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Kidney Week

Abstract: PO0532

Kidney Outcomes Associated with Fibrosis and Inflammation on Kidney Wedge Sections

Session Information

Category: CKD (Non-Dialysis)

  • 2101 CKD (Non-Dialysis): Epidemiology, Risk Factors, and Prevention

Authors

  • Ricaurte Archila, Luisa M., Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Denic, Aleksandar, Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Mullan, Aidan F., Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Bogojevic, Marija, Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Leibovich, Bradley, Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Thompson, R. houston, Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Kremers, Walter K., Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Alexander, Mariam P., Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Lieske, John C., Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Rule, Andrew D., Mayo Clinic Minnesota, Rochester, Minnesota, United States
Background

Interstitial fibrosis and tubular atrophy (IFTA) and inflammation are prognostically important but crudely assessed in biopsy reports. We used manual morphometry to characterize different patterns of IFTA and inflammation on large biopsy sections and their associations with CKD progression.

Methods

We studied 936 patients who had a radical nephrectomy due to renal cancer and no severe renal disease. A wedge section distal to tumor was used for morphometry. All areas of cortex, glomeruli, IFTA and inflammation were annotated. We calculated glomerular volume, % globally sclerotic glomeruli (GSG), overall %IFTA, mean area of each contiguous focus of IFTA (focus area), number of IFTA stripes (from capsule toward medulla) per cortex area, % subcapsular cortex with IFTA (%SC IFTA), % total inflammation (%TI), % inflammation outside (%I-non IFTA) and within foci of IFTA (%I-IFTA). We followed patients for progressive CKD censoring at cancer recurrence or death. Progressive CKD was defined as kidney failure or 40% decline in eGFR from the baseline (4 months after surgery). Models were unadjusted, adjusted for %IFTA, and adjusted for %TI.

Results

At surgery mean age was 64 years, 64% male, 66% hypertensive, and 13% diabetic. Samples contained a mean of 349 glomeruli and mean baseline eGFR was 48 ml/min/1.73m2. After a mean follow-up of 6.4 years there were 117 CKD progression events and 299 deaths. %IFTA and %TI predicted progressive CKD independent of each other (Table). %I-non IFTA (not %I-IFTA) contributed to this risk. After %IFTA adjustment, smaller mean IFTA focus area associated with a higher risk of CKD progression. These findings persisted with adjustment for clinical characteristics including eGFR and proteinuria.

Conclusion

Both total %IFTA and %TI (particularly %I-non IFTA) are important predictors of progressive CKD. At the same %IFTA, a greater number of small IFTA foci are more predictive of progressive CKD than fewer large foci of IFTA.