Gene polymorphisms and serum alpha-2-Heremans-Schmid levels in Italian haemodialysis patients.
BACKGROUND
Vascular calcification (VC) and accelerated atherosclerosis are major causes of cardiovascular (CV) morbidity and mortality in haemodialysis (HD) patients. Inhibitory proteins are associated with reduced VC and may play a key role in preventing CV in chronic kidney disease (CKD) patients. Fetuin-A, also known as alpha(2)-Heremans-Schmid glycoprotein (AHSG), is a circulating plasma protein with inhibitory effects on VC that has been associated with inflammation and CV mortality in HD patients. In the present study, we investigated the associations between serum fetuin-A levels and its gene (AHSG) polymorphisms in an Italian HD population.


METHODS
Ninety-six patients on stable chronic HD treatment and 57 healthy controls were genotyped for the common polymorphisms on the AHSG (T256S). In addition, serum fetuin-A levels were tested.


RESULTS
In this study, serum fetuin-A levels were lower in HD patients (0.35 +/- 0.11 g/l) compared with healthy controls (0.62 +/- 0.31 g/l, p < 0.05). In both HD patients and the control group, the distribution of the AHSG gene did not show significant association between low serum fetuin-A levels and the Ser/Ser genotype, known to be associated with a higher CV mortality risk in the HD population. Moreover, the distribution of AHSG gene polymorphisms in HD patients and in healthy controls was similar.


CONCLUSIONS
In contrast with previous reports, this study suggests that CKD patients on HD treatment have a similar polymorphism distribution of the AHSG gene compared with the normal population and that the reduction in serum fetuin-A levels in Italian HD patients is not associated with an alteration in the distribution of AHSG T256S polymorphisms.
Cozzolino
Mario
M
Renal Division, S. Paolo Hospital, University of Milan, Milan, Italy. mariocozzolino@hotmail.com
Biondi
Maria Luisa
ML
Galassi
Andrea
A
Gallieni
Maurizio
M
d'Eril
Gian Vico Melzi
GV
Brancaccio
Diego
D
D000368:Aged; D050197:Atherosclerosis / Q000235:genetics / Q000378:metabolism; D001798:Blood Proteins / Q000032:analysis / Q000235:genetics*; D002114:Calcinosis / Q000235:genetics* / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000235:genetics* / Q000378:metabolism; D016022:Case-Control Studies; D005260:Female; D005838:Genotype; D006801:Humans; D007558:Italy; D007676:Kidney Failure, Chronic / Q000150:complications / Q000628:therapy; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D006435:Renal Dialysis; D060749:alpha-2-HS-Glycoprotein
C556354:AHSG protein, human; D001798:Blood Proteins; D060749:alpha-2-HS-Glycoprotein