ABC | Volume 113, Nº6, December 2019

Original Article Impact of Transcatheter Aortic Valve Implantation on Kidney Function Rita Calça, 1 Rui C. Teles, 2 P atrícia Branco, 1 Augusta Gaspar, 1 João Brito, 2 Tiago Nolasco, 3 Manuel D. Almeida, 2 José P. Neves, 3 Miguel Mendes, 2 Domingos S. Machado, 1 André Weigert 1 Nephrology department, Hospital de Santa Cruz, Centro Hospitalar de Lisboa Ocidental, 1 Lisboa – Portugal Cardiology department, Hospital de Santa Cruz, Centro Hospitalar de Lisboa Ocidental, 2 Lisboa – Portugal Cardiotoracic Surgery department Hospital de Santa Cruz, Centro Hospitalar de Lisboa Ocidental, 3 Lisboa – Portugal Mailing Address: Rita Calça • Hospital de Santa Cruz - Av. Prof. Dr. Reinaldo dos Santos, 27-29. Postal Code 2790-134 Carnaxide - Portugal E-mail: arrcalca@gmail.com Manuscript received November 23, 2018, revised manuscript February 06, 2019, accepted March 10, 2019 DOI: https://doi.org/10.36660/abc.20180356 Abstract Background: Chronic kidney disease (CKD) is frequently present in patients with aortic valve disease. Decreased kidney perfusion as a consequence of reduced cardiac output may contribute to renal dysfunction in this setting. Objective: Given the potential reversibility of kidney hypoperfusion after valve repair, this study aimed to analyze the impact of percutaneous transcatheter aortic valve implantation (TAVI) on kidney function. Methods: We performed a retrospective analysis of 233 consecutive patients who underwent TAVI in a single center between November 2008 and May 2016. We assessed three groups according to their baseline estimated glomerular filtration rate (eGFR) (mL/min/1.73 m 2 ): Group 1 with eGFR ≥ 60; Group 2 with 30 ≤ eGFR < 60; and Group 3 with eGFR < 30. We analyzed the eGFR one month and one year after TAVI in these three groups, using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula to calculate it. Results: Patients from Group 1 had a progressive decline in eGFR one year after the TAVI procedure (p < 0.001 vs. pre-TAVI). In Group 2 patients, the mean eGFR increased one month after TAVI and continued to grow after one year (p = 0.001 vs. pre-TAVI). The same occurred in Group 3, with the mean eGFR increasing from 24.4 ± 5.1 mL/min/1.73 m 2 before TAVI to 38.4 ± 18.8 mL/min/1.73 m 2 one year after TAVI (p = 0.012). Conclusions: For patients with moderate-to-severe CKD, kidney function improved one year after the TAVI procedure. This outcome is probably due to better kidney perfusion post-procedure. We believe that when evaluating patients that might need TAVI, this ‘reversibility of CKD effect’ should be considered. (Arq Bras Cardiol. 2019; 113(6):1104-1111) Keywords: Aortic Valve Stenosis/complications;renal Insufficiency,Chronic; Calcinosis; Renal Dialysis; Diabetes Mellitus; Cardyomyopathies; Hypertension. Introduction Since Bright 1 first described the association between chronic kidney disease (CKD) and heart disease in 1836, many epidemiological studies have confirmed and extended this finding. With higher life expectancy, the prevalence of valvular heart disease, such as aortic valve disease, is increasing, and patients needing intervention are older and display multiple comorbidities. 2 Surgical intervention is the most effective therapeutic option, but transcatheter aortic valve implantation (TAVI) has become an important treatment choice for inoperable or high-risk patients. 2-4 Many studies show poor short- and long-term outcomes in patients with CKD submitted to TAVI. 5,6 Other studies on this field focus on acute kidney injury (AKI) after TAVI, showing that AKI is not merely an independent predictor of adverse outcome but also predisposes to the development of CKD. Cases of AKI requiring dialysis have a poor prognosis (50% in-hospital mortality), and a significant proportion of patients progress to end-stage kidney disease. 7–9 Aortic valve disease is frequently seen in CKD patients 10 due to progressive and accelerated leaflet calcification, a well‑known complication of kidney failure. The key modulators in this field have not been totally identified, but might include calcification inhibitors (e.g., fetuin-A and matrix Gla protein), calcification promotors (e.g., hyperphosphatemia, calcium-phosphate product, parathyroid hormone), and leptin. On the other hand, long-standing aortic stenosis may contribute to CKD by impairing forward blood flow from the heart, causing chronic hypoperfusion and resulting in organ damage, and by increased renal venous pressure associated with right-sided heart failure. 11,12 Hypothetically, these pathological CKD mechanisms can be reversed after correction of aortic valve stenosis. Little is known about the reversibility of CKD after aortic valve replacement. The dynamic changes in kidney function after TAVI have not been described and are not fully understood. Given the potential reversibility of the pathological CKD mechanism after the correction of aortic valve disease, this study aimed at analyzing the variations in kidney function after TAVI. 1104