INFLUENCE OF DIALYSIS MODALITY ON PLASMA AND TISSUE CONCENTRATIONS OF PENTOSIDINE IN PATIENTS WITH END-STAGE RENAL-DISEASE

被引:82
作者
FRIEDLANDER, MA
WU, YC
SCHULAK, JA
MONNIER, VM
HRICIK, DE
机构
[1] CASE WESTERN RESERVE UNIV,SCH MED,DEPT MED,CLEVELAND,OH
[2] CASE WESTERN RESERVE UNIV,SCH MED,DEPT SURG,CLEVELAND,OH
[3] CASE WESTERN RESERVE UNIV,SCH MED,INST PATHOL,CLEVELAND,OH
关键词
ADVANCED GLYCATION END-PRODUCTS; NONENZYMATIC GLYCATION; DIABETES MELLITUS; HEMODIALYSIS; PERITONEAL DIALYSIS;
D O I
10.1016/0272-6386(95)90107-8
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Plasma and tissue concentrations of pentose-derived glycation end-products (''pentosidine'') are elevated in diabetic patients with normal renal function and in both diabetic and nondiabetic patients with end-stage renal disease. To determine the influence of dialysis modality and other clinical variables on the accumulation of pentosidine, we used high-performance liquid chromatography to measure this advanced glycation end-product in plasma, skin, and peritoneal samples obtained from 65 hemodialysis and 45 peritoneal dialysis patients. Plasma pentosidine levels were significantly lower in peritoneal dialysis patients, Concentrations of pentosidine in skin were similar in the two groups. In contrast, peritoneal concentrations of pentosidine were significantly higher in the patients maintained on peritoneal dialysis. Our results demonstrate that dialysis modality influences the plasma and tissue distribution of pentosidine. Compared with hemodialysis, peritoneal dialysis is associated with lower levels of this glycation end-product in plasma, but with higher levels in the peritoneum. The mechanisms accounting for lower circulating levels of pentosidine in peritoneal dialysis patients remain to be determined. Higher levels in peritoneal tissues may reflect chronic exposure to the high concentrations of glucose in peritoneal dialysate. (C) 1995 by the National Kidney Foundation, Inc.
引用
收藏
页码:445 / 451
页数:7
相关论文
共 27 条
[1]   NONENZYMATIC GLYCOSYLATION AND THE PATHOGENESIS OF DIABETIC COMPLICATIONS [J].
BROWNLEE, M ;
VLASSARA, H ;
CERAMI, A .
ANNALS OF INTERNAL MEDICINE, 1984, 101 (04) :527-537
[2]  
CANCARINI GC, 1986, PERITON DIALYSIS INT, V6, P77
[3]  
CHATENOUD L, 1994, KIDNEY INT, V45, pS92
[4]  
Dinarello C A, 1988, Kidney Int Suppl, V24, pS21
[5]  
DYER DG, 1991, J BIOL CHEM, V266, P11654
[6]   ROLE OF DIALYSIS MODALITY IN RESPONSES OF BLOOD MONOCYTES AND PERITONEAL-MACROPHAGES TO ENDOTOXIN STIMULATION [J].
FRIEDLANDER, MA ;
HILBERT, CM ;
WU, YC ;
RICH, EA .
AMERICAN JOURNAL OF KIDNEY DISEASES, 1993, 22 (01) :11-23
[7]  
GRANDHEE SK, 1991, J BIOL CHEM, V266, P11649
[8]   INFLUENCE OF UREMIA AND HEMODIALYSIS ON CIRCULATING INTERLEUKIN-1 AND TUMOR NECROSIS FACTOR-ALPHA [J].
HERBELIN, A ;
NGUYEN, AT ;
ZINGRAFF, J ;
URENA, P ;
DESCAMPSLATSCHA, B .
KIDNEY INTERNATIONAL, 1990, 37 (01) :116-125
[9]   EFFECTS OF KIDNEY OR KIDNEY-PANCREAS TRANSPLANTATION ON PLASMA PENTOSIDINE [J].
HRICIK, DE ;
SCHULAK, JA ;
SELL, DR ;
FOGARTY, JF ;
MONNIER, VM .
KIDNEY INTERNATIONAL, 1993, 43 (02) :398-403
[10]   ALBUMIN HOMEOSTASIS IN PATIENTS UNDERGOING CONTINUOUS AMBULATORY PERITONEAL-DIALYSIS [J].
KAYSEN, GA ;
SCHOENFELD, PY .
KIDNEY INTERNATIONAL, 1984, 25 (01) :107-114