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P10 IL-16 expression in kidney biopsies from patients with SLE- and antiphosholipid syndrome- associated renal thrombotic microangiopathy and renal IgA vasculitis
  1. Aliisa Häyry1,
  2. Vilija Oke1,2,
  3. Elisabet Svenungsson1,3,
  4. Francesca Faustini1,3 and
  5. Iva Gunnarsson1,3
  1. 1Division of Rheumatology, Dept. of Medicine, Karolinska Institutet, Stockholm, Sweden
  2. 2Center for Rheumatology, Academic Specialist Center, Stockholm Region, Sweden
  3. 3Rheumatology, Karolinska University Hospital, Stockholm, Sweden

Abstract

Objective Renal involvement in SLE is most commonly characterized by immunocomplex-mediated glomerulonephritis denoted lupus nephritis (LN). Renal thrombotic microangiopathy (TMA) occurs in a minority and constitutes a diagnostic and therapeutic challenge.

IL-16 was recently described as a promising urinary biomarker of active proliferative lupus nephritis by us and others, and detected in kidney biopsies of LN patients. IL-16 expression in other types of renal disease remains unexplored, while necessary to further characterize the biomarker potential of IL-16 in LN.

Methods IL-16 expression was studied by immunohistochemistry in kidney biopsies from 2 patients with SLE, triple-positive antiphospholipid syndrome (APS) and renal TMA, and in 4 patients with renal IgA vasculitis (IgAV). One TMA patient had history of biopsy-proven LN. Half of the patients in both groups had no ongoing treatment. All had albuminuria, erythrocyturia and/or reduced estimated glomerular filtration rate.

Results Histopathological diagnosis of TMA or IgAV was confirmed by renal pathologist, in parallel with lack of signs of active LN. Renal IL-16 was detected in both TMA patients, localized in the rich chronic interstitial inflammatory infiltrate observed in both cases (figure 1a-b). No glomerular or vascular staining was noted in either case. Furthermore, interstitial staining of varying intensity was seen in all 4 IgAV patients (figure 1c-d). In two cases, strong staining was observed in interstitial inflammatory infiltrate in parallel with glomerular staining. Both IgAV patients who expressed glomerular IL-16 had necrotic glomerular lesions.

Conclusions IL-16 can be detected in renal interstitial infiltrate in SLE- and APS-associated renal TMA and in IgAV, similarly to our previous descriptions of IL-16 expression in membranous and active proliferative LN. Furthermore, glomerular IL-16 may be observed in IgAV, which appears to occur in parallel with glomerular necrosis. This indicates potential diversity of IL-16 expression in kidney disease beyond LN.

Next, besides renal expression, urinary IL-16 levels should be investigated in other types of renal disease than LN to further characterize the biomarker properties of IL-16. This is an ongoing process.

Acknowledgements This work is funded by the Stig and Gunborg Westman Foundation.

Abstract P10 Figure 1

Immunohistochemical stainings for IL-16.

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