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Kidney Week

Abstract: FR-OR045

MRI Kidney Parenchymal Volume Identifies a Hidden CKD-Risk Phenotype in Adults with Normal eGFR: UK Biobank Analysis of 34,646 Adults

Session Information

Category: CKD (Non-Dialysis)

  • 2202 CKD (Non-Dialysis): Clinical, Outcomes, and Trials

Authors

  • Lee, Yongwoo, Chungnam National University Hospital, Daejeon, Korea (the Republic of)
  • Choi, Yeolim, Chungnam National University Hospital, Daejeon, Korea (the Republic of)
  • In, Seungyong, Chungnam National University Hospital, Daejeon, Korea (the Republic of)
  • Han, Eun Kyu, Chungnam National University Hospital, Daejeon, Korea (the Republic of)
  • Lee, Eu Jin, Chungnam National University Hospital, Daejeon, Korea (the Republic of)
  • Ham, Youngrok, Chungnam National University, Daejeon, Korea (the Republic of)
  • Na, Ki Ryang, Chungnam National University, Daejeon, Korea (the Republic of)
  • Choi, Dae Eun, Chungnam National University, Daejeon, Korea (the Republic of)
Background

eGFR captures aggregate filtration but not structural kidney reserve, so adults with reduced nephron-bearing tissue can present with biochemically normal kidney function. We tested whether discordance between preserved eGFR and low MRI-derived kidney parenchymal volume (KPV) identifies a structural CKD-risk phenotype missed by biochemistry, and which metabolic factors most accelerate disease in structurally smaller kidneys.

Methods

In 34,646 UK Biobank participants (40–80 y) with abdominal MRI and no prevalent CKD, BSA-adjusted KPV was derived by automated neural-network segmentation. Discordance was defined as eGFR ≥60 mL/min/1.73m2 with KPV below the sex- and age-decade-specific 10th percentile of a healthy reference. Incident CKD (ICD-10 N18.3–N18.6) was ascertained from Hospital Episode Statistics. Cox models with full covariate adjustment including eGFR estimated CKD risk; discrimination used C-statistic and NRI.

Results

Discordance was present in 9.2% of eGFR-preserved adults, with markedly lower KPV (102 vs 137 mL/m2) despite similar eGFR. Over 4.94-year median follow-up (418 events), Discordance conferred a 2.20-fold elevated CKD risk (95% CI 1.66–2.90), rising to 5.07-fold (95% CI 2.07–12.4) at eGFR ≥90 mL/min/1.73m2 and persisting after excluding diabetics. Adding KPV improved the clinical model's C-statistic (0.834→0.853; NRI 0.41), whereas metabolic syndrome added nothing. Hypertension and hyperglycemia—not abdominal obesity—were the dominant accelerants in structurally smaller kidneys. A Clinical Burden Score (low KPV + hypertension + high glucose) stratified 5-year CKD incidence from 0.30% to 9.05% (HR 7.09), robust across prespecified sensitivity analyses for biochemistry–imaging temporal separation.

Conclusion

One in 11 adults with normal eGFR harbors a structural kidney risk phenotype invisible to biochemical screening but conferring substantial excess CKD risk. KPV adds discriminative value beyond eGFR; hypertension and hyperglycemia are the dominant modifiable accelerants. Imaging-based detection of low parenchymal reserve offers a complementary screening axis for CKD prevention.

Funding

  • Government Support – Non-U.S.