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Article: Mannose binding lectin level and polymorphism in patients on long-term peritoneal dialysis

TitleMannose binding lectin level and polymorphism in patients on long-term peritoneal dialysis
Authors
KeywordsGene mutation
Haemodialysis
Mannose binding lectin
Peritoneal dialysis
Peritonitis
Issue Date2005
PublisherOxford University Press. The Journal's web site is located at http://ndt.oxfordjournals.org/
Citation
Nephrology Dialysis Transplantation, 2005, v. 20 n. 11, p. 2489-2496 How to Cite?
AbstractBackground. Infection is a leading cause of mortality and morbidity in patients with end-stage renal disease. The increased susceptibility to infection is probably secondary to the impaired immune defence in uraemia and other co-morbid factors such as diabetes mellitus. Peritonitis remains the most common and major complication in the treatment modality of peritoneal dialysis (PD) for uraemic patients. Mannose binding lectin (MBL) is a calcium dependent C-type lectin that acts as an important first line defence mechanism against infection by its capability to activate the complement system and enhance phagocytosis. Methods. We examined whether serum concentration of MBL and the point mutation of MBL may act as a risk factor in PD-related peritonitis. We studied four groups of dialysis patients: PD patients with two or more episodes of peritonitis, peritonitis-free PD patients, haemodialysis (HD) patients not previously on PD, and HD patients who were converted from PD due to technique failure following peritonitis-related abdominal adhesion. Results. Both homozygous and heterozygous patients had profoundly reduced serum level of MBL. The codon 54 point mutation rate amongst our dialysis patients was comparable with that of healthy subjects. Dialysis patients had a significantly lower serum level of MBL than healthy controls independent of the MBL gene mutation or the mode of dialysis treatment. Patients on PD with codon 54 point mutation were found to have a lower serum MBL level compared with HD patients with similar MBL gene mutation. However, we found no difference in the serum MBL level or frequency of codon 54 point mutation between four groups of dialysis patients. Conclusions. Dialysis patients have lower MBL levels that may increase the susceptibility of infection. However, the existence of other risk factors such as connection technique, nasal bacterial carriers, bowel pathology and personal hygiene precludes the MBL level as the sole primary factor for peritonitis in patients on maintenance PD treatment. © The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/78080
ISSN
2015 Impact Factor: 4.085
2015 SCImago Journal Rankings: 1.780
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLam, MFen_HK
dc.contributor.authorLeung, JCKen_HK
dc.contributor.authorTang, CCSen_HK
dc.contributor.authorLo, WKen_HK
dc.contributor.authorTse, KCen_HK
dc.contributor.authorYip, TPen_HK
dc.contributor.authorLui, SLen_HK
dc.contributor.authorChan, TMen_HK
dc.contributor.authorLai, KNen_HK
dc.date.accessioned2010-09-06T07:38:57Z-
dc.date.available2010-09-06T07:38:57Z-
dc.date.issued2005en_HK
dc.identifier.citationNephrology Dialysis Transplantation, 2005, v. 20 n. 11, p. 2489-2496en_HK
dc.identifier.issn0931-0509en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78080-
dc.description.abstractBackground. Infection is a leading cause of mortality and morbidity in patients with end-stage renal disease. The increased susceptibility to infection is probably secondary to the impaired immune defence in uraemia and other co-morbid factors such as diabetes mellitus. Peritonitis remains the most common and major complication in the treatment modality of peritoneal dialysis (PD) for uraemic patients. Mannose binding lectin (MBL) is a calcium dependent C-type lectin that acts as an important first line defence mechanism against infection by its capability to activate the complement system and enhance phagocytosis. Methods. We examined whether serum concentration of MBL and the point mutation of MBL may act as a risk factor in PD-related peritonitis. We studied four groups of dialysis patients: PD patients with two or more episodes of peritonitis, peritonitis-free PD patients, haemodialysis (HD) patients not previously on PD, and HD patients who were converted from PD due to technique failure following peritonitis-related abdominal adhesion. Results. Both homozygous and heterozygous patients had profoundly reduced serum level of MBL. The codon 54 point mutation rate amongst our dialysis patients was comparable with that of healthy subjects. Dialysis patients had a significantly lower serum level of MBL than healthy controls independent of the MBL gene mutation or the mode of dialysis treatment. Patients on PD with codon 54 point mutation were found to have a lower serum MBL level compared with HD patients with similar MBL gene mutation. However, we found no difference in the serum MBL level or frequency of codon 54 point mutation between four groups of dialysis patients. Conclusions. Dialysis patients have lower MBL levels that may increase the susceptibility of infection. However, the existence of other risk factors such as connection technique, nasal bacterial carriers, bowel pathology and personal hygiene precludes the MBL level as the sole primary factor for peritonitis in patients on maintenance PD treatment. © The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://ndt.oxfordjournals.org/en_HK
dc.relation.ispartofNephrology Dialysis Transplantationen_HK
dc.rightsNephrology, Dialysis, Transplantation. Copyright © Oxford University Press.en_HK
dc.subjectGene mutationen_HK
dc.subjectHaemodialysisen_HK
dc.subjectMannose binding lectinen_HK
dc.subjectPeritoneal dialysisen_HK
dc.subjectPeritonitisen_HK
dc.subject.meshAdulten_HK
dc.subject.meshAscitic Fluid - metabolismen_HK
dc.subject.meshDNA - geneticsen_HK
dc.subject.meshEnzyme-Linked Immunosorbent Assayen_HK
dc.subject.meshExonsen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Frequencyen_HK
dc.subject.meshGenetic Markersen_HK
dc.subject.meshGenotypeen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMannose-Binding Lectin - genetics - metabolismen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshPeritoneal Dialysis, Continuous Ambulatory - adverse effectsen_HK
dc.subject.meshPeritonitis - etiology - genetics - metabolismen_HK
dc.subject.meshPoint Mutationen_HK
dc.subject.meshPolymerase Chain Reactionen_HK
dc.subject.meshPolymorphism, Geneticen_HK
dc.subject.meshRetrospective Studiesen_HK
dc.subject.meshRisk Factorsen_HK
dc.subject.meshUremia - metabolism - therapyen_HK
dc.titleMannose binding lectin level and polymorphism in patients on long-term peritoneal dialysisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0931-0509&volume=20&spage=2489&epage=2496&date=2005&atitle=Mannose+binding+lectin+level+and+polymorphism+in+patients+on+long-term+peritoneal+dialysisen_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.emailChan, TM: dtmchan@hku.hken_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.identifier.authorityChan, TM=rp00394en_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1093/ndt/gfi089en_HK
dc.identifier.pmid16115848-
dc.identifier.scopuseid_2-s2.0-27644522825en_HK
dc.identifier.hkuros117891en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-27644522825&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume20en_HK
dc.identifier.issue11en_HK
dc.identifier.spage2489en_HK
dc.identifier.epage2496en_HK
dc.identifier.isiWOS:000232593600030-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLam, MF=35300050600en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.scopusauthoridTang, CCS=9036754800en_HK
dc.identifier.scopusauthoridLo, WK=7201502414en_HK
dc.identifier.scopusauthoridTse, KC=7102609864en_HK
dc.identifier.scopusauthoridYip, TP=7004283977en_HK
dc.identifier.scopusauthoridLui, SL=7102379130en_HK
dc.identifier.scopusauthoridChan, TM=7402687700en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.citeulike353099-

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