[Clinical value of TNF, IL-6, and IL-10 gene polymorphic markers in chronic glomerulonephritis].
OBJECTIVE
To study the association of the polymorphic markers (PMs) G(-238)A of the TNF gene, G(-174)C of the IL-6 gene, and G(-1082)A of the IL-10 gene with the clinical characteristics of chronic glomerulonephritis (CGN) and a response to immunosuppressive therapy (IST).


METHODS
Clinical syndromes at the time of diagnosis, the morphological types of nephritis, and a response to IST were analyzed in relation to the carriage of the examined PMs of the TNF, IL-6, and IL-10 genes in 102 patients with CGN.


RESULTS
No association was found between the PM G(-238)A of the TNF gene and the clinical features of CGN. The carriers of the C allele of the PM G(-174) C of the IL-6 gene versus the homozygous individuals were observed to have more frequently kidney dysfunction at the time of diagnosis (р=0.014). Hypertension was more common in the carriers of the AA genotype of the PM G(-1082)A of the IL-10 gene (p=0.023); moreover, they tended to have a more frequent concurrence of nephrotic syndrome and hypertension (p=0.082). Analysis of the distribution of the morphological types of CGN disclosed that the proliferative variants were more common in the patients with the GG genotype (the TNF gene) as compared to the A allele carriers (p=0.067); and the nonproliferative forms were in the individuals homozygous for GG (the IL-6 gene) as compared to the C allele carriers (p=0.067). Examination of an IST response showed that a complete response at 12 months of treatment occurred more frequently in the carriers of the C allele of the IL-6 gene (p=0.045) and in those of the GG genotypes of the IL-10 gene (p=0.030).


CONCLUSIONS
There was an association of the PMs G(-174)C of the IL-6 gene and G(-1082)A of the IL-10 gene with the clinical features of CGN and a response to IST.
I.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia, Moscow, Russia.
E S
ES
Kamyshova
I.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia, Moscow, Russia; M.V. Lomonosov Moscow State University, Moscow, Russia.
M Yu
MY
Shvetsov
I.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia, Moscow, Russia.
I M
IM
Kutyrina
Research Institute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences, Moscow, Russia; N.M. Emanuel Institute of Biochemical Physics, Russian Academy of Sciences, Moscow, Russia.
A M
AM
Burdennyi
M.V. Lomonosov Moscow State University, Moscow, Russia.
A
A
Zheng
N.M. Emanuel Institute of Biochemical Physics, Russian Academy of Sciences, Moscow, Russia.
V V
VV
Nosikov
I.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia, Moscow, Russia.
I N
IN
Bobkova
D000328:Adult; D002908:Chronic Disease; D005260:Female; D005819:Genetic Markers; D020022:Genetic Predisposition to Disease; D005921:Glomerulonephritis / Q000175:diagnosis / Q000235:genetics / Q000503:physiopathology / Q000628:therapy; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D016753:Interleukin-10 / Q000235:genetics*; D015850:Interleukin-6 / Q000235:genetics*; D007677:Kidney Function Tests; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
D005819:Genetic Markers; D007166:Immunosuppressive Agents; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10