American journal of kidney diseases : the official journal of the National Kidney Foundation · 2009
Potential role of soluble ST2 protein in idiopathic nephrotic syndrome recurrence following kidney transplantation.
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Bruneau Sarah, Le Berre Ludmilla, Hervé Caroline, Valanciuté Asta, Kamal Maud, Naulet Jeanne, Tesson Laurent, Foucher Yohann, Soulillou Jean-Paul, Sahali Djillali, Dantal Jacques
Аннотация
BACKGROUND: Corticosteroid-resistant idiopathic nephrotic syndrome (INS) recurs rapidly after transplantation in 30% to 50% of transplant recipients, suggesting the presence of 1 or more circulating factors that alter the glomerular filtration barrier. We investigated the possible role in INS recurrence of soluble ST2 (sST2) protein, a marker of T helper type 2 (T(H)2) cells and a factor predicted to be regulated by the transcription factor c-Maf; involvement of sST2 protein would be consistent with the observation that both T(H)2 cells and c-Maf appear to be activated during INS relapse.
STUDY DESIGN: Retrospective observational study.
SETTING & PARTICIPANTS: Patients with biopsy-proven corticosteroid-resistant INS who had undergone kidney transplantation between September 1983 and April 2007 (n = 71). A control group consisting of proteinuric transplant recipients with kidney failure unrelated to INS (n = 34).
PREDICTOR: Patients who developed INS recurrence after transplantation (n = 31) were compared with those in whom INS did not recur (n = 40) and the control group. Recurrence of INS was defined as urine protein excretion greater than 2 g/d immediately after transplantation that persisted at greater than 1 g/d despite treatment or a kidney graft biopsy showing minimal change glomerulonephritis or focal segmental glomerulosclerosis.
OUTCOMES & MEASUREMENTS: Urine protein excretion in the 3 groups was 5.0 g/d (range, 1.3 to 10.5), 0.14 g/d (range, 0 to 0.46), and 4.3 g/d (range, 3 to 6.2). The sST2 protein was analyzed both quantitatively and qualitatively in patient sera, and its activity was tested in vitro on a mouse podocyte cell line and in vivo in rats.
RESULTS: sST2 protein levels were significantly increased after transplantation in patients with INS recurrence compared with the 2 other groups (617.5 versus 23 pg/mL; P < 0.001 and 158.5 pg/mL; P < 0.01 respectively). However, patients with recurrence expressed a normal sST2 isoform, and the sST2 protein was unable to induce podocyte injury in vitro or trigger proteinuria in rats.
LIMITATIONS: Pretransplantation and posttransplantation sera do not always represent paired samples.
CONCLUSIONS: These data suggest that sST2 protein is a marker of INS recurrence that does not seem to be involved in the development of INS.
STUDY DESIGN: Retrospective observational study.
SETTING & PARTICIPANTS: Patients with biopsy-proven corticosteroid-resistant INS who had undergone kidney transplantation between September 1983 and April 2007 (n = 71). A control group consisting of proteinuric transplant recipients with kidney failure unrelated to INS (n = 34).
PREDICTOR: Patients who developed INS recurrence after transplantation (n = 31) were compared with those in whom INS did not recur (n = 40) and the control group. Recurrence of INS was defined as urine protein excretion greater than 2 g/d immediately after transplantation that persisted at greater than 1 g/d despite treatment or a kidney graft biopsy showing minimal change glomerulonephritis or focal segmental glomerulosclerosis.
OUTCOMES & MEASUREMENTS: Urine protein excretion in the 3 groups was 5.0 g/d (range, 1.3 to 10.5), 0.14 g/d (range, 0 to 0.46), and 4.3 g/d (range, 3 to 6.2). The sST2 protein was analyzed both quantitatively and qualitatively in patient sera, and its activity was tested in vitro on a mouse podocyte cell line and in vivo in rats.
RESULTS: sST2 protein levels were significantly increased after transplantation in patients with INS recurrence compared with the 2 other groups (617.5 versus 23 pg/mL; P < 0.001 and 158.5 pg/mL; P < 0.01 respectively). However, patients with recurrence expressed a normal sST2 isoform, and the sST2 protein was unable to induce podocyte injury in vitro or trigger proteinuria in rats.
LIMITATIONS: Pretransplantation and posttransplantation sera do not always represent paired samples.
CONCLUSIONS: These data suggest that sST2 protein is a marker of INS recurrence that does not seem to be involved in the development of INS.
Предметные рубрики MeSH
AdolescentAdultAnimalsBiomarkersCOS CellsCell Line, TransformedChildChlorocebus aethiopsFemaleHumansInterleukin-1 Receptor-Like 1 ProteinKidney TransplantationMaleMiceMiddle AgedNephrotic SyndromeRatsRats, Inbred BUFRats, Inbred LewRats, Sprague-DawleyReceptors, Cell SurfaceRetrospective StudiesSecondary PreventionYoung Adult