primary Sjögren syndrome

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primary Sjögren syndrome Figure 1 Possible mechanisms involved in the pathophysiology of renal disease during primary Sjögren syndrome Figure 1 | Possible mechanisms involved in the pathophysiology of renal disease during primary Sjögren syndrome. Environmental factors, genetic factors and viruses can contribute to epithelial lesions and the release of autoantigens from the salivary glands. These events trigger the release of type 1 and type 2 interferon (IFN) in genetically susceptible individuals, as well as T-cell activation leading to continuous B-cell activation and autoantibody synthesis. Immune complexes formed by autoantigens and autoantibodies (1), autoantibodies alone (2), and activated T cells, B cells, and plasma-cells (3) can be found in the circulation of the patient. Immune complexes are trapped within the glomeruli where they can form deposits and precipitates and trigger mesangial proliferation and extracellular matrix protein synthesis (corresponding to membranoproliferative glomerulonephritis secondary to cryoglobulinaemia). Autoantibodies to various specific renal transporters in the distal collecting ducts are trapped within the kidney where they might trigger electrolyte disturbances and distal renal tubular acidosis. In addition, activated T cells, B cells and plasma cells reach the kidney interstitium leading to the development of tubulointerstitial glomerulonephritis. These last two events may be enhanced by local expression of autoantigens within the tubules. Local renal inflammation contributes to tubular lesions, including tubulitis, and triggers renal interstitial fibrosis and tubular atrophy contributing to chronic kidney disease. NCCT, NaCl cotransporter. François, H. & Mariette, X. (2015) Renal involvement in primary Sjögren syndrome Nat. Rev. Nephrol. doi:10.1038/nrneph.2015.174