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Abstract: TH-PO306

A Novel Mouse Model of Renal Tubular Protein-Induced Nephropathy Mimics Sjögren Syndrome With Kidney Injury

Session Information

Category: Fluid‚ Electrolyte‚ and Acid-Base Disorders

  • 1001 Fluid‚ Electrolyte‚ and Acid-Base Disorders: Basic


  • Ma, Tiantian, Peking Union Medical College Hospital, Dongcheng-qu, Beijing, China
  • Shi, Xiaoxiao, Peking Union Medical College Hospital, Dongcheng-qu, Beijing, China
  • Chen, Limeng, Peking Union Medical College Hospital, Dongcheng-qu, Beijing, China

By immunization with allogeneic renal tubular homogenate, we tried to establish an experimental mouse model of primary Sjögren's syndrome (SS) with renal injuries which was not available now.


Proteins extracted from the salivary glands (SG) of normal mice were emulsified in an equal volume of Freund’s complete adjuvant at a concentration of 2 mg/mL (the SG group), while renal tubular proteins at a concentration of 1 mg/mL or 3 mg/mL (the RT group). For disease induction, each 8-week-old female C57BL/6 mouse received subcutaneous multiinjections on the back with 0.1 mL of the above emulsion on days 0 and 7, respectively. On day 14, a booster injection was carried out with a half dose of the proteins emulsified in Freund’s incomplete adjuvant. Mice injected with phosphate buffered saline (PBS) served as the control group. At 5 weeks postimmunisation, serum creatinine, 24-hour water intake, urine volume and urine electrolyte excretion were determined. Serum levels of anti-SSA and anti-SSB autoantibodies were determined by ELISA. The pathology of SG tissues and the proximal tubular injury was evaluated by light microscopy and electron microscope.


Both the SG group and the RT group developed a typical disease profile of SS, including increased water intake, reduced saliva secretion, positive serum anti-SSA and anti-SSB autoantibodies and pathologically lymphocytic infiltrations in SG. For kidney, despite similar serum creatinine and urea nitrogen levels, both the SG group and the RT group presented with renal tubular dysfunctions including decreased urine osmolality, increased urine output, proteinuria, decreased serum potassium levels, and increased urinary potassium and phosphorus excretion compared to the control group. Kidney pathology showed swollen and exfoliated tubular epithelial cells, brush border cilia lodging and dissolving with focal lymphocytic infiltrations in both the two groups. By electron microscope, we observed the disorderly dissolution of brush border cilia, smaller, ruptured mitochondria and increased mitochondrial membrane density were observed in the 1 mg/mL RT group, but not in the 3 mg/mL RT group.


This study first established a mouse model of SS with kidney injuries which was induced by immunizing mice with renal tubular protein and adjuvant.


  • Government Support – Non-U.S.