Anatomically unbiased analysis of renal BOLD magnetic resonance images reveals disruption of corticomedullary gradient during chronic angiotensin II infusion

Oxygenation defects may contribute to renal disease progression but are difficult to define in vivo without invasive methods. BOLD MRI provides a non-invasive alternative but the signal is physiologically complex and data analysis often rely on region of interest selection, excluding biological information.

We present an analysis pipeline that compartmentalizes voxels into distinct clusters. In control rats, low R2* clustering was located predominantly within the cortex and higher R2* clustering within the medulla, consistent with a cortico-medullary oxygen gradient. An intravenous bolus of acetylcholine caused a transient reduction of the R2* signal in both clustered segments. This was nitric oxide dependent and temporally distinct from hemodynamic effects. Rats were then chronically infused with angiotensin II and rescanned three days later. Clustering demonstrated a disruption of the cortico-medullary gradient, producing less distinctly segmented mean R2* clusters. The acetylcholine-induced attenuation of the R2* signal was abolished by chronic angiotensin II infusion, indicative of reduced nitric oxide bioavailability

Our more inclusive analysis pipeline may be more robust in defining deficits in renal oxygenation than the absolute magnitude of R2* in small, manually selected and averaged regions of interest.