IgA nephropathy is the most common chronic glomerulopathy. In addition to the defining mesangial IgA deposition, codeposition of IgG and C3 is typically found in the condition. More rarely, IgM and/or C1q mesangial label is reported. No systematic examination of the significance of these reactants or the mechanism by which they occur has been reported.

Complete clinical, histopathologic, and immunohistochemical data were available in 74 children (age at onset 2 to 17 years). All had typical primary IgA nephropathy, with codeposition of IgG and C3. The presence and intensity(trace to 3+) of codeposited C1q or IgM was examined, as was a number of clinical features including the urinalysis performed at the time of kidney biopsy.

Fourteen children had C1q or IgM deposition of more than trace intensity; of these, all 14 had IgM and 5 had IgM and C1q. C1q was not found in the absence of IgM. These 14 children did not differ from those without significant IgM or C1q labeling in age at onset, sex distribution, length of follow-up, or disease severity (as assessed by most recent serum creatinine).

All 14 (100%) of these children had urine protein concentration of>1+ at the time of biopsy. In contrast, only 4 of 40 (10%) children whose glomeruli were completely negative for C1q and IgM had urine protein >1+ at the time of biopsy. Of the 20 children with trace mesangial label for C1q or IgM, an intermediate frequency of>1+ proteinuria (11 of 20 = 55%) was found.

Of the entire group, 31 children had urine protein >1+. Of these, 25(81%) had at least a trace label of IgM or C1q. In contrast, only 9 of the 43 children (21%) with no proteinuria had IgM labeling; in none was it greater than trace in intensity. None of these children had a C1q label.

Significant mesangial labeling with IgM, with or without C1q, is a common finding in childhood primary IgA nephropathy. It appears to be of no clinical importance. As is the case in nephrotic syndrome with C1q or IgM mesangial label, our data suggest that the finding may represent nonspecific mesangial trapping in the presence of heavy proteinuria. It is unlikely that these reactants are important in this immunopathogenesis of this glomerulopathy.