Kidney Week

Abstract: FR-PO142

Renal Hypertrophy in End-Stage Liver Disease

Session Information

• AKI Clinical: Outcomes and Biomarkers
  November 03, 2017 | Location: Hall H, Morial Convention Center
  Abstract Time: 10:00 AM - 10:00 AM

Category: Acute Kidney Injury

• 003 AKI: Clinical and Translational

Authors

• Saad, Marc, Emory University, Atlanta, Georgia, United States

Marc Saad,

• Ellis, Carla L., Emory University, Atlanta, Georgia, United States

Carla L. Ellis,

• O'Neill, W. Charles, Emory University, Atlanta, Georgia, United States

W. Charles O'Neill,

Background

Renal failure has been extensively studied in liver disease but the normal physiologic responses to liver dysfunction remain unknown. We hypothesized that decreased clearance of metabolic products by the liver increases metabolic demand on the kidneys, leading to hypertrophy.

Methods

Renal parenchymal volume (RPV) was measured on outpatient CT scans performed in 29 patients with end-stage liver disease (ESLD) and 30 controls without liver disease. Cross-sectional kidney areas (excluding the renal sinus, vessels, collecting system, and cysts) from sequential transverse images were summed and muliplied by the slice thickness to derive RPV, which was normalized to body height. Renal histology was evaluated in 5 autopsies that were suitable for analysis and compared to 8 autopsies in patients without liver disease. Glomerular size was estimated from the area of Bowman's capsule measured at maximal cross-section (7-29 glomeruli/patient, mean 22). Subjects with diabetes, kidney stones, serum creatinine > 1.2 mg/dl, or proteinuria > 100 mg/dl by dipstick were excluded.

Results

The characteristics of the patients in whom RPV was measured are shown in the table. There were no significant differences between the groups. RPV/height was 21% greater in ESLD than in controls: 230 ± 7 ml/m vs 190 ± 7 ml/m (mean ± SE; p= 0.0002). This difference remained significant (p<0.001) in a multivariate analysis that included age, gender, serum creatinine, and degree of ascites . Glomerular volume was 24% greater in ESLD than in controls (3.68 ± 0.46 vs. 2.96 ± 0.41 μm³x10⁶) but significance was limited by the small sample size. No edema or vascular congestion was noted in any ESLD kidney.

Conclusion

Renal parenchymal volume is increased in patients with ESLD without evidence of renal disease. This cannot be explained by interstitial edema, vascular congestion, or ascites. There appears to be a similar increase in glomerular volume consistent with renal hypertrophy. This enlargement needs to be considered when evaluating kidney size in ESLD, and the hypertrophy could contribute to the increased risk of acute renal failure in ESLD.

Funding

• Clinical Revenue Support