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Updated: Aug 5, 2026

Isolation of Glomeruli and In Vivo Labeling of Glomerular Cell Surface Proteins
Published on: January 18, 2019
Circulating immune complexes in idiopathic glomerular disease
Circulating immune complexes (CIC) could be found in the majority of 271 sera from 131 patients with idiopathic minimal change, membranous and mesangial proliferative glomerulonephritis when a combination of CIC assays detecting different properties of CIC were used. In neither individual patients nor in any of the three groups as a whole did CIC levels reflect the state of the renal lesion. No correlation was found between the class of immunoglobulin in the CIC and that deposited in the kidney. With the exception of minimal change disease in which non-C1q binding IgG CIC predominated, a range of CIC was found in the patients examined. The pattern of CIC detected did not allow different forms of renal disease to be distinguished. IgA CIC could be found in mesangial proliferative glomerulonephritis both with and without IgA deposition and in some patients with membranous and minimal change disease, as well as in a high proportion of sera from 12 patients with the Henoch-Schönlein syndrome. CIC size was estimated in six patients, but only in one did a specific size of complex predominate. The CIC which may be found in the majority of sera from patients with idiopathic glomerulonepohritis provide little information of clinical value; no direct relationship can be demonstrated between the CIC found and the renal lesion.
Circulating immune complexes (CIC) could be found in the majority of 271 sera from 131 patients with idiopathic minimal change, membranous and mesangial proliferative glomerulonephritis when a combination of CIC assays detecting different properties of CIC were used. In neither individual patients nor in any of the three groups as a whole did CIC levels reflect the state of the renal lesion. No correlation was found between the class of immunoglobulin in the CIC and that deposited in the kidney. With the exception of minimal change disease in which non-C1q binding IgG CIC predominated, a range of CIC was found in the patients examined. The pattern of CIC detected did not allow different forms of renal disease to be distinguished. IgA CIC could be found in mesangial proliferative glomerulonephritis both with and without IgA deposition and in some patients with membranous and minimal change disease, as well as in a high proportion of sera from 12 patients with the Henoch-Schönlein syndrome. CIC size was estimated in six patients, but only in one did a specific size of complex predominate. The CIC which may be found in the majority of sera from patients with idiopathic glomerulonepohritis provide little information of clinical value; no direct relationship can be demonstrated between the CIC found and the renal lesion.
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