Abstract:
BACKGROUND:Chronically elevated vasopressin (VP) plasma levels have been shown to induce accelerated renal function decline in rats with chronic renal failure. Whether endogenous VP is a renal risk factor in humans has not been investigated yet. We aimed to investigate whether, in renal transplant recipients, VP concentration is associated with change in renal function during follow-up. METHODS:In this prospective study, all consecutive patients visiting our kidney transplant outpatient clinic between August 2001 and July 2003 were asked to participate. Serum creatinine was assessed at baseline and at follow-up. Copeptin, the C-terminal portion of the precursor of VP, was determined at baseline (immunoassay). Univariate and multivariate regression analyses were performed to investigate the association between copeptin and renal function decline. RESULTS:Overall, 548 patients were included 6.0 (2.8-11.6) years after transplantation (men 54%, age 52 [43-60] years). Median follow-up was 3.2 (2.7-3.7) years. Median copeptin level was 9.1 (5.0-18.6) pmol/L at baseline. Copeptin was significantly associated with change in estimated Glomerular Filtration Rate (eGFR; MDRD) during follow-up. When our study population was subdivided according to gender-stratified tertiles of increasing copeptin concentration, mean changes in eGFR during follow-up were -0.03, -0.44, and -1.06 mL/min/1.73 m2 per year. In multivariate regression analysis, the association of copeptin at baseline with change in eGFR during follow-up remained significant after adjustment for age, gender, baseline eGFR, and known risk factors for renal function decline. CONCLUSIONS:These findings suggest that in renal transplant patients, VP may play a role in renal function decline.
journal_name
Transplantationjournal_title
Transplantationauthors
Meijer E,Bakker SJ,de Jong PE,Homan van der Heide JJ,van Son WJ,Struck J,Lems SP,Gansevoort RTdoi
10.1097/TP.0b013e3181b11ae4subject
Has Abstractpub_date
2009-08-27 00:00:00pages
561-7issue
4eissn
0041-1337issn
1534-6080pii
00007890-200908270-00017journal_volume
88pub_type
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