Association between CT-evaluated Poststenotic Dilatation in Human Renal Artery Stenosis and Kidney Release of MCP-1

Background Renal artery stenosis (RAS) can trigger the development of renal damage and poststenotic dilatation (PSD). However, the clinical relevance and mechanisms are ill-characterized. Purpose To characterize the mechanisms underlying PSD development distal to the site of RAS in humans. Materials and Methods Forty-nine individuals with RAS were prospectively consecutively recruited from October 2013 to September 2024. The characteristics of the stenosis, including the dilatation-diameter ratio (DDR), and single-kidney volumes, perfusion, and glomerular filtration rate (GFR) were measured at three-dimensional multidetector abdominal CT. Additional characteristics included stenotic kidney (STK) oxygenation (blood oxygen level-dependent MRI), cytokine levels in the STK renal vein (RV) and inferior vena cava (blood sampling), and measured GFR (iothalamate clearance). Seven participants subsequently underwent percutaneous transluminal renal angioplasty (PTRA). Data were analyzed with Spearman correlation and linear regression. Results Of 49 participants with RAS (median age, 73 years [IQR, 67-75 years]; 28 male participants), age, blood pressure, measured GFR, and STK oxygenation were comparable between participants with PSD (n = 31) and participants without PSD (n = 18), but participants with PSD had a lower median STK cortical volume. DDR positively correlated with the STK RV levels of neutrophil gelatinase-associated lipocalin, interferon-γ, and monocyte chemoattractant protein-1 (MCP-1), which were elevated in participants with PSD versus participants without PSD or in the STK RV versus the IVC (all P < .05). The regression coefficient between STK RV MCP-1 level and DDR was 0.813 (95% CI: 0.328, 1.298; P = .002) in an unadjusted model and 0.889 (95% CI: 0.246, 1.532; P = .009) after multivariable adjustment for potential confounders; that is, each 1-ng/mL increase in STK RV MCP-1 level was independently associated with a 0.889-unit DDR increase. DDR also correlated positively with urinary protein level (r = 0.33; P = .04) and negatively with estimated GFR (r = -0.51; P = .004), but there was no evidence of a correlation of DDR with renal hemodynamics, arterial morphologic features, or blood flow velocity at Doppler US. PTRA did not improve estimated GFR but did induce PSD regression, the extent of which correlated negatively with STK RV MCP-1 level. Conclusion PSD, as evaluated at abdominal CT, may be associated with STK damage and the release of MCP-1. Clinical trial registration nos. NCT02266394 and NCT04508049 © RSNA, 2026 Supplemental material is available for this article.