Degree of Portal and Systemic Hemodynamic Alterations Predict Recurrent AKI and Chronic Kidney Disease in Patients With Cirrhosis.

The relevance of hemodynamic derangements on the incidence of recurrent acute kidney injury (AKI) and chronic kidney disease (CKD) in patients with cirrhosis is largely unknown. Consecutive patients with cirrhosis with a complete record of baseline hemodynamics were followed for identifying risk factors for the development of recurrent AKI and CKD by using negative binomial regression and competing risk analysis, respectively. Consecutive patients with cirrhosis (n = 2013, age 50.1 ± 11.8 years, 80% male, Child A:B:C percentage 13.7:52.9:33.4, and mean Child-Turcotte-Pugh score 8.6 ± 1.8) were enrolled, 893 (44.3%) of whom received beta-blockers, with 44.2% responders. Prior AKI was noted in 12.4% at enrollment. At a median follow-up of 379 (interquartile range: 68-869) days, AKI developed at a rate of 0.37 episodes per person-year, and 26% patients developed CKD. A lower mean number of AKI episodes (0.05 ± 0.25 vs. 0.42 ± 0.868;  < 0.001), CKD (subdistribution hazard ratio 0.74 [0.54-1.02]), and mortality (hazard ratio 0.21 [0.06-0.73]) were observed in beta-blocker responders. Albuminuria was an independent risk factor for recurrent AKI, CKD, and mortality ( < 0.05). Lower systemic vascular resistance index predicted hemodynamic response (odds ratio 2.04 [1.29-3.22]), cumulative AKI episodes (ratio of means 0.10 [0.08-0.14]), and development of CKD (subdistribution hazard ratio 0.70 [0.58-0.83]). Higher hepatic venous pressure gradient (≥17 mm Hg) predicted AKI episodes (ratio of means 1.76 [1.32-2.35]) but not CKD. High portal pressure and severe vasodilatation predispose patients with cirrhosis to repeated AKI episodes and development of CKD. Response to beta-blockers and therapies targeting the vasodilatory state could prevent frequent AKI and the risk of CKD development. Albuminuria could serve as an early marker of renal dysfunction in patients with cirrhosis.