HYPERLEPTINAEMIA OF END-STAGE RENAL-DISEASE IS CORRECTED BY RENAL-TRANSPLANTATION

Citation
N. Landt et al., HYPERLEPTINAEMIA OF END-STAGE RENAL-DISEASE IS CORRECTED BY RENAL-TRANSPLANTATION, Nephrology, dialysis, transplantation, 13(9), 1998, pp. 2271-2275
Citations number
36
Categorie Soggetti
Urology & Nephrology",Transplantation
ISSN journal
09310509
Volume
13
Issue
9
Year of publication
1998
Pages
2271 - 2275
Database
ISI
SICI code
0931-0509(1998)13:9<2271:HOERIC>2.0.ZU;2-K
Abstract
Background. Previous studies have reported that patients with end-stag e renal disease (ESRD) have elevated plasma leptin concentrations, but the cause and significance of the elevations are unknown. We studied leptin concentrations in 29 adults undergoing renal transplantation, t o determine if restoration of renal function reduced leptin concentrat ions in ESRD. Methods. Leptin concentrations were measured by radioimm unoassay in plasma specimens collected within 1 week before transplant , 6 days post-transplant, and 60 days post-transplant. Results. Mean p lasma leptin concentrations were higher in both male and female ESRD p atients compared with a control population of similar age and body mas s index (BMI), but most of the disparity was due to a minority of pati ents with grossly elevated concentrations; the majority of ESRD patien ts had normal or near-normal leptin concentrations after accounting fo r their adiposity with BMI. Six days after successful renal transplant ation, average plasma leptin concentrations decreased to control level s. The grossly elevated pretransplant concentrations in a minority of patients were greatly reduced in relation to BMI, and the reduction pe rsisted to 60 days post-transplant. The decrease in creatinine with tr ansplant did not correlate with the decrease in leptin. Conclusions. T hese results demonstrate that restoration of renal function in ESRD pa tients reduces hyperleptinaemia, which provides further evidence of a cause/effect relationship between impaired renal function and abnormal leptin metabolism.