more susceptible to these clots, including the kidney.  Thus, when fully expressed, HUS presents with the triad of hemolytic anemia (destruction of red blood cells), thrombocytopenia (low platelet count), and renal failure (loss of kidney function).[4]  

There is no cure or effective treatment for HUS.[5]  Approximately half of the children who suffer HUS require dialysis to survive the acute stage of the illness.  Those who do survive almost invariably suffer irreversible damage to the kidneys.  The damage sustained in the short term then places the patient at risk for long-term kidney complications, including end stage renal disease (ESRD).  Five percent or more of those who survive have long-term kidney impairment.[6]

Hyperfiltration Injury

“Hyperfiltration injury” is a term used to describe chronic, progressive damage in kidneys that have already sustained significant damage during an HUS illness, resulting in the destruction of a substantial percentage of nephrons.  Nephrons are the functional units of the kidney and are comprised of glomeruli connected to kidney tubules.

Where hyperfiltration injury has occurred, the remaining healthy glomeruli attempt to adapt to their reduced number by enlarging (hypertrophy) and by hyper-filtrating.  In other words, the remaining glomeruli work extra hard in an attempt to meet the needs of the body. For a time, they are usually able to compensate.  The glomeruli, however, are being over-worked.  This overworking of glomeruli is manifested by the spillage of protein (albumin) in the urine.  This phenomenon is called proteinuria.

Over time, the hyperfiltration injury causes progressive loss of the remaining glomeruli due to the formation of scar tissue, or fibrosis.  Once the remaining functional nephron population drops below 10 percent, the person’s survival requires initiation of “renal replacement therapy”.

There are some medications that can help slow the need for renal replacement therapy.  The use of angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) is usually helpful in slowing the fibrotic process, but no known treatment can stop it. ESRD, also known as stage 5 kidney disease, eventually occurs.

End Stage Renal Disease

Common problems associated with the development of ESRD include:

Reduced ability to excrete waste products and maintaining fluid and electrolyte balance:   As kidney function declines, waste products will accumulate.  The patient will experience uremic toxicity characterized by weakness, loss of appetite, nausea, and vomiting, and if not treated with dialysis, seizures, coma and death.  

Accumulation of body acid:  The patient will need to take a base such as sodium bicarbonate to neutralize remaining body acid.  Failure to do so results in poor appetite and weakened bones.

Anemia:  The patient may require hormone injections that would begin no later than the start of dialysis, and probably sooner.

Loss of bone density:  The patient is at high risk for bone pain and fractures.

High blood pressure: High blood pressure afflicts the majority of kidney failure patients.   Failure to maintain normal blood pressure increases the risk of heart failure, heart attack and stroke.

Once ESRD is reached there are two survival options:  long-term dialysis treatment or a kidney transplant.  Dialysis is a treatment designed to replace what damaged kidneys can no longer do. Treatments are usually 3-4 hours three times a week.  Receiving regular dialysis presents several challenges.  

At some point, kidney transplant may be preferable to dialysis or become necessary for survival.  The wait for a kidney is months to years, depending on the availability of a donor and the recipient’s blood type.  Since all kidneys except those from an identical twin are recognized as “foreign” by the recipient’s immune system, it will be necessary, for the rest of a transplant recipient’s life, to use immunosuppressive medications to reduce the risk of rejection.   Common complications of renal transplant include the following:

Acute rejection of the transplanted kidney.  This often requires a biopsy of the graft, and the use of very powerful medications (probably requiring hospital stays).

Infections (viral, fungal and bacterial) that can be life threatening.

Cancer due to the Epstein- Barr virus, and goes by the term of Post Transplant Lymphoproliferative Disease (PTLD).  

Osteopenia, an additional post-transplant risk is osteopenia (loss of bone calcium).

Premature coronary artery disease–coronary artery disease (including myocardial infarction) is the most common cause of death in the transplant population.

There is no known treatment to stop the progression of HUS–at either the acute stage or long-term.  Likewise, while not all those infected develop HUS, there is no way of preventing the development of HUS in a person infected with E. coli O157:H7.  As a result, there is only one avenue to reducing the impact of E. coli O157:H7 on kidney health–preventing food from becoming contaminated with E. coli O157:H7 in the first place.  


1.  Chinyu Su, MD & Lawrence J. Brandt, MD, Escherichia coli O157:H7 Infection in Humans, 123 Annals Intern.  Med. (Issue 9), 698-707.

2.  Amit X. Garg, MD, MA, et al.  Long-term Renal Prognosis of Diarrhea-Associated Hemolytic Uremic Syndrome: A Systematic Review, Meta-Analysis, and Meta-regression, 290 JAMA (No. 10) 1360, 1360 (Sept. 10, 2003).

3.  Richard L. Siegler, MD, The Hemolytic Uremic Syndrome, 42 Ped. Nephrology, 1505 (Dec. 1995), at 1509-11 (describing what Dr. Siegler refers to as the “pathogenic cascade” that results in the progression from colitis to HUS).

4.  Nasia Safdar, MD, et al.  Risk of Hemolytic Uremic Syndrome After Treatment of Escherichia coli O157:H7 Enteritis: A Meta-analysis, 288 JAMA (No. 8) 996, 996 (Aug. 28, 2002).  at 1360.  See also Su & Brandt, at 700.

5.  Id., at 996.  See also Siegler, supra note 3, at 1379.  (“There a
re no treatments of proven value, and care during the acute phase of the illness, which is merely supportive, has not changed substantially during the past 30 years.”)

6.  Safdar, supra note 4, at 996 (going on to conclude that administration of antibiotics to children with E. coli O157:H7 appeared to put them at higher risk for developing HUS).

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