Abnormal glucose metabolism and galactose-deficient immunoglobulin A1 (IgA1) synthesis: a possible mechanism of IgA nephropathy.

It is widely accepted that a possible etiopathogenic factor associated with IgA nephropathy is the glycosylation of IgA1 molecule O-glycans. The present study aimed to determine if galactose-deficient IgA1 is related to glucose metabolism. IgA nephropathy was identified from the renal biopsies of 108 adult patients enrolled in our study with 60 healthy controls. The concentration of serum lactose, galactose, and lactase was measured. The relationship between glucose metabolism, proteinuria, and renal pathological changes was studied. The circulating lactose level was higher in IgAN patients compared to that in the healthy controls [143.9 (93.9-225.6) vs. 77.9 (54.9 - 209.6); p < 0.001]. The circulating lactase level was lower in IgAN patients than that in the healthy controls (229.9 ± 57.56 vs. 270.0 ± 69.30; p < 0.001). Serum galactose level of IgAN patients was lower than that of healthy controls but without significant differences. Lactose levels showed a significant positive correlation with 24-h proteinuria (r = 0.222; p = 0.021). The differences in lactose and lactase from the IgAN patients and healthy controls may be an indicator of the possible pathogenesis of IgAN. The level of serum lactose was correlated with the level of 24-h urinary protein during the same period, suggesting that it plays a role in IgA kidney disease progression. Future studies are required to validate our findings during the follow-up and investigate the underlying mechanisms.