[Impact of interleukin-10 and interleukin-28 gene polymorphisms on the development and course of lupus nephritis].
OBJECTIVE
To assess the relationship of the carriage of IL-10-1080 G/A and IL-28 rs8099917 C/T polymorphisms to the course of lupus nephritis (LN).


METHODS
Ninety-nine patients with systemic lupus erythematosus (SLE), including 68 with LN, were examined. Gene polymorphisms were analyzed using standard molecular genetic techniques. The frequency of the clinical manifestations of LN was analyzed; renal survival (RS) was estimated by the Kaplan-Meier method.


RESULTS
Ten-year RS rates were 80 and 86% of the patients with and without the mutant IL-10 allele, respectively (p = 0.78). The 10-year RS was lower (75%) in carriers of the mutant IL-28 rsl2979860 allele than in patients without this mutant allele (83%; p = 0.049) and in those of the mutant IL28 rs8099917 allele than in patients without the above mutant allele (67 and 88%, respectively; p = 0.047). LN patients, carriers of the mutant IL-10-1028 G/A allele, were observed to have higher-grade proteinuria in the presence of nephritic syndrome (mean 6.1 g/l) than those without the mutant allele of this gene (mean 2.9 g/l; p = 0.034). However, the mutant allele carriers responded to treatment better (p = 0.050). The mutant IL-10 and IL-28 alleles were unassociated with the development of rapidly progressive nephritis, the activity of a renal lupus process, and the rate of onset of SLE and LN.


CONCLUSIONS
In the LN patients, the carriage of the mutant IL-10 allele A is associated with a better response to treatment and that of the mutant IL-28 allele is linked to the severe course of the disease.
Department of Internal Medicine, Faculty of Fundamental Medicine, M.V. Lomonosov Moscow State University, Moscow, Russia.
T N
TN
Krasnova
Laboratory of Gene and Cell Technologies, Department of Biochemistry and Molecular Medicine, Faculty of Fundamental Medicine, M.V. Lomonosov Moscow State University, Moscow, Russia.
L M
LM
Samokhodskaya
Department of Internal Medicine, Faculty of Fundamental Medicine, M.V. Lomonosov Moscow State University, Moscow, Russia.
L V
LV
Ivanitsky
E.M. Tareev Clinic of Nephrology, Internal and Occupational Diseases, I.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia, Moscow, Russia.
A D
AD
Korogodina
Department of Internal Medicine, Faculty of Fundamental Medicine, M.V. Lomonosov Moscow State University, Moscow, Russia.
E N
EN
Borisov
E.M. Tareev Clinic of Nephrology, Internal and Occupational Diseases, I.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia, Moscow, Russia.
N V
NV
Nikiforova
E.M. Tareev Clinic of Nephrology, Internal and Occupational Diseases, I.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia, Moscow, Russia.
P I
PI
Novikov
Medical Research and Education Center, M.V. Lomonosov Moscow State University, Moscow, Russia.
A A
AA
Kamalov
Department of Internal Medicine, Faculty of Fundamental Medicine, M.V. Lomonosov Moscow State University, Moscow, Russia.
N A
NA
Mukhin
D000328:Adult; D000483:Alleles; D004247:DNA / Q000235:genetics*; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D016753:Interleukin-10 / Q000097:blood / Q000235:genetics*; D007378:Interleukins / Q000097:blood / Q000235:genetics*; D008181:Lupus Nephritis / Q000097:blood / Q000235:genetics*; D008297:Male; D009154:Mutation; D011110:Polymorphism, Genetic; D000095022:Interferon Lambda
D004247:DNA; D016753:Interleukin-10; D007378:Interleukins; C000624353:interferon-lambda, human; D000095022:Interferon Lambda