Renal failure · 2025
Contrast-enhanced ultrasound and elastography predict histopathology and recovery in acute kidney injury.
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Wang Xiangyu, Liu Jiajia, Chen Luzeng, Su Tao
Аннотация
PURPOSE: Acute kidney injury (AKI) progression involves complex microcirculatory and structural changes poorly captured by conventional metrics. This study investigates contrast-enhanced ultrasound (CEUS) and shear wave elastography (SWE) to evaluate hemodynamic redistribution and fibrosis in AKI patients.
METHODS: Prospective cohort study of 16 biopsy-confirmed tubulointerstitial (TI) nephritis patients and matched controls. We aim to explore the potential correlation of CEUS-SWE derived parameters (peak intensity (PI), rise time (RT), time to peak (TTP), and shear wave velocity (SWV)) with renal histopathology and 3-month outcomes (renal recovery: estimated glomerular filtration rate (eGFR) ≥45 mL/min/1.73 m2).
RESULTS: CEUS revealed stage-specific perfusion patterns: milder AKI (eGFR >25 mL/min/1.73 m2) showed medullary hyperemia (cortical-to-medullary PI ratio: 0.80 ± 0.24 vs. 1.12 ± 0.18 in controls; p < .05), a potential compensatory response to medullary hypoxia. Cortical-to-medullary ratios of PI, RT, and TTP significantly correlated with chronic TI injury (r = 0.501/-0.576/-0.547), reflecting capillary rarefaction's role in disease severity and fibrosis. Patients with severe renal dysfunction (eGFR <25 mL/min/1.73 m2) exhibited elevated renal artery resistive indices. In stage 3 AKI, PI ratio demonstrated positive correlation with glomerulosclerosis (r = 0.690, p = .03), cortical RT/TTP correlated inversely with chronic TI injury (r = -0.807/-0.821, p = .005/.004), reflecting cortical hypoperfusion and impaired compensatory perfusion redistribution during AKI. Prognostically, patients with lower PI ratio (indicating preserved medullary hyperemia) experienced better renal recovery (64.3% achieving eGFR ≥45 mL/min/1.73 m2; p = .02). SWE-derived SWV declined with AKI severity (p < .05) but lacked fibrosis specificity due to edema/necrosis confounders.
CONCLUSIONS: CEUS-derived PI ratios quantify microcirculatory dysfunction in AKI, correlating with chronic TI injury and predicting recovery.
METHODS: Prospective cohort study of 16 biopsy-confirmed tubulointerstitial (TI) nephritis patients and matched controls. We aim to explore the potential correlation of CEUS-SWE derived parameters (peak intensity (PI), rise time (RT), time to peak (TTP), and shear wave velocity (SWV)) with renal histopathology and 3-month outcomes (renal recovery: estimated glomerular filtration rate (eGFR) ≥45 mL/min/1.73 m2).
RESULTS: CEUS revealed stage-specific perfusion patterns: milder AKI (eGFR >25 mL/min/1.73 m2) showed medullary hyperemia (cortical-to-medullary PI ratio: 0.80 ± 0.24 vs. 1.12 ± 0.18 in controls; p < .05), a potential compensatory response to medullary hypoxia. Cortical-to-medullary ratios of PI, RT, and TTP significantly correlated with chronic TI injury (r = 0.501/-0.576/-0.547), reflecting capillary rarefaction's role in disease severity and fibrosis. Patients with severe renal dysfunction (eGFR <25 mL/min/1.73 m2) exhibited elevated renal artery resistive indices. In stage 3 AKI, PI ratio demonstrated positive correlation with glomerulosclerosis (r = 0.690, p = .03), cortical RT/TTP correlated inversely with chronic TI injury (r = -0.807/-0.821, p = .005/.004), reflecting cortical hypoperfusion and impaired compensatory perfusion redistribution during AKI. Prognostically, patients with lower PI ratio (indicating preserved medullary hyperemia) experienced better renal recovery (64.3% achieving eGFR ≥45 mL/min/1.73 m2; p = .02). SWE-derived SWV declined with AKI severity (p < .05) but lacked fibrosis specificity due to edema/necrosis confounders.
CONCLUSIONS: CEUS-derived PI ratios quantify microcirculatory dysfunction in AKI, correlating with chronic TI injury and predicting recovery.