# Visceral Adipose Tissue Alters Podometrics and Renal Compensation After Uninephrectomy

## TL;DR

This study shows that visceral obesity, even in people with normal BMI, is linked to kidney damage and reduced kidney function after surgery.

## Contribution

The study reveals new associations between visceral adipose tissue and impaired renal compensation after uninephrectomy.

## Key findings

- Visceral obesity is associated with larger glomerular volume and podocyte nuclear hypertrophy.
- VO is linked to reduced podocyte density and impaired eGFR compensation after nephrectomy.
- Structural kidney changes correlate with reduced renal function recovery.

## Abstract

Obesity is an established risk factor for chronic kidney disease (CKD). However, excess visceral adipose tissue (VAT) termed visceral obesity (VO) can occur in individuals with normal body mass index (BMI) or overweight. VO is associated with impaired kidney function but its effect on kidney morphology remains unclear. This study aimed to examine the association of VO with glomerular ultrastructure, podocyte morphometry (podometrics), and the kidneys’ ability for compensation after uninephrectomy in normal BMI and overweight individuals.

VAT was retrospectively quantified in computed tomography (CT) of 52 patients (BMI < 30 kg/m2) who underwent nephrectomy for nonmetastatic renal tumor without previous chemotherapy or immunotherapy. VO was defined as VAT area ≥ 100 cm2. Histological sections from nontumorous kidney regions were examined using deep learning–supported glomerular morphometry and podometrics (podocyte count, density, and nuclear volume). Renal compensation in the first year after nephrectomy (change in estimated glomerular filtration rate [ΔeGFR]) was assessed using linear regression.

Of the 52 subjects with normal BMI or overweight, 35 were diagnosed with VO and exhibited a larger glomerular volume (2.6 ± 0.7 vs. 2.0 ± 0.5 ×106 μm3; P = 0.004), lower podocyte density (194 ± 50 vs. 243 ± 59 per 106 μm3; P = 0.003), and podocyte nuclear hypertrophy (226 ± 27 vs. 195 ± 22 μm3; P < 0.001). VO was associated with impaired eGFR compensation after uninephrectomy (ΔeGFR: −24 ± 15 vs. −12 ± 12 ml/min per 1.73 m2, P = 0.03). Structural changes, including glomerular enlargement (P = 0.005), podocyte density (P = 0.01), and nuclear hypertrophy (P = 0.003), were significantly associated with reduced ΔeGFR.

VO was associated with glomerular and podocyte changes, and impaired kidney function compensation after nephrectomy in normal BMI and overweight individuals. These data suggest that VAT quantification could guide individual decision making in subjects planned for nephrectomy.