Renal artery involvement in acute aortic dissection: Prevalence and impact on renal atrophy in non-interventional treatment patients

Abstract

BackgroundTo evaluate the frequency of renal artery dissection (RAD) and renal hypoperfusion in aortic dissection (AD) and its effect on subsequent renal atrophy in patients who did not undergo therapeutic intervention. MethodsInitial CT data of 155 patients with acute AD (Stanford type A = 88, B = 67) were retrospectively analyzed. The false lumen statuses were patent (n = 94), partially thrombosed (n = 25), and completely thrombosed (n = 36) (also called as intramural hematoma (IMH)). Follow-up CT images of the surviving 122 patients (6–62.6 months, median, 28.9 months) were reviewed for analysis of sequential changes in renal volume. A regional decrease of ≧20 Hounsfield units in the renal cortex was defined as a renal hypo-enhancement sign (RHS). Simplified CT estimations of renal volume and estimated glomerular filtration rates (eGFR) were calculated. The generalized estimating equations (GEE) method was used to predict renal atrophy. ResultsFifty of the 122 patients presented with 59 RAD in the current study, and a positive RHS was noted in 33.9% (20/59) of these involved kidneys. GEE analysis showed hypertension, surgical treatment for AD, presence of RAD, and positive RHS as significant risk factors for renal atrophy. Patients with RHS had the most severe form of renal atrophy. The severity of renal atrophy was mildly correlated with GFR change (γ2 = 0.044, p < 0.001). ConclusionRenal atrophy in AD was predicted by the CT findings of RAD and RHS. The severity of renal atrophy was weakly reflected by eGFR.