Renal elastography in kidney disease: Current evidence, limitations, and future directions

Figure 1 From isolated stiffness to multiparametric decision-making. Limitations of interpreting renal shear-wave elastography in isolation and the rationale for a multiparametric approach in glomerulonephritis. In inflammatory or hyperemic kidneys, increased stiffness may be driven more by perfusion and inflammation than by fibrosis. In advanced fibrotic disease, stiffness values may vary according to renal perfusion, and a “soft” kidney does not exclude significant fibrosis. Therefore, a multiparametric model integrating shear-wave elastography-derived mechanical properties (stiffness and viscosity), renal function parameters, and selected biomarkers may provide a more accurate non-invasive renal phenotyping, risk stratification, and assessment of disease progression. SWE: Shear-wave elastography; eGFR: Estimated glomerular filtration rate; TGF-β1: Transforming growth factor beta 1; CTGF: Connective tissue growth factor; NGAL: Neutrophil gelatinase-associated lipocalin; KIM-1: Kidney injury molecule 1.

Figure 2 Effect of renal anisotropy on shear wave elastography measurements. Renal tissue anisotropy significantly influences shear wave propagation and, consequently, stiffness measurements obtained by shear wave elastography. When the ultrasound beam is aligned parallel to the corticomedullary axis, shear waves travel along tubular and vascular structures with less resistance, resulting in higher measured velocities and increased apparent stiffness. In contrast, perpendicular orientation results in slower wave propagation and lower stiffness due to higher structural impedance. These orientation-dependent differences highlight the impact of renal architecture on elastographic measurements and underscore the need for standardized probe positioning to improve reproducibility and interpretation in clinical practice. SWE: Shear-wave elastography; SWS: Shear-wave speed.