Arthritis Treated with Alternative Medicine

ScienceDaily (Feb. 25, 2010) — Simple urine tests for four proteins might be able to detect early kidney disease in people with lupus, researchers at UT Southwestern Medical Center have found in an animal study.

See Also:Health & MedicineKidney DiseaseLupusJoint PainPain ControlDiseases and ConditionsUrologyReferenceInflammation of the kidneyExcretory systemKidneyKidney stone

Although it might take years before such tests could be used clinically, the findings suggest they could pinpoint kidney disease better than tests currently in use, the researchers said.

"Our goal was to accurately detect something in the urine that appears only in disease," said Dr. Chandra Mohan, professor of internal medicine and immunology at UT Southwestern and senior author of the study, available online and in the February 16 issue of The Journal of Immunology.

"If this testing regimen proves effective in humans, physicians might be able to predict and diagnose kidney damage noninvasively, as well as monitor whether treatments are working."

Kidney disease is the major cause of death and disability in lupus patients, Dr. Mohan said. Early detection and treatment lead to a longer and better-quality life.

The researchers found that in mice, four proteins — protease, PGDS, SAP and SOD — show up in larger quantities in urine as kidney damage progresses. Each of these proteins is either present in humans or has a human equivalent. The researchers currently are studying whether the same correlation between urinary protein levels and disease occurs in humans.

Lupus is one of many autoimmune diseases that attack internal organs, tissues, joints and other parts of the body. The researchers focused on systemic lupus erythematosus affecting the kidneys, the most common and serious form of lupus.

Currently, kidney damage in humans is detected by performing a kidney biopsy, Dr. Mohan said. A kidney biopsy involves taking a tissue sample with a needle, a process that is invasive and can be stressful to patients.

In the current study, the researchers used mice that have a condition similar to human lupus. They screened urine for proteins both before and after the mice showed symptoms of kidney disease and found that 71 proteins appeared in urine after the illness became physically evident.

The researchers then focused on four proteins that were present in high levels after symptoms appeared. These proteins or their analogs had not previously been known to be present in the urine of patients or mice with lupus kidney disease.

Dr. Mohan said monitoring urinary levels of these four proteins might also reveal more about the mechanisms of lupus. Each protein is involved in a different biochemical process, so the stage of the disease at which each appears in urine might prove informative, he said.

Testing for these proteins might also have the potential to monitor kidney damage that results from diabetes, hypertension and other conditions, said Dr. Mohan.

Other UT Southwestern researchers participating in the study were Dr. Tianfu Wu, assistant professor of internal medicine; Dr. Yuyang Fu, former postdoctoral fellow in internal medicine; Dr. Deirdre Brekken, adjunct assistant professor of pharmacology; research associate Mei Yan; Dr. Xin Jin Zhou, professor of pathology and internal medicine; research associate Kamala Vanarsa; research intern Nima Deljavan; and Dr. Chul Ahn, professor of clinical sciences.

Dr. Chaim Putterman of the Albert Einstein College of Medicine also participated in this study.

The research was supported by the Lupus Research Institute and the National Institutes of Health.

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ScienceDaily (May 3, 2010) — Lupus is a disease where the immune system attacks healthy cells of the body. This leads to progressive damage of different tissues and organs. The classical characteristic of the disease is the so-called butterfly rash in the face. Many Lupus patients eventually die of kidney failure. Scientists at the Max Planck Institute for Infection Biology in Berlin together with medical scientists from the University of Erlangen succeeded in elucidating basic principles of the disease. This opens up new perspectives for methods that might enable early diagnosis and treatment of Lupus patients with a high risk at kidney failure.

See Also:Health & MedicineLupusJoint PainKidney DiseasePain ControlImmune SystemDiseases and ConditionsReferenceInflammation of the kidneyTransplant rejectionHuntington’s diseaseArthritis

Lupus is one of the most common autoimmune diseases. The symptoms vary from patient to patient and can include rashes, muscle and joint pain, fatigue, inflammation, and miscarriage. One third of the patients die of kidney failure. Little is known about the origin and the pathogenesis of this disease. Diagnosis is difficult because many symptoms are common with other diseases. The hallmark of Lupus is that the body produces antibodies against its own DNA, certain proteins of the nucleus and of white blood cells. The course of the disease is characterized by flares which are often triggered by infections. After a flare the health of the patient improves but often there are sequelae, resulting in a continuous exacerbation of the disease.

Scientists of the Max Planck Institute for Infection Biology suspected that an immune mechanism that was only recently discovered by them, plays a key role in Lupus: During an infection, white blood cells are stimulated and extrude nets in which they trap and kill pathogens. This NET (an acronym for Neutrophil Extracellular Traps) is composed of exactly those components against which a Lupus patient produces antibodies: DNA, as well as proteins of the nucleus and the white blood cells. In co-operation with clinical scientists from the University of Erlangen, the Max Planck scientists could show for the first time that, in contrast to healthy persons, a part of the Lupus patients could not degrade NETs after the infection.

The scientists also discovered that NETs are degraded by the enzyme DNase-1, a protein which normally is found in the blood. Lupus patients, however, either lack this enzyme or their DNase-1 is blocked. Further examination of this patient group revealed that the remains of NETs together with the auto-antibodies are deposited in the kidneys of SLE patients. Indeed, the scientists showed a strong correlation between the inability to degrade NETs in Lupus and a high risk of kidney failure. These results provide a starting point for the development of a test that might allow an early diagnosis and treatment of these high risk patients.

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ScienceDaily (May 4, 2010) — Researchers at Karolinska Institutet have discovered a new control mechanism in our immune system. The discovery is of potential significance to the treatment of serious diseases such as MS (multiple sclerosis), rheumatoid arthritis, and SLE (systemic lupus erythematosus).

See Also:Health & MedicineImmune SystemStem CellsLymphomaLupusBrain TumorJoint PainReferenceT cellNatural killer cellImmune systemDiabetes mellitus type 1

"Now that we’ve started to understand the regulatory mechanisms involved in these autoimmune diseases, we are hopeful that new treatments can be found," says Mikael Karlsson, associate professor at the Department of Medicine at Karolinska Institutet in Solna, and one of the team behind the study now published in the highly reputed periodical, The Journal of Experimental Medicine.

An important component of our immune defence is a type of cell called a B cell. Normally, the job of these cells is to produce antibodies, which in turn bind to and neutralise invasive microorganisms, such as bacteria and viruses. In people with an autoimmune disease, explains Dr Karlsson, these B cells actually have an injurious effect and instead of serving the body, are activated against its own tissues, which they start to break down.

Patients with SLE and other autoimmune diseases have lower levels of so-called NKT cells. Previously, it was not known what part these cells play in the origin and development of the disease; now, however, the research group at KI has shown that this deficiency is a contributory pathogenic factor.

"We’ve demonstrated that NKT cells can regulate how B cells become activated against healthy tissue, and that a lack of NKT cells results in greater misguided B cell activation," says Dr Karlsson. "So now we can mechanically link the NKT cell defect in patients to the disease."

The study also shows that the NKT cells directly impede faulty B cell activation, and that they do so early in the misdirected process. The team managed to inhibit the activity of pathogenic B cells by adding NKT cells — a result that may one day lead to new types of treatment.

"This means that new treatments specifically targeting the protective NKT cells can help this patient group," concludes Dr Karlsson.

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