Tumour necrosis factor-alpha and microalbuminuria in patients with inflammatory bowel disease

To determine whether tumour necrosis factor-alpha (TNF-alpha) is important in the pathogenesis of microalbuminuria in patients with inflammatory bowel disease (IBD).

We measured serum TNF-alpha, interleukin (IL)-6, the erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) levels and microalbuminuria in 48 patients with IBD. Serum TNF-alpha was measured by enzyme-linked immunosorbent assay and microalbuminuria was measured using an immunoturbiditimetric method. Clinical disease activity was quantified using the simple index of Harvey and Bradshaw.

Microalbuminuria was more severe in patients with IBD than in controls, and in patients with active versus inactive disease. TNF-alpha levels were higher in patients with IBD than in controls (mean +/- SE 16.4 +/- 1.4 versus 6.6 +/- 1.3 pg/ml, respectively; P < 0.01) and in patients with active versus inactive IBD (means +/- SE 20.1 +/- 2 versus 12.8 +/- 2.7 pg/ml; respectively P = 0.056). Microalbuminuria correlated strongly with TNF-alpha (r = 0.60; P < 0.009), ESR (r = 0.67, P < 0.02) and CRP levels (r = 0.935, P < 0.001). TNF-alpha correlated significantly with CRP (r = 0.54, P < 0.01). IL-6 levels were raised significantly in patients with IBD (7 +/- 4 pg/ml, controls undetectable; P < 0.05). Patients with active IBD had higher IL-6 levels than those with inactive IBD (mean +/- SE 13 +/- 8 versus 0.90 +/- 0.35 pg/ml, respectively; P < 0.05). However, IL-6 levels did not correlate with microalbuminuria in patients with IBD (r = 0.105, P = 0.256).

Our findings suggest that TNF-alpha may be important in the pathogenesis of microalbuminuria in patients with IBD, possibly through TNF-induced damage to the glomerular basement membrane. The mechanism for this has not been defined but may relate to TNF-induced disruption of sulphated glycosaminoglycans.