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Paraoxonase 1 192 and 55 polymorphisms in nephrotic children

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dc.contributor.authorALPAY, HARİKA
dc.contributor.authorsBiyikli, NK; Alpay, H; Yildiz, N; Agachan, B; Ergen, A; Zeybek, U; Bozkurt, N; Ispir, T
dc.date.accessioned2022-03-12T17:21:44Z
dc.date.available2022-03-12T17:21:44Z
dc.date.issued2006
dc.description.abstractHuman paraoxonase 1 (PON1) is a serum enzyme related to high-density lipoprotein which has a major role in preventing oxidative modification of low-density lipoprotein. Due to its amino acid substitution PON1 has two genetic polymorphisms. These polymorphisms are characterized by the location of glutamine (A genotype) and arginine (B genotype) at position 192, and leucine (L genotype) and methionine (M genotype) at position 55. Hyperlipidemia and increased lipid oxidation in nephrotic syndrome may lead to glomerulosclerosis and progression of the glomerular disease. In this study we aimed to investigate PON1 192 and PON1 55 polymorphisms in children with focal segmental glomerulosclerosis (FSGS) and control subjects. The study included 25 children with biopsy-proven FSGS and 30 healthy controls. We demonstrated a statistically significant difference between FSGS patients and control subjects with respect to the distribution of the PON1 polymorphism. The AA genotype was less frequent and the AB+BB genotype was more frequent in FSGS patients than in controls (48 versus 73% for AA genotype and 52 versus 27% for AB+BB genotype, p < 0.05). Distributions of PON1 55 genotypes of FSGS and control subjects were also statistically different (76 versus 43% for LL genotype and 24 versus 57% for LM+MM genotype, p < 0.05) (case-control study, dominant model, Fisher's exact test). The distributions of both genotypes in subgroups of FSGS (stable renal function versus declining renal function) were not statistically different. We conclude in this preliminary study that presence of B allele and/or L allele may be risk factors for the development of FSGS in children.
dc.identifier.doi10.1007/s00467-006-0073-y
dc.identifier.issn0931-041X
dc.identifier.pubmed16565923
dc.identifier.urihttps://hdl.handle.net/11424/228360
dc.identifier.wosWOS:000237189700007
dc.language.isoeng
dc.publisherSPRINGER
dc.relation.ispartofPEDIATRIC NEPHROLOGY
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectparaoxonase 1 192 polymorphism
dc.subjectparaoxonase 1 55 polymorphism
dc.subjectnephrotic syndrome
dc.subjectchild
dc.subjectFOCAL SEGMENTAL GLOMERULOSCLEROSIS
dc.subjectCORONARY-HEART-DISEASE
dc.subjectMOLECULAR-BASIS
dc.subjectRISK
dc.subjectDNA
dc.titleParaoxonase 1 192 and 55 polymorphisms in nephrotic children
dc.typearticle
dspace.entity.typePublication
local.avesis.idaee32a6b-b645-4e66-90af-e1dd5039704d
local.import.packageSS17
local.indexed.atWOS
local.indexed.atSCOPUS
local.indexed.atPUBMED
local.journal.numberofpages6
oaire.citation.endPage654
oaire.citation.issue5
oaire.citation.startPage649
oaire.citation.titlePEDIATRIC NEPHROLOGY
oaire.citation.volume21
relation.isAuthorOfPublication102b331c-4c62-4795-880d-234f6b72fa6a
relation.isAuthorOfPublication.latestForDiscovery102b331c-4c62-4795-880d-234f6b72fa6a

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