Abstract 743 Evaluation of N-acetyl-ß-D-glucosaminidase and kidney injury molecule-1 as prognostic markers for acute kidney injury in patients with severe aortic valve stenosis and TAVR

Clin Res Cardiol (2023). https://doi.org/10.1007/s00392-023-02180-w
Evaluation of N-acetyl-ß-D-glucosaminidase and kidney injury molecule-1 as prognostic markers for acute kidney injury in patients with severe aortic valve stenosis and TAVR
A. Schober¹, C. Heidel¹, N. Roth¹, C. M. Xu², A. Schober¹, M. Schober³, U. Hubauer¹, M. Schlossbauer¹, A. Luchner⁴, L. S. Maier¹, K. Debl¹, C. G. Jungbauer¹
¹Klinik und Poliklinik für Innere Med. II, Kardiologie, Universitätsklinikum Regensburg, Regensburg; ²Klinik und Poliklinik für Innere Medizin II, Universitätsklinikum Regensburg, Regensburg; ³Nephrologie, Universitätsklinikum Regensburg, Regensburg; ⁴Klinik für Kardiologie, Krankenhaus Barmherzige Brüder Regensburg, Regensburg;
Background Patients with severe aortic valve stenosis and TAVR are at severe risk of suffering from acute kidney injury (AKI) due to the underlying disease and exposure to contrast medium. The aim of the present study was to examine the tubular markers N-acetyl-ß-D-glucosaminidase (NAG) and kidney injury molecule-1 (KIM-1) as predictors for acute kidney injuries in patients with severe aortic valve stenosis and TAVR. Methods 133 patients with severe aortic valve stenosis undergoing preparation for TAVR and TAVR were included in this prospective study. The tubular markers NAG and KIM-1 were measured in urine samples before TAVR, 6h and 24h after TAVR and the eGFR (crea) was measured on a regular basis. All biomarker concentrations were related to urinary creatinine to minimize dilutional bias. Results 39 (29,3%) patients suffered from an acute kidney injury after TAVR. Patients who suffered from acute kidney injury were significantly older and had more often a history of AKI (each p <0,05). However, there was no significant difference regarding hypertension, diabetes, and cardiovascular diseases in patients with and without acute kidney injury (p =n.s.). Patients with an AKI after TAVR had significant elevated levels of NAG before TAVR as well as 6h and 24h after TAVR (each p < 0,05). KIM-1 was not significantly different between patients without and with AKI (p=n.s.). ROC analysis showed an AUC of 0,65 for NAG, collected 6h after TAVR to predict an acute kidney after TAVR. Especially in patients with preserved renal function (eGFR > median) NAG was able to predict an AKI after TAVR with an AUC of 0,74 in ROC analyses. Furthermore, NAG proved itself as a significant, independent predictor for acute kidney injury in multivariate binary logarithmic regression analysis alongside STS-Score and history of AKI (each p <0,05). Age, stage of chronic kidney disease, arterial hypertension, CHD, sex, diabetes, PAOD and NTproBNP were also included, but were no significant predictors. In addition, in patients with and without AKI after TAVR, NAG showed a significant increase during the first 24h after TAVR, indicating a tubular damage during TAVR. However, this tubular damage did not always lead to an AKI. Conclusion In this study, NAG presented itself as putative predictor for an acute kidney injury in patients with severe aortic valve stenosis and TAVR in the short term. In addition, there was a significant increase in NAG during the first 24h after TAVR in patients with AKI after TAVR as well as in patients without AKI after TAVR, indicating a tubular damage. These findings could not be shown for KIM-1.
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