A hidden kidney threat—and new treatments that make detecting it critical

March 17, 2026

8 min read

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A hidden kidney threat—and new treatments that make detecting it critical

IgA nephropathy, an immune assault on the kidneys, is often missed. New treatments mean that spotting it sooner might save lives

By Charles Schmidt edited by Lauren Gravitz

Chiara Vercesi

This article is part of “Innovations In: Kidney Disease,” an editorially independent special report that was produced with financial support from Vertex.

The man in his 50s arrived at Ellie Kelepouris’s office carrying a sheaf of medical records. They contained years’ worth of laboratory test results that showed microscopic traces of blood in his urine. Kelepouris, a nephrologist at the University of Pennsylvania’s Perelman School of Medicine, wasn’t the first kidney specialist he had consulted about the problem. “I don’t want to have blood in my urine,” the man said. “I don’t know what’s going on.” Kelepouris suspected the cause, but it took a kidney biopsy, done in 2024, to confirm it. Her patient had IgA nephropathy (IgAN), an autoimmune disease that is an important cause of kidney failure.

IgAN is far from the most common cause of kidney disease, but up to 40 percent of people who have it will eventually require dialysis or a kidney transplant. Kelepouris’s patient was diagnosed while he was still in the early stages of the illness, but that’s uncommon. IgAN can develop asymptomatically for years, and by the time it’s detected, most patients are already at advanced stages. Today there are emerging precision therapies that can preserve kidney function and potentially stop IgAN in its tracks. But early diagnosis is crucial. The sooner treatment gets underway, the better the odds that “we can push off the need for dialysis, hopefully permanently,” says Brad Rovin, a nephrologist at the Ohio State University Wexner Medical Center.

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Usually an antibody protein known as immunoglobulin A, or IgA, patrols the inner walls of the body’s organs, blocking pathogens from entering cells. But in people who have IgAN, IgA is misshapen and not recognized by the rest of the immune system, prompting an attack against the perceived invader. When defective IgAs and their attackers bind, they aggregate into clumps that trigger inflammation in capillary networks in the kidneys called glomeruli. Inflamed blood vessels become scarred and unable to filter properly. The damaged kidneys leak proteins and red blood cells into the urine and allow too much salt and water to be retained in the body, raising blood pressure and putting undue stress on the remaining glomeruli.

For many, the first sign of the disease is urine turned bright red with blood. That typically happens after a cold or other virus. The virus increases immune activity, which ramps up IgA production and leads to an influx of new antibody clumps in the kidney. This inflammation damages the glomerular barrier, letting blood leak into the urine and “scaring the heck out of everybody,” Rovin says.

Ideally, nephrologists would identify patients before the disease becomes this advanced. But that has been difficult. A simple urine test can hint at early warning signs, but it takes a kidney biopsy to prove conclusively that someone has IgAN rather than some other condition. For a biopsy, doctors must push a needle from the patient’s back into one of their kidneys and pull out “two or three teeny pieces of tissue about the length of long grains of rice,” says Melanie Hoenig, a nephrologist at Beth Israel Deaconess Medical Center in Boston. Then a pathologist looks for IgA deposits in these specimens.

When patients have few to no symptoms, a kidney biopsy seems like an expensive and unreasonable ask. So it’s not done as often as nephrologists might like. In developing countries, the procedure is often not an option because of limited resources. But even in wealthier nations, doctors have hesitated to biopsy people with suspected cases of IgAN because—until the past few years—a confirmed diagnosis wouldn’t change their treatment.

Until recently, doctors could offer only harsh immunosuppressing drugs or basic supportive care to people in late stages of the disease. Instead of getting a biopsy, patients would be treated as having “chronic kidney disease of unknown etiology,” says Krzysztof Kiryluk, a nephrologist and physician scientist at Columbia University. “They would progress to end-stage renal disease without a proper diagnosis.”

Without biopsy-confirmed data, it’s difficult