†These authors contributed equally in this study.Recent findings in idiopathic membranous nephropathy (MN) suggest that in most patients, the disease is because of anti-phospholipase A 2 receptor (PLA 2 R1) autoantibodies. Our aim was to analyze the prevalence and significance of anti-PLA 2 R1 antibodies in recurrent and de novo MN after transplantation. We assessed circulating PLA 2 R1 autoantibodies by a direct immunofluorescence assay based on human embryonic kidney cells transfected with a PLA 2 R1 cDNA, and the presence of PLA 2 R1 antigen in immune deposits. We showed that PLA 2 R1 was involved in 5 of 10 patients with recurrent MN, but in none of the 9 patients with de novo MN. We also showed a marked heterogeneity in the kinetics and titers of anti-PLA 2 R1, which may relate to different pathogenic potential. We provide evidence that some patients with PLA 2 R1-related idiopathic MN and anti-PLA 2 R1 antibodies at the time of transplantation will not develop recurrence. Because PLA 2 R1 autoantibody was not always associated with recurrence, its predictive value should be carefully analyzed in prospective studies.

Objective-Plasma concentration of adiponectin is positively correlated with high-density lipoprotein (HDL) cholesterol level. However, the role of adiponectin on HDL metabolism remains unknown. This prompted us to perform an in vivo kinetic study of apoA-I, the main apolipoprotein of HDL, using stable isotopes, in 22 subjects with a wide range of plasma adiponectin, including 11 patients with metabolic syndrome (8 with type 2 diabetes, 3 without type 2 diabetes) and 11 normal individuals. Methods and Results-In the 22 studied subjects, plasma adiponectin levels ranged from 2.57 to 14.44 g/mL and apoA-I fractional catabolic rate (FCR) values ranged from 0.142 to 0.340 day Ϫ1 . A strong negative correlation was found between adiponectin and apoA-I FCR (rϭϪ0.66, PϽ0.001) in the whole studied population and, to a similar extent, in patients with metabolic syndrome (rϭϪ0.73, Pϭ0.010) and normal subjects (rϭϪ0.68, Pϭ0.020), separately. In multivariable analysis, apoA-I FCR was associated negatively with adiponectin (Pϭ0.005) and positively with HDL triglycerides/cholesterol ratio (Pϭ0.006), but not with age, sex, body mass index (BMI), waist circumference, plasma triglycerides, HDL cholesterol, fasting glycemia, and QUICKI. Both adiponectin and HDL triglycerides/cholesterol ratio explained 62% of the variance of apoA-I FCR and adiponectin on its own explained 43%. Conclusions-Our kinetic study shows a strong negative correlation between adiponectin and apoA-I FCR, which can explain the positive link between HDL cholesterol and adiponectin. This association is independent of obesity, insulin resistance, and the content of triglycerides within HDL particles. These data suggest that adiponectin may have a direct role on HDL catabolism. Key Words: adiponectin Ⅲ apoA-I Ⅲ HDL cholesterol Ⅲ insulin-resistance Ⅲ kinetic A diponectin is a peptide predominantly synthesized in the adipose tissue that plays an important role in carbohydrate and lipid metabolism and vascular biology. 1,2 It has been suggested to be a link between obesity, insulin resistance, and cardiovascular disease. Plasma adiponectin levels are reduced in individuals with abdominal obesity, metabolic syndrome, and/or type 2 diabetes. 1,3-5 Adiponectin concentration has been found negatively correlated with abdominal obesity and insulin resistance in humans 6,7 and has been shown to predict the development of type 2 diabetes. 8,9 Furthermore, several studies indicate that plasma adiponectin levels are significantly decreased in patients with coronary heart disease 10,11 and high plasma adiponectin predict a lower risk of future myocardial infarction in nondiabetic 12 and diabetic individuals. 13 However, the link between adiponectin and cardiovascular disease could be partly mediated by its effects on lipids, because several studies indicate that the inverse association between adiponectin and coronary disease is importantly attenuated or no more significant after adjustment for lipids, particularly high-density lipoprotein (HDL) cholesterol. 12,13 Adiponectin ...

Apolipoprotein Cs (apoC-1, apoC-II, and apoC-III) are lipoprotein components that have regulatory effects on enzymes involved in lipoprotein metabolism. Owing to their low molecular weights, apoCs can adsorb onto and/or pass through dialysis membranes. Our study determines the consequence of hemodialysis (HD) on plasma concentrations of apoCs and on the activities of enzymes modulated by apoCs. Plasma samples were collected from 28 patients with chronic renal failure before and after HD. Plasma apoC-II levels were unchanged, whereas apoC-III levels were slightly decreased in post-dialysis plasmas. The apoC-I content was markedly reduced during HD. This was due to a significant decrease in the apoC-I content of very low-density lipoprotein (VLDL), whereas the apoC-I content of high-density lipoprotein (HDL) was unchanged. Although HDL bound apoC-I is thought to inhibit cholesterol ester transfer protein, no change in the ability of pre- and post-dialysis VLDL to interact with the transfer protein were observed. Complementary experiments confirmed that VLDL-bound apoC-I has no transfer protein inhibitory potential. In contrast, an increase in the ability of post-dialysis apoC-I-poor VLDL to act as substrate for lipoprotein lipase (LPL) was found compared to pre-dialysis VLDL. Our study shows that apoC-I losses during HD might be beneficial by improving the ability of VLDL to be a substrate for LPL thus improving plasma triglyceride metabolism.