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Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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The infection risk in lupus nephritis (LN) remains uncertain. There is limited data on the correlation between the FCGR3A-F158V, FCGR2A-H131R polymorphisms and susceptibility to infection in LN. Our study aims to determine in LN: (1) The distribution of FCGR3A-F158V and FCGR2A-H131R polymorphisms; (2) The association of the FCGR3A-F158V, FCGR2A-H131R polymorphisms and infection.
A cross-sectional study was conducted at Cho Ray Hospital (12/2021- 07/2023) in 207 LN participants. All LN participants met the Systemic Lupus International Collaborating Clinics 2012 criteria with 24-hour proteinuria > 0.5g/day or urine protein creatinine ratio > 500mg/g. Kidney failure was defined as estimated glomerular filtration rate (CKD-EPI 2009) on admission ≤ 60 ml/min/1.73m2. Three categories of infection were identified using the combination of (1) microbiology results, (2) infectious signals, and (3) the systemic inflammatory response syndrome: group 1 (no infection if none of 3 positive), group 2 (possible infection if (2) and/or (3) positive but negative microbiology results), and group 3 (definite infection if positive microbiology results with (2) and/or (3) positive). Histology results were based on the 2018 revised International Society of Nephrology/Renal Pathology Society classification. Participants on long-term dialysis and those with pregnancy were excluded. FCGR3A-F158V and FCGR2A-H131R genotypes were identified by polymerase chain reaction and reverse hybridization. The distribution of genotypes and haplotypes was compared using the χ2-test with the predicted values of Hardy-Weinberg equilibrium. Linkage disequilibrium (LD) between 2 loci was measured by the r2 and D’ methods. p < 0.05 was statistically significant.
There were 44 in group 1, 92 in group 2, and 71 in group 3. Groups 2 and 3 had higher percentages of participants with ≥ 2 extrarenal damaged organs, higher proportions of kidney failure, higher C-reactive protein levels, and higher percentages of acute tubulointerstitial nephritis than group 1 (p<0.05). The majority was class III/IV LN (74/76, 93.7%). There were 80 episodes of infection among 207 LN participants. The common organisms as Gram-negative bacteria (30/80, 37.5%) and Candida spp. (24/80, 30%). The skewed allelic and genotypic distributions in group 1, 2, and 3 of F158 were 0.577, 0.712, and 0.511 (p=0.002); VF were 0.568, 0.446, and 0.563 (p=0.009), respectively. No significant skewing in the distribution of FCGR2A-H131R was found in group 1, 2, and 3: H131 were 0.682, 0.598, and 0.711, p=0.085, respectively; HR were 0.409, 0.522, and 0.408, p=0.229, respectively. The FF genotype was susceptible to possible infection compared to VV (OR=6.49, p=0.005). FCGR2A-H131R did not confer risks of infection in LN participants. There was no LD of allelic inheritance in our cohort (D’= 0.122, r2 = 0.01, p = 0.021).
Alleles F158 and H131, VF and HR genotypes were common in Vietnamese LN individuals. No association was found between FCGR2A-H131R and infection; however, the FF genotype could be linked with susceptibility to possible infection in such a population.
