Renal Tubular Complement 3 Deposition in Children with Primary Nephrotic Syndrome

Abstract

Background This study aimed to investigate the clinical significance of complement 3 (C3) deposition in renal tubules of children with primary nephrotic syndrome (PNS). Methods The clinical and pathological characteristics of PNS were retrospectively reviewed in 99 PNS pediatric patients, who were divided into the C3 deposition and the non-C3 deposition groups. Results A total of 39 patients (39.39%) had renal tubule C3 deposition. In the C3 deposition group, the ratios of urine N-acetylglucosaminidase/creatinine (UNAG/Cr), urine β2 microglobulin/creatinine (Uβ2MG/Cr), and urine transferrin/creatinine (UTRF/Cr) were significantly higher than those of the non-C3 deposition group. The patients of the C3 deposition group had lower serum total protein and albumin, higher cholesterol and D-dimer (DD), lower proportion of CD3+CD8+ cells, and higher proportion of CD19+CD23+ cells. The number of the patients with interstitial fibrosis, renal cell vacuolar degeneration, renal tubular immunoglobulin deposition, and severe tubulointerstitial injury in the C3 deposition group was higher than that of the non-C3 deposition group. The C3 deposition intensity was positively correlated with the number of recurrences. Conclusion PNS pediatric patients with C3 deposition in renal tubules have more severe disease condition, tubulointerstitial injury, and recurrence suggesting a worse long-term prognosis.

C3a and suPAR drive versican V1 expression in tubular cells of focal segmental glomerulosclerosis

“…Liu et al reported that compared with FSGS patients with no or mild tubulointerstitial injury, those with moderate or severe tubulointerstitial injury exhibited a lower level of serum C3 (31). Wang et al reported that nephrotic syndrome patients with C3 deposition in their renal tubules have more severe disease conditions, tubulointerstitial injury, and recurrence (32). We found that C3a bound to the tubular cells of FSGS patients and that C3a promoted the transcription of versican in tubular cells.…”