Anti-Tumor Necrosis Factor Therapy for IBD Tied to Kidney Function Decline – Renal and Urology News

Anti-tumor necrosis factor (anti-TNF) therapy may increase the risk for kidney function decline in patients with inflammatory bowel disease (IBD), according to investigators.

In a study of 10,689 US veterans with new-onset IBD (93.5% male; mean age, 67.4 years), 14.2% initiated anti-TNF therapy, including adalimumab, infliximab, certolizumab, and golimumab. At baseline, mean estimated glomerular filtration rate (eGFR) was 77.2 mL/min/1.73 m², and 31.4% had diabetes.

Over a median 4.1 years, 3367 patients experienced at least a 30% decline in eGFR. In adjusted multivariable analyses, TNF inhibitor users had a significant 34% increased risk for eGFR decline compared with nonusers, Csaba P. Kovesdy, MD, of Memphis VA Medical Center in Tennessee, and colleagues reported in JAMA Network Open. The risk for kidney function decline was significantly increased 40% among patients with Crohn disease and 25% among patients with ulcerative colitis. Results were consistent across age, body mass index, and diabetes status.

Anti-TNF therapy was not associated with the risk for eGFR decline among patients using corticosteroids.

No association was found between anti-TNF use and all-cause mortality.

According to Dr Kovesdy’s team, the association of TNF inhibitor use with progressive eGFR decline suggest “the need for careful assessment and monitoring of kidney function when initiating anti-TNF therapy in patients with IBD.”

Among the study’s limitations, the investigators could not account for all confounders. The veteran population included few women.

Other research has also found an association between IBD, chronic kidney disease (CKD) and acute kidney injury (AKI) among adults without a genetic predisposition. IgA nephropathy is more common among patients with IBD and predicts kidney failure.

Disclosure: One study author declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of authors’ disclosures.