Increased urinary excretion of macrophage-colony-stimulating factor (M-CSF) in patients with IgA nephropathy: Tonsil stimulation enhances urinary M-CSF excretion

Upper respiratory tract infection including chronic tonsillitis is consider ed to be involved in the onset and/or the progression of IgA nephropathy. I t is well known that deterioration of urinary findings occurs after episode s of upper respiratory tract infection in patients with IgA nephropathy. We previously showed that the expression of macrophage-colony-stimulating fac tor (M-CSF) is increased in the glomeruli of patients with IgA nephropathy and correlated with glomerular mesangial proliferation, suggesting that M-C SF plays an important role in the progression of IgA nephropathy. In the pr esent study, we measured the serum and urinary concentrations of M-CSF in p atients with IgA nephropathy associated with chronic tonsillitis. Furthermo re, we evaluated the effects of the local provocation test of tonsils (mech anical tonsil stimulation) on the serum and urinary concentrations of M-CSF in the following three groups: (1) IgA nephropathy with severe mesangial p roliferation, (2) IgA nephropathy with mild mesangial proliferation, and (3 ) patients with chronic tonsillitis without renal disease. The serum and ur inary levels of M-CSF in the groups with severe and mild IgA nephropathy we re significantly higher than those in the chronic tonsillitis group. The ur inary M-CSF level but not the serum M-CSF level was positively correlated w ith the degrees of mesangial proliferation and glomerular M-CSF expression in the renal biopsy specimens. The urinary M-CSF concentration was signific antly increased after tonsillitis stimulation in both mild and severe IgA n ephropathy groups. Enhanced urinary excretion of M-CSF prolonged for 7 days after tonsil stimulation in the severe IgA nephropathy group; in contrast, the urinay M-CSF level was increased for only 2 days after tonsil stimulat ion in the mild IgA nephropathy group. The urinary M-CSF level was not chan ged in the chronic tonsillitis group after tonsil stimulation. The serum co ncentrations of M-CSF were not changed after tonsil stimulation in these th ree groups. Our present results suggest that tonsil stimulation contributes to the progression of IgA nephropathy via enhancement of glomerular produc tion of M-CSF. The urinary excretion of M-CSF may be a useful predictor to evaluate the relevance of chronic tonsillitis to the disease and the indica tion of tonsillectomy in patients with IgA nephropathy.