In a study published Dec. 12 in the journal Nature Medicine, a research team announced they have identified a type of immature myeloid cell, located in the bone marrow, as the source of abnormal levels of suPAR.

The protein has been identified in recent years as a potential biomarker for chronic kidney disease and a pathogen of the condition.

“These immature myeloid cells appear as a main source of circulating suPAR,” said Jochen Reiser, MD, PhD, principal investigator and senior author of the study presented in Nature Medicine, who has been working on solving the mysteries of suPAR for more than a decade. Reiser is Ralph C. Brown, MD, Professor and chairperson of the Department of Internal Medicine at Rush University Medical Center.


Everyone has urokinase plasminogen activator receptor (uPAR), a healthy molecule “tethered” in place to various types of cells. It’s the soluble variety, circulating in the blood stream, suPAR, that damages the kidneys.

In two papers published in Nature Medicine in 2008 and 2011, Reiser’s team showed that uPAR and its soluble form suPAR may be causative for FSGS. In 2015, Reiser and colleagues published work in the New England Journal of Medicine that showed that circulating suPAR associates with future chronic kidney disease in general, likely by delivering a “systemic insult” to the organs.

“SuPAR is not just a biomarker; it may also be a cause of the disease,” Reiser said. That finding was “a game changer. You could predict new disease in people that by any available test still had normal kidney function.”

Reiser’s team used a “humanized” mouse model that utilizes patients’ peripheral blood stem cells to communicate signals to mouse bone marrow immature myeloid cells.

Further research will be necessary to establish solid connections between the suPAR production site in mice and the human cell types, Reiser said. It also might be possible to establish a genetic link to the process that unleashes suPAR on a person’s system.