Abstract:
Chronic glomerulonephritis (CGN) is associated with significant intrarenal hemodynamic alterations that correlate with disease
severity and structural changes. Doppler ultrasound studies reveal reduced blood flow velocities in interlobar and arcuate arteries in CGN patients,
with resistivity indices remaining elevated compared to controls [1]. These hemodynamic disorders are present in up to 94.9% of pediatric CGN
patients and manifest as decreased blood flow rates and increased vascular resistance in both renal and ocular vessels. Importantly, intrarenal he modynamic parameters correlate with histological findings. The pulsatile index and renal resistive index show positive correlations with glomerular
sclerosis percentage and crescent formation, while severe arteriolosclerosis significantly increases both indices [3]. Standard therapy alone provides
limited improvement in hemodynamic parameters, though anticoagulation with rivaroxaban may offer modest benefits at the interlobar artery
level [1]. Central hemodynamic indicators also differ between disease stages. Computational simulations further demonstrate that stagedependent
modulation of myogenic responsiveness and tubuloglomerular feedback underlies these central hemodynamic differences [3]
