According to a recent article, a recent study shows evidence that anti-Semaphorin 3B antibodies are pathogenic and therefore patients diagnosed with membranous nephropathy should be monitored after a kidney transplant.
Membranous nephropathy is a kidney disorder in which small blood vessels in the kidney (glomeruli) that filter wastes from the blood become inflamed and thickened. As a result, proteins leak from the damaged blood vessels into the urine (proteinuria). For many, loss of these proteins eventually causes signs and symptoms characteristic of nephrotic syndrome.
The following are symptoms of membranous nephropathy:
- Edema (swelling) in any area of the body
- Foamy urine
- Poor appetite
- Weight gain
- Excessive urination, usually at night
- Elevated fat levels in the blood (hyperlipidemia)
- Increased protein levels in the urine (proteinuria)
- Decreased protein levels in the blood, particularly of the protein albumin
Researchers performed biopsies on patients’ kidneys at 1 month and 5 months after their kidney transplant. Using immunohistochemistry and confocal microscopy, researchers were able to detect the Semaphorin 3B antigen.
Researchers discovered a boy, who was seven years old, had early recurrence after transplantation, and he had both severe nephrotic syndrome and advanced kidney failure. Using a Western blot analysis of serum, they found the boy had anti-Semaphorin 3B antibodies. This means that recurrence happened just 25 days after his kidney transplantation despite the use of conventional immunosuppressive therapy. Rituximab, a monoclonal antibody, was then used to treat the boy, and after 40 days of treatment, there were no anti-Semaphorin 3B antibodies found in his system.
Researchers, therefore, concluded that anti-Semaphorin 3B antibodies are pathogenic (causing or capable of disease) and patients with membranous nephropathy should be closely monitored after a kidney transplant.