Potential Role of Soluble ST2 Protein in Idiopathic Nephrotic Syndrome Recurrence Following Kidney Transplantation

Abstract

France.DS and JD contributed equally to this work. No differences were detected in these sera before transplantation. Moreover, recurrent patients displayed the same sST2 isoform as the two control groups. In vitro, a mouse podocyte cell line was profoundly altered by incubation with sera of recurrent patients. However, purified sST2 from these patients was not able to reproduce these damages. In addition, induction of high sST2 levels in rats did not trigger proteinuria. Collectively, these data suggest that sST2 is a marker of INS recurrence that could be of interest for its diagnosis in ambiguous clinical situations. Nonetheless, sST2 does not seem to be directly implicated in INS development. This work was supported in part by

Deficiency of liver sinusoidal scavenger receptors stabilin-1 and -2 in mice causes glomerulofibrotic nephropathy via impaired hepatic clearance of noxious blood factors

“…Nevertheless, unequivocal identification of a single factor as the decisive permeability-inducing and disease-causing factor in the FSPF has not yet been established. Therefore, it seems reasonable to assume that several factors interact or act in sequence to induce FSGS, some of which may even act indirectly to induce posttransplantation recurrence without directly influencing permeability, such as sST2 (53). In addition to the fact that the FSPF(s) are still elusive, the mechanisms of their accumulation in the circulation are so far unknown.…”

Characterization of Interleukin-33 and Soluble ST2 in Serum and Their Association with Disease Severity in Patients with Chronic Kidney Disease

“…ST2 is found to be selectively expressed on a subset of Th2 cells but not Th1 cells and mediates Th2 functions [2]. A recent study has indicated that elevated sST2 seems to be a consequence of renal pathologies not involved in the pathogenesis of idiopathic nephrotic syndrome [26]. Although patients with recurrence expressed a normal sST2 isoform, elevated serum sST2 suppresses IL-6, IL-12, and TNF-α production via inhibition of NF-kB activation and mitogen-activated protein kinase pathways to result in the development of CKD.…”

“…The specificity for elevated sST2 in CKD is consistent with the relative predominance of the immune inflammatory response. Also, a recent study suggests that sST2 protein is a marker of idiopathic nephrotic syndrome recurrence [26].…”

From IL-15 to IL-33: the never-ending list of new players in inflammation. Is it time to forget the humble aspirin and move ahead?

“…This spliced isoform is produced by antigen presenting cells such as monocytes and macrophages and acts as decoy receptor and thus antagonizes the effects of IL-33 [119,120]. In fact, patients suffering chronic inflammatory diseases have high levels of soluble ST2 [121,122].…”