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NDT Advance Access originally published online on August 22, 2005
Nephrology Dialysis Transplantation 2005 20(11):2489-2496; doi:10.1093/ndt/gfi089
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org


Original Article

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

Man Fai Lam, Joseph C. K. Leung, Colin C. S. Tang, Wai Kei Lo, Kai Chung Tse, Terrance P. Yip, Sing Leung Lui, Tak Mao Chan and Kar Neng Lai

Nephrology Division, Department of Medicine, University of Hong Kong, Pokfulam Road, Hong Kong

Correspondence and offprint requests to: Professor K. N. Lai, Department of Medicine, University of Hong Kong, Queen Mary Hospital, 102 Pokfulam Road, Hong Kong. Email: knlai{at}hkucc.hku.hk

Background. 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.

Keywords: gene mutation; haemodialysis; mannose binding lectin; peritoneal dialysis; peritonitis


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