a 44-year-old man
IgA nephropathy (Oxford M1,E0,S1,T1,C0) linked to adalimumab, in a man with seronegative rheumatoid arthritis
A 44-year-old man had seronegative rheumatoid arthritis. He took adalimumab starting in 2014, and it controlled his arthritis for five years. In 2019 he developed protein in his urine (1 gram a day), ongoing blood in his urine, and low complement levels. A kidney biopsy showed IgA nephropathy. His doctors suspected the adalimumab was linked to the kidney problem, so they stopped it. His urine protein dropped to 0.1 gram a day and his creatinine returned to normal. A later drug called tofacitinib did not control his arthritis well. In 2021 he started certolizumab, which controlled his arthritis and kept his kidney disease in remission at 0.2 gram of protein a day.
In one man, an arthritis drug (adalimumab) appears to have triggered IgA nephropathy, and stopping it brought his kidney numbers back down.
- His kidney trouble showed up in 2019 after five years on adalimumab, with 1 gram of protein a day in the urine, blood in the urine, and low complement (C3/C4) levels.
- A kidney biopsy confirmed IgA nephropathy before any treatment changes were made, so the diagnosis was not a guess.
- After his doctors stopped the adalimumab, his urine protein dropped to 0.1 gram a day and his creatinine returned to normal.
- Switching to a different arthritis drug, certolizumab, in 2021 controlled his arthritis and kept his kidney disease quiet at 0.2 gram of protein a day.
- Not every TNF inhibitor behaved the same way for him, which is why the specific drug mattered.
Why it might work
The paper frames this as a possible drug-triggered kidney injury. Adalimumab is a TNF inhibitor, a class of arthritis drugs that dampen part of the immune system. The authors suspect that in this man the drug set off IgA nephropathy, where a protein called IgA builds up in the kidney's tiny filters and inflames them, letting protein and blood leak into the urine. Because the timing lined up with the drug, they stopped it, and the kidney numbers improved. That improvement after removing the suspected trigger is the main reason they think the drug was the cause.
The honest limits
- This is a single patient (n=1), so it cannot tell us how often this happens or whether it would happen to you.
- The story shows the timing lined up, but a case report cannot prove the drug caused the kidney disease.
- The abstract reports urine protein and creatinine but does not give an eGFR number, so we cannot see his exact kidney filtering rate.
- The abstract lists no conflict-of-interest or funding disclosures, so we cannot judge those from it.
- Should my urine protein and kidney function be checked regularly while I am on a TNF inhibitor like adalimumab?
- If a medication might be affecting my kidneys, how would we safely test whether stopping or switching it helps?
- Do my current medicines carry any known kidney risks I should watch for?