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Peer reviewed Dramatic slowing pharmaceutical checked against the paper

a 73-year-old woman

IgA nephropathy with cellular crescents, in a patient with polycythemia vera carrying a JAK2 V617F mutation

Beforehematuria, proteinuria, and renal dysfunction
Afterover the following year urinary protein decreased and serum creatinine stabilized; clinical remission after two years of tapering corticosteroids

Doctors avoided steroids at first because steroids could worsen her blood cancer. Instead they started a JAK inhibitor called ruxolitinib. Over the next year her urine protein went down and her serum creatinine held steady. Later she took a two-year tapering course of corticosteroids and reached clinical remission. The authors say this is the first reported case of IgA nephropathy improving after JAK inhibitor treatment.

In one older woman whose IgA nephropathy came alongside a blood cancer called polycythemia vera, the JAK inhibitor ruxolitinib was tied to less protein in the urine and steady kidney function before steroids were ever used.

Key takeaways

Why it might work

The authors think the JAK inhibitor may help in two ways. First, blocking JAK signaling can lower IL-6 and IL-11, which drive platelet-derived growth factor. Less of that growth factor could mean less overgrowth of the mesangial cells in the kidney filter. Second, the drug may calm the abnormal blood-cell production that makes faulty IgA antibodies, the same antibodies that build up in IgA nephropathy. So the same medicine that settles the blood cancer may also cool the inflammation in the kidney.

The honest limits

Questions to bring your nephrologist

Researchers: Takahashi-Kobayashi M · Nishikii H · Shimizu T · Kaneko Y · Sakata-Yanagimoto M · Usui J

PubMed ↗added 2026-08-15