At a recent medical congress, scientists announced a major step forward in understanding and treating kidney diseases linked to nephrotic syndrome—a condition where too much protein leaks into urine because of kidney damage.
This important research, also featured in a leading medical journal, highlights a new way to track the disease using a special marker in the blood.
Nephrotic syndrome can cause several kidney diseases, including ones known as minimal change disease, primary focal segmental glomerulosclerosis, and membranous nephropathy. These conditions often harm the kidney’s filtering cells, leading to protein leakage.
Children are particularly affected by minimal change disease and primary focal segmental glomerulosclerosis. These are grouped under a category called idiopathic nephrotic syndrome, which means doctors don’t know what causes the problem.
Often, these children don’t undergo kidney biopsies, which are procedures to take small samples of kidney tissue for testing, because these can be tough on the patient.
Traditionally, doctors have faced difficulties diagnosing these conditions due to similar signs among them and the risks involved in taking kidney samples, especially from children.
However, certain proteins called anti-nephrin autoantibodies, which the body mistakenly produces against its own kidney cells, have been found in some patients but their exact role was unclear until now.
In this study, researchers from Europe and the U.S. used a combination of two testing methods—immunoprecipitation and enzyme-linked immunosorbent assay—to find these autoantibodies in a reliable way.
They discovered that these autoantibodies were present in most adults with minimal change disease and in 90% of children with untreated idiopathic nephrotic syndrome.
This suggests that these antibodies are strongly linked to active disease and can serve as markers to monitor how the disease progresses.
Interestingly, when researchers injected a laboratory-made version of the nephrin protein into mice, it triggered changes in the mice similar to those seen in human kidney disease.
This experiment helped to show that the antibodies attacking nephrin play a direct role in kidney damage. The model was especially significant because the disease developed quickly in the mice with just one round of injection, even with a low dose of antibodies.
Dr. Nicola M. Tomas, one of the leading researchers, stated, “Finding these autoantibodies and being able to measure them accurately is a big step in how we can diagnose and track these kidney diseases.”
He also mentioned that their method improves how we can watch the disease get better or worse over time.
Professor Tobias B. Huber, another lead researcher, explained, “These results help us understand better what causes these diseases at a molecular level, which is crucial for developing targeted treatments.
This could lead to highly personalized medicine approaches for these patients in the future.”
This discovery opens new paths for diagnosing and treating nephrotic syndrome in a more refined and less invasive way, offering hope for better management of kidney diseases associated with this condition.
If you care about kidney health, please read studies about pesticide linked to chronic kidney disease, and this drug may prevent kidney failure in people with diabetes.
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