MO243: Intestinal Fatty-Acid Binding Protein: A Potential Biomarker of Enterocyte Damage in IGA Nephropathy?

Abstract BACKGROUND AND AIMS An abundance of inflammatory cells has been found in duodena of IgA nephropathy (IgAN) patients [1, 2]. The degree of intestinal inflammation was shown to correlate with the amount of proteinuria and haematuria in IgAN [3]. Serum intestinal fatty-acid-binding protein (I-FABP) has shown to correlate with the degree of enterocyte damage in untreated coeliac disease (CD) patients [4]. The median level of I-FABP in untreated CD patients was 785 pg/mL and 173 pg/mL in healthy controls [5]. We conducted this study hypothesizing that I-FABP would be elevated in IgAN as a potential biomarker for the presence of subclinical enterocyte damage and intestinal inflammation. CD was excluded with coeliac autoantibody tests. METHOD This study was carried out at the Tampere University Hospital and Tampere University, Finland. Altogether 85 IgAN patients participated (median age 55 years, 54% males). None of the patients had progressed to end-stage kidney disease, nor had they a diagnosed enteropathy. Fifteen healthy controls (median age 57 years, 47% males) were participants from our previous CD studies. Coeliac autoantibodies were determined from the serum samples by measuring IgA class endomysial antibodies (EmA) and transglutaminase antibodies (tTGAb). EmA was determined by an in-house indirect immunofluorescence method using human umbilical cord as substrate. A serum dilution of 1: ≥ 5 was considered positive. tTGAb levels were determined with EliA Celikey assay (ThermoFisher Scientific, Waltham, MA, USA, cut-off for positivity 7.0 U/mL). The serum levels of I-FABP were determined with a commercially available ELISA kit (Hycult Biotech, Uden, The Netherlands, detection limit 47 pg/mL). Current kidney function was available in 68 IgAN patients (80%), and eGFR >60 mL/min/1.73 m2 was regarded as preserved kidney function. RESULTS I-FABP levels among IgAN patients (median 830 pg/mL, IQR 475–1378) were higher (P < .001) compared with healthy controls (289 pg/mL, IQR 199–568). A total of 57% of the IgAN patients from whom the data on current kidney function were available had preserved kidney function. Also, I-FABP levels in IgAN patients with preserved kidney function (650 pg/mL, IQR 419–880) were higher compared with healthy controls (P .006). tTGAb levels in IgAN patients (1.3, 0.8–1.9 U/mL) were higher (P <.001) compared with healthy controls (0.6, 0.3–0.7 U/mL). One IgAN patient had a borderline elevated tTGAb of 7.1 U/mL. No one had an elevated EmA test result. I-FABP and tTGAb levels had no correlation (rS 0.182, P = .051). CONCLUSION The clear difference in the levels of I-FABP in IgAN patients with preserved kidney function compared with healthy controls was of utmost interest. Elevated I-FABP may represent enterocyte injury and intestinal inflammation present in IgAN. Even though CD was excluded serologically, also the tTGAb levels were higher among IgAN patients. These findings spur us in search for an intestinal process in the pathophysiology of IgAN.