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Abstract: FR-OR057

Progressive CKD and Mortality as Predicted by Renal Histology After Radical Nephrectomy

Session Information

Category: CKD (Non-Dialysis)

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

Authors

  • Elsherbiny, Hisham, Mayo Clinic, Rochester, Minnesota, United States
  • Denic, Aleksandar, Mayo Clinic, Rochester, Minnesota, United States
  • Lopez, Camden, Mayo Clinic, Rochester, Minnesota, United States
  • Thompson, R. houston, Mayo Clinic, Rochester, Minnesota, United States
  • Ricaurte Archila, Luisa M., Mayo Clinic, Rochester, Minnesota, United States
  • Narasimhan, Ramya, Mayo Clinic, Rochester, Minnesota, United States
  • Alexander, Mariam P., Mayo Clinic, Rochester, Minnesota, United States
  • Lieske, John C., Mayo Clinic, Rochester, Minnesota, United States
  • Rule, Andrew D., Mayo Clinic, Rochester, Minnesota, United States
Background

Nephron hypertrophy and nephrosclerosis may be important determinants of mortality and kidney failure. However, the study of adverse outcomes with renal histology has been limited to select patient populations with small tissue specimens.

Methods

We studied patients who underwent a radical nephrectomy for tumor between 2000 and 2012. Wedge sections distal to the tumor were stained and scanned into high resolution images. The areas of cortex and glomeruli (sclerotic and non-sclerotic) were annotated to calculate glomerular volume and percentage globally sclerotic glomeruli (%GSG). The percentage luminal stenosis (arteriosclerosis) and interstitial fibrosis/tubular atrophy (IFTA) of the cortex were morphometrically measured. Patients were followed with annual visits or phone calls for non-cancer death or kidney failure, censoring at cancer death. Progressive chronic kidney disease (CKD) was defined as dialysis, kidney transplant, or a 40% decline in estimated glomerular filtration rate (eGFR) from the post-nephrectomy baseline. Models adjusted for age, sex, BMI, hypertension, diabetes, smoking, and eGFR.

Results

There were 712 patients (mean age 63y, 64% male, 64% hypertension, 14% diabetic, and mean postoperative eGFR 48 ml/min/1.73 m2) with a mean follow-up of 8.0±4.2 years, 77 progressive CKD events, 170 non-cancer deaths, and 104 cancer deaths. Larger non-sclerotic glomerular volume predicted progressive CKD, but this was no longer evident after adjustment for proteinuria. Higher %GSG and more severe arteriosclerosis predicted progressive CKD, which persisted with adjustment for proteinuria. Higher %IFTA predicted non-cancer morality, and this persisted with adjustment for proteinuria. No kidney structural finding predicted cancer mortality.

Conclusion

Larger nephron size predicts kidney failure along the same pathway as proteinuria. Subclinical glomerulosclerosis and arteriosclerosis predict kidney failure, whereas subclinical IFTA predict non-cancer mortality.

Hazard ratio of outcomes by renal histology (p-values)
 Predicted progressive CKDNon-cancer MortalityCancer Mortality
Glomerular volume, log2.17 (0.003)1.11 (0.52)1.18 (0.44)
IFTA %1.07 (0.25)1.16 (0.0002)1.04 (0.43)
%GSG1.32 (0.01)1.11 (0.18)0.98 (0.81)
Luminal stenosis %1.90 (0.02)1.39 (0.10)0.95 (0.81)

Funding

  • NIDDK Support