Math Model May Replace Kidney Biopsy
Researchers at Ohio State University have developed a math model that can predict the progression of kidney damage in lupus patients from nephritis to interstitial fibrosis, scarring in the kidney that current treatments cannot reverse.
Researchers at Ohio State University have developed a math model that can predict the progression of kidney damage in lupus patients from nephritis to interstitial fibrosis, scarring in the kidney that current treatments cannot reverse.
A kidney biopsy is the only existing way to reach a definitive diagnosis of the damage and its extent. However, the model could also be used to monitor the effectiveness of experimental treatments for inflammation and fibrosis.
This fibrosis can follow development of lupus nephritis, which occurs in about 60 percent of lupus patients, according to the National Institutes of Health. Inflammation is linked to the most common type of lupus, called systemic lupus erythematosus. The cause of lupus is unknown and it cannot be cured.
The math model comprises a series of equations that account for the complex inflammatory process leading from nephritis to fibrosis in damaged kidneys. As designed, the model can detect the extent of kidney damage and predict how inflammatory processes will react to different therapies. The research is published online in the Proceedings of the National Academy of Sciences.
The most important use of this model will be improving the design of clinical trials for new medications to treat the kidneys before they develop fibrosis, said lead author Avner Friedman. Establishing a dose of an experimental therapy is the most difficult part of testing new drugs. The model could give a starting point for an effective dose.
Further validation and refinement of the model is required, said Friedman, who is also founding director of the Mathematical Biosciences Institute at Ohio State. But in this study, a comparison with human patient data showed that levels of inflammatory proteins in the urine of patients with mild, moderate or severe fibrosis matched levels predicted by the model.
The model also allows scientists to simulate the scarring injury and detect how the damage would respond to the therapies that target specific pathways to disease--either the inflammatory process or the scarring itself. By identifying vulnerabilities in the process from inflammation to scarring, the model could even point to the cells and proteins that would be the most promising treatment targets, Friedman said.
The study is available here.
A kidney biopsy is the only existing way to reach a definitive diagnosis of the damage and its extent. However, the model could also be used to monitor the effectiveness of experimental treatments for inflammation and fibrosis.
This fibrosis can follow development of lupus nephritis, which occurs in about 60 percent of lupus patients, according to the National Institutes of Health. Inflammation is linked to the most common type of lupus, called systemic lupus erythematosus. The cause of lupus is unknown and it cannot be cured.
The math model comprises a series of equations that account for the complex inflammatory process leading from nephritis to fibrosis in damaged kidneys. As designed, the model can detect the extent of kidney damage and predict how inflammatory processes will react to different therapies. The research is published online in the Proceedings of the National Academy of Sciences.
The most important use of this model will be improving the design of clinical trials for new medications to treat the kidneys before they develop fibrosis, said lead author Avner Friedman. Establishing a dose of an experimental therapy is the most difficult part of testing new drugs. The model could give a starting point for an effective dose.
Further validation and refinement of the model is required, said Friedman, who is also founding director of the Mathematical Biosciences Institute at Ohio State. But in this study, a comparison with human patient data showed that levels of inflammatory proteins in the urine of patients with mild, moderate or severe fibrosis matched levels predicted by the model.
The model also allows scientists to simulate the scarring injury and detect how the damage would respond to the therapies that target specific pathways to disease--either the inflammatory process or the scarring itself. By identifying vulnerabilities in the process from inflammation to scarring, the model could even point to the cells and proteins that would be the most promising treatment targets, Friedman said.
The study is available here.
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