Noninvasive In vivo assessment of renal tissue elasticity during graded renal ischemia using MR elastography

Abstract

Objectives: : Magnetic resonance elastography (MRE) allows noninvasive assessment of tissue stiffness in vivo. Renal arterial stenosis (RAS), a narrowing of the renal artery, promotes irreversible tissue fibrosis that threatens kidney viability and may elevate tissue stiffness. However, kidney stiffness may also be affected by hemodynamic factors. This study tested the hypothesis that renal blood flow (RBF) is an important determinant of renal stiffness as measured by MRE.

Material and methods: : In 6 anesthetized pigs MRE studies were performed to determine cortical and medullary elasticity during acute graded decreases in RBF (by 20%, 40%, 60%, 80%, and 100% of baseline) achieved by a vascular occluder. Three sham-operated swine served as time control. Additional pigs were studied with MRE 6 weeks after induction of chronic unilateral RAS (n = 6) or control (n = 3). Kidney fibrosis was subsequently evaluated histologically by trichrome staining.

Results: : During acute RAS the stenotic cortex stiffness decreased (from 7.4 ± 0.3 to 4.8 ± 0.6 kPa, P = 0.02 vs. baseline) as RBF decreased. Furthermore, in pigs with chronic RAS (80% ± 5.4% stenosis) in which RBF was decreased by 60% ± 14% compared with controls, cortical stiffness was not significantly different from normal (7.4 ± 0.3 vs. 7.6 ± 0.3 kPa, P = 0.3), despite histologic evidence of renal tissue fibrosis.

Conclusion: : Hemodynamic variables modulate kidney stiffness measured by MRE and may mask the presence of fibrosis. These results suggest that kidney turgor should be considered during interpretation of elasticity assessments.

Figure 1

Schematic of the experimental design for the acute and chronic studies. The acute experiment consisted of several periods in which renal blood flow (RBF), measured continuously by a flow probe, was decreased by 20,40,60, 80 and 100% of baseline, each followed by an MR elastography (MRE) study. In the Chronic RAS experiments, MRE and CT (RBF) studies were performed 6 weeks following development of RAS. RBF was not modulated in the control sham groups.

Figure 2

Representative elastograms of the stenotic and contralateral kidneys (A). Right panel: renal blood flow (RBF, B), perfusion (C), and volume (D) of stenotic (solid diamonds), contralateral (solid squares), and sham-operated control (solid triangles) kidneys, and changes in blood pressure (D), during experimental decreases in RBF to 0,20,40,60,80 and 100% of baseline. * p<0.05 vs control, † p<0.05 vs contralateral kidney in the same period.

Figure 3

Change in cortical (A) and medullary (B) stiffness of stenotic (diamonds), contralateral (squares), and sham-operated control (triangles) kidneys, and correlation between changes in cortical stiffness and renal blood flow (RBF, C), during acute graded decrements in RBF from baseline (0% stenosis). Tissue elasticity declined only in the stenotic kidneys. * p<0.05 vs baseline (0 period), † p<0.05 vs contralateral kidney in the same period.

Figure 4

Left panel: Renal blood flow (A), cortical (B), and medullary (C) stiffness in chronic experimental renal artery stenosis (RAS) and normal control kidneys. Right panel: Representative coronal elastograms (a, d), axial magnitude images (b, e), and axial elastograms (c, f) from control (a-c) and chronic RAS (d-f) animals, showing the stenotic and contralateral kidneys. * p<0.05 vs control kidney, † p<0.05 vs contralateral kidney