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Abstract: TH-PO141

Clinical and Pathological Analysis of Renal Tubulointerstitial Injury in Idiopathic Membranous Nephropathy

Session Information

Category: Glomerular

  • 1005 Clinical Glomerular Disorders

Authors

  • Li, Zilong, Department of Nephrology, First Affiliated Hospital of China Medical University, Shenyang, P. R. China, Shenyang, China
  • Zhang, Yibo, the first affiliated hospital of China Medical University, Shenyang, China
  • Wang, Juan, Department of Nephrology, First Affiliated Hospital of China Medical University, Shenyang, P. R. China, Shenyang, China
  • Liu, Linlin, The First Hospital of China Medical University, ShenYang, China
  • Ma, Jianfei, The First Affiliated Hospital of China Medical University, Shenyang, China
  • Yao, Li, The First Affiliated Hospital of China Medical University, Shenyang, China
Background

It has been revealed that renal tubulointerstitial injury (TII) plays important roles in the progression of chronic kidney diseases, while how TII affects idiopathic membranous nephropathy (IMN) remains unclear. Herein, we retrospectively studied the clinical and pathological data of 134 IMN patients, to investigate the characteristics of TII in IMN.

Methods

134 patients diagnosed as IMN via renal biopsy from January 2014 to December 2015 in our department were enrolled. All the patients didn’t administrate with either corticosteroid or immunosuppressants before undergoing renal biopsy, and accepted appropriate therapy according to the clinical and pathological features after renal biopsy. The patients were divided into two groups: TII group and non-TII group. Clinical and pathological data were accumulated after 12-month follow-up.

Results

Among the 134 IMN patients, 79 were males (58.96%) and 55 were females(41.04%), age from 14 to 74 years. The pathological results suggested 65 cases (48.51%) existed TII in IMN. Compared to non-TII group, TII group appeared significantly higher levels of 24-hour urinary protein,urinary α1-microglobulin,urinary β2-microglobulin,urinary albumin, serum creatinine and cystatin C (p<0.05), and significantly declined eGFR (p<0.05). Renal tubulointerstitial injury score was positively associated with serum creatinine(r=0.304,p=0.00), cystatin C(r=0.372,p=0.00), 24-hour urinary protein(r=0.207,p=0.016), α1-microglobulin(r=0.174,p=0.044), β2-microglobulin(r=0.246,p=0.004) and urinary albumin(r=0.206,p=0.017), and negatively associated with eGFR(r=-0.304,p=0.00). After 12-month follow-up, patients in TII group showed higher incidence of eGFR decrease.

Conclusion

TII occurs in IMN patients, which may be prompted by some clinical indicators. TII may affect the the progression and prognosis of IMN, and further researches are needed to elaborate the mechanisms and explore effective therapies.