ESPN 50th Annual Meeting

ESPN 2017


 
IL-10 as a potential mediator in parenchymal damage in children with congenital anomalies of the kidney and urinary tract
EMILIYA KOSTADINOVA 1 LYUBA MITEVA 1 SPASKA STANILOVA 1

1- TRAKIA UNIVERSITY, MEDICAL FACULTY, Bulgaria
 
Introduction:

IL-10 has essential role in the regulation of the tissue healing/regeneration, fibrosis and regulation of immune response. Since, the parenchymal damage is frequently observed among patients with congenital anomalies of the kidney and urinary tract (CAKUT) we aimed to evaluate the relationship between IL-10 serum levels and parenchymal damages in children with CAKUT. Therefore, we also aimed to clarify whether the IL10 rs1800896 polymorphism has implication in the CAKUT pathogenesis. 

Material and methods:

 The quantitative determination of IL-10 in sera was performed by ELISA test in 79 CAKUT patients and 18 age-sex-matched unaffected children from Bulgarian population. Genotyping of IL10 rs1800896 was performed by allele specific-PCR reaction.

Results:

 Serum IL-10 was elevated in total group of CAKUT cases compared to controls with marginal significance (28.6±36pg/ml vs. 12.4±8.5; p=0.066). Patients with renal hypo/dysplasia showed higher IL-10 levels compared to patients with renal agenesis and controls (37.3±49.5pg/ml; 17.1±9.5pg/ml; 12.4±8.5pg/ml, respectively). Cases with high-grade hydronephrosis elevated IL-10 than controls (34.4 ±32.2pg/ml; p=0.01), in contrast to cases with low-grade hydronephrosis. Also, we observed that almost all extremes values of serum IL-10 belongs to CAKUT patients with -1082*GG-genotype of IL10 rs1800896. Among CAKUT patients with parenchymal damage, GG-genotype was associated with higher serum IL-10 (48.7±63.5pg/ml) compared to AA (26.03±27pg/ml; p=0.05) and AG (22.7±27pg/ml; p=0.045) genotypes as well as compared to controls with the same genotype (14.1±9pg/ml, p=0.03)     

Conclusions:

IL-10 might be involved into pathogenesis of parenchymal damage in CAKUT. Higher IL-10 level, at least partially determined by -1082*GG genotype may contribute to IL-10 mediated renal damage in renal hypo/dysplasia, high-grade hydronephrosis and reflux nephropathy.