title: Serum paraoxonase activity changes in uremic and kidney-transplanted patients.
abstract: Serum paraoxonase (PON) is a high-density lipoprotein (HDL)-associated hydrolase, which inhibits low-density lipoprotein oxidation. Uremic and kidney-transplanted patients have an increased risk of atherosclerosis, to which an increased lipoprotein oxidation may contribute. The aim of our study was to determine whether the PON activity or phenotype is altered in uremic and kidney-transplanted patients, and to compare the values with those of healthy controls. 117 uremic patients on long-term hemodialysis treatment, 115 renal-transplanted patients, and 110 healthy controls were involved in the study. The PON activity was significantly reduced in the uremic patients compared to controls (PON 101.36+/-30. 12 vs. control 188.05+/-58.96 U/ml; p < 0.001), while in kidney-transplanted patients the values were almost identical to those of controls (PON 161.5+/-35.39 U/ml). The different immunosuppressive drug combinations did not influence PON activity. To assess whether the altered PON activity was due to a decrease HDL level, we standardized the enzyme activity for the HDL concentration (PON/HDL ratio). We found that the standardized enzyme activity was lower in the uremic (102.7+/-54.8) and kidney-transplanted patients (144.5+/-32.7) when compared to controls (194.5+/-94.5; p < 0.001). The phenotypic distribution of PON in uremic, renal transplant and control patients are as follows: AA 66.67, 56.48 and 66.67%; AB 31. 62, 33.3 and 26.67%; BB 1.71, 10.19 and 6.67%. We conclude that the decreased PON/HDL and PON/apoA-1 ratios may lead to a reduction in the antioxidant capacity of HDL, which might contribute to the accelerated development of atherosclerosis in uremic and kidney-transplanted patients.
authors.affiliation: 1st Department of Internal Medicine, University Medical School of Debrecen, Debrecen, Hungary. paragh@ibel.dote.hu
authors.forename: G
authors.initials: G
authors.lastname: Paragh
authors.forename: L
authors.initials: L
authors.lastname: Asztalos
authors.forename: I
authors.initials: I
authors.lastname: Seres
authors.forename: Z
authors.initials: Z
authors.lastname: Balogh
authors.forename: L
authors.initials: L
authors.lastname: Löcsey
authors.forename: I
authors.initials: I
authors.lastname: Kárpáti
authors.forename: J
authors.initials: J
authors.lastname: Mátyus
authors.forename: E
authors.initials: E
authors.lastname: Katona
authors.forename: M
authors.initials: M
authors.lastname: Harangi
authors.forename: G
authors.initials: G
authors.lastname: Kakuk
mesh_terms: D000328:Adult; D043303:Aryldialkylphosphatase; D002265:Carboxylic Ester Hydrolases / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D004950:Esterases / Q000097:blood*; D005260:Female; D006801:Humans; D007166:Immunosuppressive Agents / Q000494:pharmacology; D016030:Kidney Transplantation / Q000502:physiology*; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D014280:Triglycerides / Q000097:blood; D014511:Uremia / Q000097:blood*
chemical_list: D007166:Immunosuppressive Agents; D008055:Lipids; D014280:Triglycerides; D002784:Cholesterol; D004950:Esterases; D002265:Carboxylic Ester Hydrolases; C019734:arylesterase; D043303:Aryldialkylphosphatase